Neuro Exam 1

Front 1

receptor potential

Back 1

in response to mechanical, thermal, chemical and light stimulus, is a passive response, ion channels open in response to touch in receptor potential

Front 2

synaptic potential

Back 2

in response to a neurotransmitter, ion channels also involved in the synaptic potential, a passive response

Front 3

passive response

Back 3

small response, not conducted very far

Front 4

action potential

Back 4

large amplitude, conducted along the length of the entire nerve, an active response

Front 5

active response

Back 5

bigger response than the passive response, conducted and goes the entire length of the entire cell

Front 6

charge

Back 6

a basic property of matter in units of coulombs, the possession of net positive or negative charge by ions, for examples Na+, K+, Ca2+, and Cl-

Front 7

current

Back 7

the movement of charge in coulombs/sec = amps, the movement of charge into and out of cells (across the plasma membrane), flux of charge

Front 8

inward current

Back 8

is + charge entering the cell or – charge leaving the cell

Front 9

outward current

Back 9

is + charge leaving the cell or – charge entering the cell

Front 10

voltage

Back 10

voltage difference between two points is strictly the work (force * distance) needed to move a test charge from one point to another, we can ignore the distance and think of a voltage as a force acting to push charges, a transmembrane voltage pushes charges across a membrane

Front 11

potential

Back 11

another word for voltage

Front 12

membrane potentials

Back 12

difference in electrical potential between the inside and outside of the cell

Front 13

what happens to membrane potential with a stimulus

Back 13

INC the amplitude of the stimulus INC the number of the action potentials, the amplitude of the stimulus is encoded in the frequency of the action potentials, the amplitude of each action potential is not changed much

Front 14

resting potential

Back 14

unstimulated, resting neurons have 40 to 90 mV inside, negative value

Front 15

stimulating electrode

Back 15

used to alter the membrane potential by injecting charge into the cell

Front 16

initiation of passive responses

Back 16

result from injection of negative charge and small amounts of positive charge, amplitude typically nearly linearly related to the amount of charge injected, the amplitude DEC with distance from the site of injection

Front 17

initiation of action potential

Back 17

result from injection of larger amounts of positive charge, amplitude is independent of the amount of current, the action potential is conducted along the length of the entire nerve

Front 18

initiation transmembrane potentials

Back 18

result from gradients of permenant ions (i.e. ions that can cross the membrane), the permeability of the membrane to individual ions

Front 19

permeability

Back 19

is a measure of the ease of movement of a solute molecule across a membrane, determined by ion channels, if a lot of Na+ channels are open, then Pna will be high

Front 20

conductance

Back 20

another measure of the ease of movement of a solute molecule across a membrane

Front 21

how are ion gradients established

Back 21

pumps use energy to create ion gradients (Na-K ATPase), created by active transport, main ones are the Na+/K+ pump and the Ca2+ pump

Front 22

ion gradients across the plasma membrane

Back 22

1. K+ (140 intracellular, 5 extracellular, -90 potential)
2. Na+ (5-15 intracellular, 145 extracellular, +60 to +90 potential)
3. Cl- (4-30 intracellular, 110 extracellular, -88 to -35 potential)
4. Ca2+ (0.0001 intracellular, 1-2 extracellular, +100 potential)

Front 23

Nernst equation

Back 23

equation that allows one to use gradient of ions to measure voltage
E = RT/zF * ln [X]o/[X]i

Front 24

goldman-hodgkin-katz equation

Back 24

states that the contribution of an ion gradient to potential of the membrane is weighted by the permeability of the cell membrane to that ion
Em = 58 log (Pk [K]o + Pna [Na]o + Pcl [Cl]i) / (Pk [K]i + Pna [Na]i + Pcl [Cl]o)
***Cl- is upside down because of the z value, Ca2+ is divalent and is not used (putting it in would cause an explosion

Front 25

ion channels

Back 25

transmembrane proteins that provide a pathway for rapid movement of ions across the membrane (can be gated and are selective)

Front 26

ion channel gating

Back 26

channels typically can be opened and closed by specific stimuli including voltage, ligands, heat, light and mechanically, opening and closing of channels INC and DEC membrane permeability

Front 27

ion channel selectivity

Back 27

many ion channels are specific for a single ion or class of ions, many are less selective, voltage gated

Front 28

resting membrane

Back 28

is relatively highly permeable to K+, typically relatively close to Ek, at rest Pk > Pna, during an action potential PNa > Pk to cause depolarization, then Pk > Pna to cause repolarization, this is all done by opening and closing channels

Front 29

encoding stimulus intensity

Back 29

the intensity of a stimulus (natural or artificial) is encoded in the frequency of action potentials, commonly the freq. INC with the intensity of the stimulus but the response can be complex, properties of the ion channels determine the encoding, neurons can alter their encoding by altering the opening and closing of their channels (this is called learning)

Front 30

apamin (bee venom)

Back 30

blocks a specific type of K+ channel

Front 31

shapes of action potentials

Back 31

the shape of the action potential will influence the maximum frequency at which a neuron can generate action potentials, the shape will influence the amount of Ca2+ that enters during an action potential (or a train of action potentials) and this will influence the amount of transmitter that is released

Front 32

voltage-gated Ca2+ channels

Back 32

in many cells, voltage-gated Ca2+ channels open during depolarization, Ca2+ enters the cell and triggers biochemical events: release or neurotransmitter or hormone, contraction of muscle, the longer the depolarization, the more Ca2+ enters

Front 33

sodium pump

Back 33

has little or no effect on the amplitude or time course of the action potential, it generates the Na+ and K+ gradients that produce Ena and Ek, once these are generated the pump’s contribution to the action potential is done

Front 34

channelopathies

Back 34

disorders due to mutations in genes encoding for ion channels, typically each channel gene has multiple mutations, there are no rules for channelopathies, mutations giving rise to similar syndromes can be scattered all over the channel sequence (episodic ataxia due to mutations in the Ca2+ channel gene), it is generally impossible to link symptoms to a location on a channel or even to a particular channel

Front 35

passive conduction

Back 35

in the absence of activity by ion channels a depolarization will be conducted with decrement over a short distance, if there are no changes in membrane permeabilities, a depolarization or a hyperpolarization will be conducted for a relativelyl short distance (<1 or 3 mm) with decrement, not regenerative and does not go very far

Front 36

active conduction

Back 36

if the right ion channels are activated they will boost the signal along the length of the neuron, APs are conducted long distances without decrement, also in skeletal, cardiac, and smooth muscle, if there are voltage-gated Na+ channels an AP can be conducted for long distances (>100 m) essentially without decrement, myelination and larger axon diameter will speed conduction

Front 37

conduction of membrane potential

Back 37

speed matters, larger cells conduct faster, myelinated cells conduct faster, the AP essentially jumps from node to node (salutatory conduction)

Front 38

dendrites

Back 38

there are voltage-gated conductances in dendrites

Front 39

Luigi Galvani

Back 39

showed that electrical stimulation of muscular tissue produces contraction and force

Front 40

Guillaume Ducheene and the muscles of facial expression

Back 40

He applied electric stimulation to intact skeletal muscles, systematically mapped out functions of nearly every facial muscle, discovered that the muscles around the eyes are only active during a genuine smile, an insincere smile involves only the muscles of the mouth

Front 41

tendon reflex

Back 41

demonstrates reciprocal innervation in CNS, excites enxtensor and inhibits flexor, an AP in the sensory neuron produces a depolarizing response (an EPSP) in the extensor motor neuron, an AP in the interneuron produces a hyperpolarizing response (an IPSP) in the flexor motor neuron

Front 42

posture

Back 42

is not controlled by the brain, but rather the spinal cord, it is purely due to reflexes

Front 43

muscle spindle

Back 43

senses stretch

Front 44

junctional folds

Back 44

deep foldes in the cell membrane of the muscle fiber, beneath which the sarcoplasm contain numerous mito

Front 45

terminal swelling of the motor axon

Back 45

have abundant neurosecretory granules (acetylcholine) and mito

Front 46

curare

Back 46

binds to ACh receptors (nicotinic receptors)

Front 47

end plate potential

Back 47

EPP, has a depolarizing synaptic potential at the end plate, postsynaptic potential induced at the NMJ by the opening of the nicotinic receptors, is not an AP, but it partially depolarizes the membrane and can initiate an AP, not continuous, but quantized, MEPP is the fundamental unit of the EPP, undergoes passive (electrotonic spread), spreads and decays, not regenerative like the AP

Front 48

end plate current

Back 48

EPC, has an inward synaptic current at the end plate

Front 49

MEPPS

Back 49

miniature end plate potentials, spontaneous depolarizations of consistent amplitude in the absence of nerve stimulation, very small, brief depolarizations which occur even when there has been no AP in the nerve, about 150 MEPPS = 1 EPP, spontaneous MEPP can resemble the evoked EPP, MEPP due to spontaneous vesicles from the presynaptic membrane

Front 50

stastical relationship between MEPPs and EPP

Back 50

MEPPs are clustered around 0.4 mV in amplitude, for the evoked EPPs, can get 5X the amplitude of the MEPP, some at 0.4, 0.8, 1.2 or 1.6

Front 51

neurotransmitter release

Back 51

is also qantized

Front 52

rise in presynaptic Ca2+

Back 52

is essential for neurotransmitter release, if inject Ca2+ buffer in the presynaptic terminal, then buffer binds to Ca2+ and when stimulate an AP it blocks the response in the postsynaptic cell, showing Ca2+ is necessary in the release of vesicles for transmission

Front 53

location of Ca2+ channels in the presynaptic membrane

Back 53

Ca2+ channels in the presynaptic membrane line up where the vesicles are, Ca2+ channels also line up with the nicotinic receptors on the postsynaptic terminal

Front 54

transmission across the NMJ

Back 54

get an AP in the nerve, passes id down the branches and depolarizes the nerve terminal, Ca2+ comes in and causes vesicle fusion, contents diffuse, bind to nicotinic receptors and activate Na+ channels to open and generate an AP

Front 55

spread of Na+ AP from end plate region

Back 55

if a stimulating pipette is placed over the Z line where the T-tubules are then get contraction, if over the middle of the sarcomere then there is no contraction

Front 56

coupling of Na+ AP to Ca2+ release and to contraction

Back 56

1. Na+ AP depolarizes T-tubule membrane
2. this depolarization causes voltage sensitive dyhidropyridine receptors to change conformation of ryanodine receptors
3. Ca2+ is released from ryanodine sensitive stores
4. released Ca2+ binds to troponin, revealing cross-bridge binding sites on actin molecules

Front 57

SR

Back 57

stores Ca2+

Front 58

ryanodine receptor

Back 58

allows Ca2+ to flow out of the sarcoplasmic spaces where it can activate the filament

Front 59

T-tubule

Back 59

where AP propagates, causes the ryanodine receptors to change their conformation to depolarization, they unplug and allow Ca2+ to flow out of the sarcoplasmic spaces

Front 60

excitation-contraction coupling

Back 60

shows that when an AP is fired, Ca levels don’t rise until a small delay

Front 61

heart and the discovery of chemical neurotransmission via ACh

Back 61

two hearts are placed in two separate beakers connected by a tube that allows for the transfer of solution from heart 1 to heart 2, heart 1 has a vagus nerve attachment while heart 2 has no vagus nerve attachment, when stimulate with the vagus nerve then there was a dec in the beats in heart 1, then shortly thereafter a decrease in heart 2

Front 62

synthesis and breakdown of acetylcholine

Back 62

the synthesis of ACh from choline and acetyl CoA is derived from pyruvate generated by glycolysis, synthesized by the enzyme choline acetyltransferase, choline is transported into the terminal via a Na+ dependent transporter, ACh is loaded into synaptic vesicles by a vesicular transporter, after release, ACh is rapidly metabolized acetylcholinesterase, choline is transported back into terminal

Front 63

nicotini receptors

Back 63

blocked or antagonized by curare, binds nicotine, are ligand gated ion channels, the reversal potential of the receptors implies that it is a non-selective cation channel

Front 64

muscarini receptors

Back 64

also bind ACh, blocked or antagonized by atropine, a G-protein coupled receptor

Front 65

strucuter of the ligand gated nicotinic ACh receptor

Back 65

has two alpha, a beta, gamma and delta subunit

Front 66

sequence of events in AP propagation

Back 66

1. an AP arrives at the end of a motor neuron at the NMJ
2. depolarization causes Ca2+ entry into nerve terminal and vesicle mobilization
3. this causes the release of the neurotransmitter acetylcholine
4. acetylcholine diffuses across synaptic cleft and binds to nicotini receprot on sarcolemma
5. activation of nicotinic receptors generates EPP
6. EPP initiates an AP in the muscle cell membrane (sarcolemma)
7. ACh broken down by acetylcholinesterase into choline plus acetate, choline reuptake into nerve terminal
8. this AP is carried quickly into the large muscle cell by invaginations in the cell membrane called T-tubules
9. the AP causes depolarization of the T-tubule membrane that opens ryanodine receptor on the SR
10. activation of ryanodine receptors leads to the store release of calsium into the myofribirls
11. Ca2+ causes tropomyosin to be displaced uncovering myosin binding sites on actin
12. myosin cross bridges can now attach and the cross bridge cycle can take place
13. relaxation is the reverse of these steps

Front 67

vesicle synaptic proteins

Back 67

synaptobrevin and synaptotagmin on the vesicle, SNAP-25 and snytaxin on the cell membrane, steps of endocytosis
1. vesicle docks
2. entering Ca2+ binds to synaptotagmin
2. SNARE complexes form to pull membranes together
3. entering Ca2+ binds to synaptotagmin
4. Ca2+ gound synaptotagmin catalyzes membrane fusion

Front 68

diseases associated with exocytosis and endocytosis

Back 68

various steps in the exocytosis and endocytosis cycle are targets for disease that is associated with weakness and fatigability of skeletal muscle, botulinum and tetanus toxins affect SNARE proteins involved in vesicle fusion, LEMS attacks presynaptic Ca2+ channels

Front 69

Lambert-Eaton myasthetnic syndrome (LEMS)

Back 69

an autoimmune disease, complication in patients with certain kinds of cancer, recordings from muscle biopsies suggest amplitude of EPPs is reduced but amplitude of MEPPs are normal, blood of such patients high in antibodies to Ca2+ channels, evidence points to an immune defect that leads to a loss of voltage gated presynaptic Ca2+ channels, removal of antibodies reduces muscle weakness, caused by antibodies to the Ca2+ channel in the nerve terminal resulting in DEC release of quanta of acetylcholine, there is a very strong association with neoplasms, particularly with bronchus carcinoma, symptoms are proximal weakness, often with autonomic features, reflexes are absent

Front 70

myasthenia gravis

Back 70

autoimmune disease of neuromuscular synapses, seen twice freq in women, there is a peak incidence in the 2nd and 3rd decades and a second in the 6th and 7th, look at the slide on lecture 2, EPPs are down because there are not so many nicotinic receptors

Front 71

botulinum toxin

Back 71

prevents release of quanta, Clostridium botulinum, hydrolyzes the synaptic proteins synaptobrevin (Bot. toxins B, D, F, G), syntaxin (Bot. toxin C), SNAP-25 (Bot toxin A, C, and E), inhibits ACh release in NMJs and other synapses, flaccid type of paralysis, usually occurs in people who have eaten improperly preserved foods, the toxin can be destroyed by heating, causes neuromuscular weakness, extreme cases respiratory failure due to paralysis of diaphragm

Front 72

tetanus

Back 72

Clostridium tetani, synaptobrevin is the synaptic protein hydrolyzed, inhibits glycine and GABA release in CNS, spastic type of paralysis, occurs when an open wound is exposed to the bacteria, blocks release of inhibitory neurotransmitters form interneurons, loss of synaptic inhibition on spinal motorneurons, results in hyper-excitation of skeletal muscle and tetanic contraction

Front 73

aminoglycosides (antibiotics) and excess Mg2+

Back 73

interfere with Ca2+ mediated release of quanta,

Front 74

black widow spider venom

Back 74

causes a complete depletion of ACh, there is initial spasms and then paralysis

Front 75

cobratoxins

Back 75

bind specifically to the ACh receptor

Front 76

tetanus toxin and botulinum toxin in common

Back 76

work by cleaving SNARE proteins involved in fusion of synaptic vesicles with the presynaptic membrane, inhibit transmitter release, lowering transmitter concentration in the synaptic cleft, produced by anaerobic soil bacteria, both protease enzymes

Front 77

BOTOX

Back 77

works by physiologically weakening facial muscles beneath the skin that are related to expression lines, contraction of these muscles results in wrinkles, BOTOX blocks the impulses from the nerve to the facial muscles thereby relaxing them, the result is that the pull of the underlying facial muscles relax causing the skin to flatten, results in smooth look

Front 78

neurotoxins

Back 78

poisonous insects, shell fish, plants and venomous animals are widespread in nature, many toxins they produce affect the nervous system, especially the neuromuscular junction since this paralyzes prey, given the essential role of ACh in mediating neuromuscular transmission in many species it is not surprising that many toxins affect this synapse

Front 79

alpha-bungarotoxin

Back 79

one of the many peptides that make up the venom of the banded krait, paralyses its prey by blocking neuromuscular neurotransmission by irreversibly binding to nicotinic ACh receptors thereby preventing ACh from opening channels on the postsynaptic membrane, other snake toxins that block ACh receptors are cobra and sea snake peptide erabutoxin

Front 80

conotoxins

Back 80

these peptides, which are produced by fish hunting marine cone snails, block various Ca2+ channels, Na+ channels, glutamate receptors and ACh receptors

Front 81

curare

Back 81

south American arrow head poison used to immobilize prey, it is derived from tree bark Chondodendrum tomentosu

Front 82

anti-cholinesterase nerve gases

Back 82

include tabun (GA), soman (GD) and sarin, tabun is an organophosphate type compound that was developed between WWI and II, it can be easily absorbed through the skin, by means of inhalation or ingestion, they symptoms of the poisoning are similar, regardless of the route of introduction, include runny nose, coma, death, drooling, nausea…

Front 83

atropine sulfate

Back 83

primary treatment for Tabun and several other nerve agents, it is commonly carried in auto-injectors by military personnel in dosages of 1-2 mgs, however in many cases, massive doses may be necessary to revers the effects of the anticholinesterase agents, freq. 20-40 mgs of atropine may be necessary

Front 84

pralidoxime chloride

Back 84

the 2nd drug that is used in the treatment of nerve gas poisoning, used to reactivate the acetylcholinesterase that is bound by the nerve agent

Front 85

What are the integral components of defense reaction in animals?

Back 85

1. INC blood flow through skeletal muscle but DEC blood flow through viscera and skin
2. INC blood pressure and heart rate
3. pupil dilation
4. sweat gland activation
5. activation of piloerector muscles (hair stands on end)
6. activation of adrenal medulla (adrenalin) and cortex (corticosteroids)

Front 86

What is the purpose of the ANS?

Back 86

with the help of the endocrine system, it regulates the activities of nearly all the tissues throughout the body, and through neural reflex arcs modulates or controls the actions of all the body’s major organ systems including the CV, reproductive, urinary, digestive, respiratory and visual system

Front 87

What activities of the body is the ANS responsible for regulating?

Back 87

body temperature (control of skin), endocrine and exocrine secretions, cell metabolism, total body water, electrolyte balance and influences the immune system

Front 88

What are the two anatomically distinct, mutually antagonistic systems of the ANS?

Back 88

the sympathetic and parasympathetic nervous systems, sympathetic stimulates the adrenal medulla to release epinephrine and norepinephrine

Front 89

Who were the researchers who first rationalized the visceral motor system (ANS)?

Back 89

Walter Gaskell and John Langley

Front 90

What is the function of autonomic ganglia?

Back 90

they harbor the primary visceral motor neurons

Front 91

What was the importance of Walter Cannon to ANS research?

Back 91

coined homeostasis, lay the basis for neuronal plasticity through understanding the effects of denervation in the ANS, used X-rays to study digestive processes

Front 92

Why is it important to have an understanding of the ANS?

Back 92

1. the accessibility of ANS structures has meant that many of our ideas about synaptic transmission and drug action were first developed by studying their effects on ANS effectors, many of these ideas are directly transferable to the CNS since many neurotransmitters are common to both systems
2. autonomic nerves are routinely cut to alleviate several conditions such as peripheral vascular disease, they are severed by trauma or during routine surgery and organ transplantation
3. disease affecting ANS systems are often serious and contribute to morbidity and mortality

Front 93

Describe what the drugs that work on the ANS do.

Back 93

they either mimic or block the ANS neurotransmitters, used to treat hypertension, asthma, impotence and constipation, but these drugs do have a variety of side effects

Front 94

What does bethanochol do?

Back 94

it is a cholinergic agonist, used in reflux disease to INC lower esophageal sphincter pressure, side effects include abdominal cramps, skin flushing, sweating, lacrimation, salivation, bronchioconstriction, and urinary urgency

Front 95

Is the ANS completely involuntary?

Back 95

no, some conscious control can be exerted over some ANS controlled organs such as the bladder and penis, can also train oneself to control BP, blood flow, body temp

Front 96

What does the SNS and PNS do during sexual arousal?

Back 96

1. erection comes from the PNS and requires a calm state
2. SNS then takes over and when the PNS is turned off ejaculation occurs
3. erectile dysfunction (ED) can be stress induced, since one needs to be calm for erection, during premature ejaculation a switch from PNS to SNS occurs too quickly

Front 97

What are the autonomic neurons (visceral efferent neurons)?

Back 97

neurons lying outside the CNS and the preganglionic neurons in the lateral horns of the spinal cord, exceptions are sensory neurons which have their cell bodies in DRG (cranial sensory ganglia), carry neural impulses to cardiac muscle, smooth muscle and glandular epithelium

Front 98

Where is the preganglionic input from nerve cell bodies located for the sympathetic neurons?

Back 98

located in thoracic and lumbar segments of spinal cord (T1-L2 or L3)

Front 99

Where is the preganglionic input from nerve cell bodies located for the parasympathetic neurons?

Back 99

located in the brainstem (the cranial parasympathetic outflows) or in the sacral levels of the spinal cord (the sacral parasympathetic outflow, S2-S3)

Front 100

Where is the preganglionic input from nerve cell bodies located for the enteric neurons?

Back 100

most have no direct preganglionic input from the CNS, consist of not only efferent (motor neurons) but also contain interneurons and afferent (or sensory) neurons

Front 101

What are the sympathetic postganglionic axons?

Back 101

are relatively long with their cell bodies situated at some distance from their effectors

Front 102

What are the parasympathetic postganglionic axons?

Back 102

have long axons which project to postganglionic parasympathetic neurons situated relatively close to or on the innervated target tissue

Front 103

What type of innervation do blood vessels get?

Back 103

only get a sympathetic innervation, regulate blood vessel diameter (vasoconstriction)

Front 104

What are the neurontransmitters, in general, for the parasympathetic and sympathetic systems?

Back 104

parasympathetic-acetycholine, sympathetic-epinephrine

Front 105

What are the different ganglia for the SNS?

Back 105

superior cervical, stellate (combination of the inferior cervical and uppermost thoracic), celiac, superior mesenteric, and inferior mesenteric ganglions

Front 106

What do the prevertebral ganglia innervate?

Back 106

1. celiac ganglia-stomach
2. superior mesenteric ganglia-small intestine, gall bladder, and pancreas
3. inferior mesenteric ganglia-large bowel and bladder
4. pelvic ganglia-bladder, large bowel, rectum, urethra and penis

Front 107

What is the purpose of the enteric nervous system (ENS)?

Back 107

controls intestinal motility and secretion of water and electrolytes

Front 108

Where is the ENS located?

Back 108

it lies within the gut wall and contains as many neurons as the spinal cord (~1 billion) capable of own reflex activity since it continas sensory neurons, interneurons and motor neurons

Front 109

What is the purpose of the myenteric (Auerbach’s) plexus?

Back 109

it regulates motility (gut movements), motor functions

Front 110

What is the purpose of the submucous (Meissner’s) plexus?

Back 110

regulates secretion of water and electrolytes across intestinal epithelium, sensory functions, chemical monitoring and glandular secretion

Front 111

Describe the parsympathetic innervation of the GI tract

Back 111

vagal parasympathetic fibers make widespread connections within the ENX, 90% of the 50,000 vagal fibers are afferent, 5,000 efferent fibers innervate > 10^8 enteric neurons, GI tract gets vagal and pelvic pathways from pre-ganglionic efferent neurons originating in the brainstem and sacral spinal cord respectively

Front 112

Describe the efferent fibers of the ENS.

Back 112

they are thin that conduct at the <2.5 m/s range, make synaptic connections with post-ganglionic neurons which are part of the ENS, Ach is the main transmitter and acts via nicotinic receptors, although in some species and regions muscarinic receptors may also be involved

Front 113

Where are the preganglionic sympathetic neurons located

Back 113

in the lateral horns of the gray matter

Front 114

Describe the sympathetic innervation of the head and neck.

Back 114

the axons of preganglionic neurons in the upper thoracic region of the spinal cord enter the sympathetic chains at the same level and then ascend the chain to synapse with sympathetic postganglionic neurons in important paravertebral ganglia (superior, middle and inferior cervical ganglia) in the neck

Front 115

Describe the sympathetic innervation of the pelvic organs

Back 115

preganglionic axons descend the chains to synapse with postganglionic neurons in sacral ganglia

Front 116

What do the paravertebral ganglia provide sympathetic innervation to?

Back 116

blood vessels, eye and lacrimal glands, heart and airways (stellate ganglion), salivary glands, sweat glands and hair follicles

Front 117

What nuclei give presynaptic parasympathetic neurons?

Back 117

Edinger-Westphal, superior and inferior salivatory, visceral motor division of the nucleus ambiguous, dorsal motor nucleus, sacral parasympathetic pelvic ganglia

Front 118

What is the location and purpose of the Edinger-Westphal (accessory oculomotor) nucleus?

Back 118

found in the midbrain and innervates the ciliary ganglion via oculomotor nerve (III) to regulate diameter of pupil in response to light

Front 119

What is the location and purpose of the superior and inferior salivatory nuclei?

Back 119

found in the pons and medulla, innervate, via facial nerve (VII) and glossopharyngeal nerve (IX), the salivary and tear glands mediating salivary secretion and production of tears

Front 120

what is the location and purpose of the visceral motor division of the nucleus ambiguus and dorsal motor nucleus (DMN) (which is a part of the vagus)?

Back 120

lie in the medulla, neurons in the ventral lateral part of the nucleus ambiguus provide an inhibitory innervation to the cardiac ganglion via the vagus, dorsal part of DMN regulates secretion of the thorax and abdomen, ventral part of the DMN controls motor responses to the heart, lungs and gut (slowing of the heart, constricting the bronchioles, contractions of the gut)

Front 121

What is the purpose of the sacral parasympathetic pelvic ganglia?

Back 121

excite bladder and colon and reproductive system

Front 122

What are the major parasympathetic ganglia?

Back 122

they are cranial ganglia and include ciliary (iris and ciliary muscle), sphenopalatine (lacrimal gland), submandibular (sublingual and submandibular gland) and otic (parotid gland)

Front 123

What are the parasympathetic ganglia that lie outside the head?

Back 123

airways, cardiac plexus, hypogastric plexus (mixed para and symp, innervate the intestine and bladder) and pelvic ganglia (bladder and intestine)

Front 124

Where do the cell bodies of preganglionic parasympathetic neurons that synapse with postganglionic neurons exit?

Back 124

exit through the cranial nerves

Front 125

Describe the neurotransmission of preganglionic neurons

Back 125

most sympathetic and parasympathetic preganglionic neurons are cholinergic, utilizing acetylcholine as a neurotransmitter, Ach excites postganglionic neurons by stimulating nicotinic receptors on their dendrites and somata

Front 126

Describe the neurotransmission of postganglionic sympathetic neurons

Back 126

are noradrenergic, uses norepinephrine (NE) as a neurotransmitter on cardiac and smooth muscle, glands and cardiac SA and VA node cells (parasympathetic only works on glands and SA and VA node), acts on adrenergic alpha or beta receptors on effector cells which usually causes excitation or inhibition of smooth muscle respectively, NE constricts blood vessels via activation of alpha receptors but relaxes parts of the bladder via beta receptors, elicit fast excitatory postsynaptic potentials (fEPSPs)

Front 127

Describe the synthesis, loading and degradation of catecholamines.

Back 127

1. synthesis-
a. Tyr + O2 -> DOPA (via tyrosine hydroxylase)
b. DOPA -> dopamine + CO2 (via DOPA decarboxylase)
c. dopamine + O2 -> NE (via Dopamine-beta-hydroxylase)
d. NE -> epinephrine (via phenylethanolamin N-methyl-transferase)
2. loading-loaded into vesicles by a vesicular monoamine transporter (VMAT), cleared from the synaptic cleft by the NE transporter (NET)
3. degradation-monamine oxidase (MAO) and catechol O-methyl-transferase (COMT) contained in glia and mito

Front 128

Describe the cholinergic receptor types and their effects.

Back 128

1. nicotinic-supply most parasympathetic targets (and all autonomic ganglion cells), their response is a relatively fast postsynaptic response
2. muscarinic-there are M1, M2, and M3 types, supply smooth muscles and glands (M1 and M3) as well as cardiac muscles (M2), responsible for smooth muscle contraction, glandular secretion and reduction in heart rate

Front 129

Describe the different types of adrenergic receptors.

Back 129

there are alpha-1 and 2 as well as beta-1, 2, and 3 subtypes, responsible for sympathetic responses

Front 130

What is the morphology of the postganglionic vascoconstrictor neuron and its neureffector synapse?

Back 130

1. neuron forms many (~1000) varicosities close to the blood vessel, are arranged close to the smooth muscle cells
2. terminal branches of the postganglionic axon form nonadrenergic plexus at the adventitial site around the blood vessel, smooth muscle cells are electrically and chemically coupled by gap junction channels forming a functional syncytium

Front 131

What do APs in smooth muscles in the blood vessels do

Back 131

synaptic nerve stimulation releases NE which activates alpha 1 receptos on the smooth muscle, blocked by parzosin, AP in smooth muscle are caused by Ca2+ influx through L-type Ca2+ channels blocked nicardinine, nifedinine and verapamil

Front 132

What does sympathetic innervation do to arteries and veins to the gut?

Back 132

it constricts arteries and veins to the gut reducing blood flow there, thus INC blood volume for the rest of the body, major targets include the vessels in the mesentery and gut wall, utilize noradrenaline (norepinephrine), ATP and often one or more peptides (NPY)

Front 133

What role does ATP and noreadrenaline play in sympathetic innervation?

Back 133

ATP causes significant depolarization of smooth muscle, noradrenaline is the major excitatory transmitter causing significant vascoconstriction which is blocked by the blocker by the blocker of adrenergic transmission (guanethidine)

Front 134

What do the cholinergic sympathetic neurons do?

Back 134

innervate eccrine sweat glands in the skin (stimulation), some cutaneous blood vessels and arteries (inhibition) in skeletal muscle, activates NO production

Front 135

What is the mechanism of ACh activated NO production

Back 135

ACh binds on muscarinic receptos, leads to an INC in Ca2+ in endothelial cells which stimulates NO synthase (NOS) to generate NO, turns L-arginine into NO and L citrilline

Front 136

How does viagra work?

Back 136

it INC NO production, can lead to hypertension, it is an inhibitor of cyclic GMP-specific phosphodiesterase INC the level of NO and blood flow through the genitals, PDE turns cGMP into GMP, by inhibiting PDE, cGMP is not broken down acting to prolong the effects of cGMP and the erection

Front 137

Where do the sympathetic and parasympathetic neurons derive from?

Back 137

they derive from neural crest cells

Front 138

What determines whether or not a neuron uses cholinergic or noradrenergic receptors?

Back 138

depends on trophic factors in the tissue environment in which the neurons reside after migration

Front 139

What are the different combinations of chemical coding of postganglionic sympathetic neurons?

Back 139

1. NE/NPY (neuropeptide Y)-cutaneous vasculature (+)
2. NE-piloerector muscles (+)
3. ACh (Chat)/VIP (vasoinhibitory polypeptide) -sweat glands (+), cutaneous vessels (-)
4. NE/NPY-skeletal muscle vasculature (+), skeletal muscle (-)
5. ACh (Chat)-vasculature

Front 140

What determines the degree of divergence in autonomic ganglia?

Back 140

the degree of divergence of individual preganglionic neurons on postganglionic neurons probably is a function of the size of target organ (and therefore body size) and of the type of autonomic final pathway (low divergence in the pupillomotor pathway and high degree of divergence in vasoconstrictor pathways)

Front 141

What determines the degree of convergence in autonomic ganglia?

Back 141

the degree of convergence varies between different autonomic pathways

Front 142

Describe the spinal autonomic reflex pathways.

Back 142

it is the building block between supraspinal centers and final autonomic pathways, usually at least one interneuron (can be excitatory or inhibitory) between primary afferent neurons and preganglionic neurons

Front 143

What is the consequence of spinal cord transaction for spinal autonomic systems?

Back 143

1. denervation of preganglionic neurons and autonomic interneurons
2. changes of geometry of preganglionic neurons
3. sprouting of afferent neurons
4. neurochemical changes of afferent neurons

Front 144

What are the important effectors in thermoregulation?

Back 144

1. eccrine sweat glands
2. cutaneous resistance vessels
3. piloerector muscles
4. nose
5. lungs

Front 145

What are the roles of NE and ACh in sympathetic innervation of the skin?

Back 145

NE is responsible for pilomotor and vasoconstriction, ACh is responsible for sudomotor and vasodilator

Front 146

What is ANS response to a lowering of body temperature

Back 146

INC metabolism, DEC cutaneous blood supply by INCing sympathetic activity to the blood vessels in the skin, and piloerection which traps a layer of insulating air in hairs near the skin surface

Front 147

What is the ANS response to an increase in body temperature?

Back 147

leads to an INC in evaporative cooling by DECing sympathetic activity to blood vessels in the skin resulting in vasodilation of cutaneous vessels, especially of the hands and feet, dilation of cutaneous blood vessels by activation of postganglionic sympathetic neurons, a release of sweat by INCing sympathetic activity to eccrine glands and hyperventilation that is more apparent in some mammals such as the dog

Front 148

What is the importance of autonomic reflexes?

Back 148

activity in the ANS depends on the integration of a variety of reflex arcs often involving integrative centers in autonomic ganglia, the spinal cord, brain stem and hypothalamus, usually involves interneurons

Front 149

Where are the cell bodies of visceral sensory afferents located?

Back 149

have cell bodies located in the DRG and in sensory ganglia associated with glossopharyngeal and vagus CN and in the trigeminal ganglia, most that mediate sensation and nociception accompany the sympathetic nerves (splanchnics) whereas those involved in reflexes regulating visceral tone and motility and secretion accompany parasympathetic nerves (vagus and pelvic nerves)

Front 150

What is the purpose of visceral afferents

Back 150

they monitor the activity in a variety of tissues, their fibers accompany both sympathetic and parasympathetic efferent nerves to their targets

Front 151

What are the components of a basic spinal reflex arc?

Back 151

1. visceral afferent neurons plus sensory receptor
2. interneuron
3. preganglionic neuron
4. postganglionic neuron
5. effector

Front 152

What are the different classes of visceral afferent receptors?

Back 152

chemoreception, mechanoreception, thermoreception, nociception

Front 153

Describe chemoreception.

Back 153

nerve endings sensitive to pH, P O2, P CO2 in intestinal tract, bladder, kidneys, blood vessels, regulation of intestinal motility and blood pressure

Front 154

describe mechanoreception.

Back 154

stretch sensitive nerve endings in hollow organs (eg heart, intestine, bladder), some are sensitive to movements of intestinal mucosal villi, piloerection, they regulate contractility of bladder and intestine and blood pressure

Front 155

describe thermoreception

Back 155

nerve endings sensitive to temperature, found in the skin, GI tract

Front 156

describe nociception

Back 156

nerve endings sensitive to pain, especially overstretching of visceral organs, they are found in most internal organs, bladder, intestine etc.

Front 157

What are the different types of visceral reflexes?

Back 157

supraspinal, viscero-cutaneous and viscero-somatic reflexes

Front 158

Describe supraspinal reflexes.

Back 158

the afferent fibers can ascend the spinal cord or directly enter supraspinal sites, neurons in reflex centers provide output to preganglionic neurons in the spinal cord or medulla

Front 159

describe viscero-cutaneous reflexes.

Back 159

stimulation of nociceptos in visceral organs can lead to a reddening of the skin over the organ as activity in postganglionic sympathetic neurons innervating blood vessels in the skin is reduced

Front 160

describe viscero-somatic reflexes

Back 160

stimulation of nociceptive afferent in viscera by noxious stimuli can lead to a tightening of skeletal muscles over sensitive viscera due to activation of somatic motor neurons in the spinal cord by visceral afferent impulses

Front 161

Describe dual afferent innervation.

Back 161

when both sympathetic and parasympathetic afferents innervate an organ, found in the major thoracic, abdominal and pelvic organs, most of these fibers are unmyelinated

Front 162

What are the percentages between afferent and efferent fibers in the body?

Back 162

20% of the total nerve fibers running with sympathetic nerves are afferent, 80% of all fibers in vagus are afferent and 50% of fibers in the pelvic nerves are afferent

Front 163

Describe pain in terms of the sympathetic and parasympathetic stimulation.

Back 163

1. splanchnic nerve stimulation elicits severe pain in conscious humans
2. chronic visceral pain (cancer, severe peripheral vascular disease) can be relieved by surgically sectioning sympathetic nerve trunks but not parasympathetic nerve trunks

Front 164

Can visceral sensations be localized?

Back 164

they are difficult to localize because of the relative lack of visceral sensory neurons compared to mechanosensory neurons to skin and deeper somatic structures visceral, visceral sensations are thus diffuse

Front 165

What is the major effect of sympathetic neurons in the gut wall?

Back 165

cause inhibition of enteric neuronal transmission, mostly by presynaptic inhibition via alpha adrenoceptors, however they also cause vascoconstriction and changes in secretion and muscle tone

Front 166

what are the two divisions of parasympathetic neurons innervating the gut?

Back 166

parasympathetic efferent neurons use acetylcholine as their primary transmitter, may also use modulatory peptides such as VIP
1. vagal efferent neurons with cell bodies in the dorsal vagal nucleus
2. sacral efferent neurons, have cell bodies in the sacral parasympathetic nucleus of spinal cord or in extrinsic pelvic ganglia near the rectum

Front 167

How do parasympathetic efferents mediate both contraction and relaxation in the gut?

Back 167

mediate it through their nicotinic synaptic input to excitatory and inhibitory motorneurons, parasympathetic efferents make exclusively excitatory synaptic outlets but the final common effector may show either net excitation or net inhibition, seen in the stomach where vagal efferent stimulation leads to relaxation of the proximal stomach but contractile activity in the distal stomach

Front 168

Where are the sympathetic neurons to the gut wall located?

Back 168

mostly located in the prevertebral ganglia (celiac, superior mesenteric and inferior mesenteric ganglions), a minority are located in the paravertebral ganglia (sympathetic chain) and a few lie in the pelvic ganglia

Front 169

What are the neurotransmitters used by the sympathetic neurons in the gut?

Back 169

most use noradrenaline as their primary transmitter, some also release modulatory substance such as neuropeptide Y, somatostatin or ATP

Front 170

What are the targets of the sympathetic neurons in the gut wall?

Back 170

different types of neurons (determined by the cotransmitters that they contain) so there is a degree of independent neural regulation, innervate separate targets in the gut wall, 3 targets are the secretomotor pathways in the submucous ganglia, motor pathways largely concentrated in myenteric ganglia and direct vasoconstrictor innervation of blood vessels

Front 171

What cotransmitters are found on each of the different types of neurons in the gut wall?

Back 171

1. adrenergic fibers on blood vessels contain peptide NPY
2. submucous ganglia lack NPY but contain somatostatin immunoreactivity
3. adrenergic fibers to the myenteric ganglia appear to lack both NPY and somatostatin

Front 172

What are the major types of synaptic input and their transmitters to the sympathetic neurons of the gut?

Back 172

sympathetic neurons to the gut receive synaptic input from 3 sources (preganglionic neurons from the spinal cord (powerful and prominent, ACh), viscerofugal (enteric) neurons (ACh) and spinal afferent neurons (ACh and peptides: SP and CGRP)

Front 173

What activates sympathetic neurons in the gut?

Back 173

are activated by cholinergic synaptic inputs form viscerofugal (enteric) neurons in the gut, these neurons have cell bodies in myenteric ganglia and which project via the mesenteric nerves to the prevertebral sympathetic ganglia

Front 174

What supplies innervation to the airways?

Back 174

supplied by autonomic fibers that are found associated with smooth muscle, submucous glands and bronchial blood vessels

Front 175

What are the roles of the parasympathetic nerve fibers in terms of the respiratory system?

Back 175

they are cholinergic, tonically contract airway smooth muscle via muscarinic receptors affecting bronchioconstriction, other nerve fibers release NO and VIP to relax airway smooth muscle, others also release ACh and VIP to promote bronchial secretion

Front 176

What are the roles of the sympathetic nerve fibers in terms of the respiratory system?

Back 176

there are adrenergic receptors on smooth muscle but there is no known sympathetic innervation of the smooth muscle of the airways, sympathetic nerves likely inhibit secretion

Front 177

What is the basis for asthma drugs?

Back 177

stimulation of beta-2 receptors leads to relaxation of the airways and gut smooth muscle through INCing cAMP, wherease beta-1 receptors INC heart rate by INCing cAMP, inhalers stimulate both the beta-1 and beta-2 receptors, so DECing asthma attacks may lead to racing heart

Front 178

what are the different drugs for asthma?

Back 178

albuterol (terbutaline and metaproterenol) and beta-2 selective agonists (bronchodilation inhalation vs. oral, less side effects)

Front 179

How does the ANS control BP?

Back 179

use baroreceptor reflexes

Front 180

what happens when the baroreceptor reflexes are compromised?

Back 180

feeling faint when standing, especially in old age, fainting while on parade due to venous pooling in legs

Front 181

Describe baroreceptors.

Back 181

are mechanosensitive sensory nerve fibers within blood vessel walls that are stimulated by stretching of the vessel wall by INC in intravascular pressure, associated with many major blood vessels, most important are those found at the bifurcation of the common carotid arteries (carotid sinus) and those found in the aorta (aortic arch baroreceptors)

Front 182

where are the cell bodies of the afferent fibers to the carotid sinus and aortic arch baroreceptors found?

Back 182

located within cranial sensory ganglia associated with the IX and X cranial nerves, they transmit their afferent signals to brainstem nuclei

Front 183

What happens when the BP falls?

Back 183

when BP falls there is a DEC in activity in the aortic arch and carotid sinus baroreceptor sensory neurons, this leads to activation of the SNS and a withdrawal of parasympathetic input, sympathetic stimulation leads to an INC in heart rate, cardiac output and activation of vasoconstrictor neurons in the paravertebral ganglia, so BP rises

Front 184

What happens when the BP rises?

Back 184

an INC in BP leads to stimulation of baroreceptors with an INC in AP firing in sensory nerves with cell bodies in superior and inferior sensory ganglion of CN IX, activity in these sensory nerves is integrated in the medulla, also INC in AP firing in CN X and DEC in preganglionic sympathetic nerves (which innervates the heart and blood vessels)

Front 185

What effect does the parasympathetic preganglionci nerve fibers have on heart rate?

Back 185

DEC heart rate by stimulating postganglionic parasympathetic neurons on the heart, these release ACh onto M1 on SA node cells to slow heart rate, a reduction in sympathetic activity leads to reduction in both heart rate and strength of contractions of the myocardium as well as vasodilation

Front 186

What controls bladder function?

Back 186

ANS via micturition centers in the pons

Front 187

Describe the filling phase of bladder control.

Back 187

the filling phase is via SNS, preganglionic sympathetic fibers originate in T10-L2, postganglionic sympathetic nerve fibers to IMG and ganglia in pelvic plexus, postganglionic neurons relaxs detrusor muscle (NE or beta-receptors), constrct trigone smooth muscle and close internal urethral sphincter (NE on alpha-receptors)

Front 188

Describe the emptying phase or micturition of bladder control.

Back 188

the emptying phase is via PNS, at a certain threshold volume sympathetic activity is switched off, preganglionic parasympathetic neurons in S2-S4 are activated, these synapses with postganglionic parasympathetic neurons in pelvic plexus to cause contraction of the detrusor muscle (ACh on muscarinic receptors).

Front 189

What senses distension in the bladder wall?

Back 189

sensory afferent fibers with cell bodies in the DRG do, moderate distension inhibits parasympathetic pathways underlying bladder emptying

Front 190

What is the somatic component of bladder control?

Back 190

the pudendal nerve is responsible for contraction of the pelvic floor musculature and is under voluntary control, thus also playing a role in voiding

Front 191

Describe bladder control in infants.

Back 191

1. in the infant, urination is purely a local reflex centered in the lower portion of the spinal cord, involuntary voiding occurs whenever the bladder is sufficiently full in infants <2, results from stretch receptors transmitting impulses to the sacral micturition center in the spinal cord, this center causes detrusor muscle contraction of the bladder
2. between 2 and 3, a special area in the brain develops and nerve pathways to that center allows the child to detect a sensation of bladder fullness
3. an area in the lower part of the brain (pontine micturition center) develops enough to coordinate sphincter relaxation during voiding
4. at ~4 to 5 years old, child learns conscious bladder control and develops the ability to inhibit the bladder center in the sacral spinal cord

Front 192

What causes continence during sleep?

Back 192

results from the unconscious inhibition of detrusor muscle contraction by an area in the brain known as the basal ganglia

Front 193

How do paraplegic patients have bladder control?

Back 193

paraplegic patients have lost descending control of the sacral spinal cord, urination is stimulated reflexly at the level of the sacral cord by sufficient bladder distension (similar to infant < 2 years, may need an indwelling catheter to ensure adequate drainage

Front 194

What type of innervation do the salivary glands have?

Back 194

thye have a dual innervation, parasympathetic postganglionic cholinergic neurons aids secretion by relaxing the smooth muscle of neighboring arterioles thereby INCing local blood flow, PNS produces a copious serous fluid, postganglionic sympathetic nerves release NE onto alpha-receptors to also INC secretion from the salivary glands, but produce a mucous secretion that makes the mouth feel dry

Front 195

What is involved in the iris-accommodation reflex?

Back 195

accommodation is an adaptation of the visual apparatus to facilitate near vision, involves an INC in the curvature (and therefore the refractive power) of the lens, papillary constriction to help sharpen the image on the retina, and convergence of the eyes to fixate on the target object

Front 196

What are the parasympathetic pathways involved in the papillary light reflex?

Back 196

walking into a bright room leads to a stong activation of Edinger-Westphal (accessory occulomotor) nucleus and constrction of pupil

Front 197

What are the sympathetic pathways involved in the papillary light reflex?

Back 197

walking into a dark room leads to strong activation of superior cervical ganglion and dilation of pupil

Front 198

Describe the pathway for the papillary light reflex.

Back 198

axons from the superior colliculi and pretectal nuclei project to both the Edinger-Westphal and oculomotor nuclei, signals from the Edinger-Westphal nuclei travel via the ipsilateral oculomotor nerve to reach the ciliary and constrictor pupilae muscles of the eye, contraction of the ciliary muscle causes the lens to INC its curvature (and thus its refractive power), while contraction of the constrictor pupillae reduces the size of the papillary aperture

Front 199

Describe Horner’s Syndrome.

Back 199

caused by damage to pathway that controls sympathetic innervation of the head (damage to the sympathetic chain in the head), symptoms include constriction of pupil on the side of the lesion, ptosis (droopy eyelids), dry face (DEC sweating) and flushed face (due to INC skin temperature)

Front 200

What determines the functional state of the penis (and clitoris)?

Back 200

whether flaccid or erect it is governed by smooth muscle tone within the corpus cavernosum and corpus spongiosum

Front 201

What maintains smooth muscle tone and flaccidity (detumescence)?

Back 201

SNS and myogenic mechanisms, SNS is responsible for ejactulation-contraction of the vas deferens, in the flaccid state a dominant sympathetic influence prevails and arterial and corporal smooth muscle are contracted, as a result only a minimal amount of blood flows through the cavernous artery into the lacunar spaces

Front 202

What induces smooth muscle relaxation and erection (tumescence)?

Back 202

PNS, NO released from both PNS and vascular endothelium by ACh is the principal mediator of tumescence (relaxation of corporal smooth muscles and erection)

Front 203

What role does Ca2+ play in detumesence?

Back 203

rhythmic activity in pacemaker (ICC) cells spreads to the smooth muscle and is responsible for myogenic tone that produces flaccidity of penis, there is also rhythmic Ca2+ transients in smooth muscle of penis

Front 204

What role does NO play in tumescence

Back 204

NO is the principal agent responsible for relaxation of penile smooth muscle,

Front 205

How is NO synthesized

Back 205

is formed from arginine by the enzyme nitric oxide synthase (NOS)

Front 206

Describe the pathway to erection

Back 206

in response to sexual stimulation, parasympathetic stimulation leads to an INC in NO production, NO causes a DEC in peripheral resistance due to vasodilation and INC blood flow through the cavernous and helicine arteries, INC blood volume, erection occurs and blood flow through the cavernous artery ceases because of compression of the dorsal vein of penis

Front 207

Describe the pathway to detumescence after erection.

Back 207

results when elevated sympathetic activity INC the tone of the helicine arteries and contraction of trabecular smooth muscle occurs

Front 208

How is the signal for NO production terminated?

Back 208

cGMP is converted into GMP by PDE, cGMP is needed in NO synthesis

Front 209

How does NO work

Back 209

Acetylcholine causes the production of inositol triphosphate (IP3), an important second messenger in many hormone signal transduction pathways. IP3 opens calcium channels in the endoplasmic membrane of the endothelial cells; the liberated calcium then activates NO synthase and causes the production of NO. Whatever the source, endothelial cells or cavernous nerve, NO diffuses across the muscle cell membrane and binds to guanylyl cyclase. Guanylyl cyclase catalyzes the synthesis of cyclic GMP from GTP. cGMP then activates a cGMP dependent protein kinase which in turn stimulates the uptake of calcium by the endoplasmic reticulum of the muscle cell. The reduced levels of cytoplasmic calcium which causes the muscle cell to relax. As a consequence of muscle cell relaxation, vasodilation occurs.

Front 210

What are the reflex centers that regulate the outflow of the sympathetic and parastympathetic nervous systems to specific organs?

Back 210

1. cardiovascular center (regulates heart rate)
2. vasomotor center (regulates blood vessel diameter)
3. micturition center (controls bladder function)
4. papillary center (controls the amount of light entering the pupil)
5. respiratory center (controls depth and rate of respiration)
6. swallowing center (coordinates peristalsis through the pharynx and esophagus)
7. vomiting center (coordinates reverse peristalsis in GI tract)

Front 211

what do neurons in these higher centers do?

Back 211

project either into the parasympathetic nuclei to either inhibit or excite preganglionic parasympathetic neurons or down the spinal cord via interneurons to either inhibit or excite preganglionic sympathetic neurons

Front 212

What functions do the afferent activity from viscera serve?

Back 212

1. it provides feedback input to local reflexes that modulate moment-to-moment visceral motor activity within individual organs
2. it informs higher integrative centers of more complex patterns of stimulation that may singnal potentially threatening conditions and/or require the coordination of more widespread visceral motor, somatic motor, neuroendocrine, and behavioral activites

Front 213

What is the purpose of the nucleus of the solitary tract in the medulla?

Back 213

it is the central structure that receives visceral information and distributes accordingly

Front 214

what is the main function of the hypothalamus?

Back 214

homeostasis (maintaining the body’s status quo), holds factors such as blood pressure, temperature, fluid and electrolyte balance and weight are held to a precise value called the set point (which can migrate over time, but from day to day it is remarkably fixed), can control every endocrine gland in the body

Front 215

How does the hypothalamus function?

Back 215

secretes hormones (neuropeptides) and growth factors that regulate the body, allows the ANS to influence the immune system

Front 216

what is the function of the limbic system?

Back 216

it links emotional responses to ideas and images with the hypothalamus

Front 217

What are the two main outputs from the hypothalamus?

Back 217

1. neural signals to the autonomic centers in the medulla-allows the hypothalamus to control heart rate, vasoconstriction, digestion, and sweating
2. endocrine signals to/through the pituitary-neurons project into the posterior pituitary where axon terminals release oxytocin and vasopressin into the bloodstream, other neurons release factors into the capillary system of the anterior pituitary, induce the anterior pituitary to secrete any one of at least six hormones (ACTH, TSH)

Front 218

What information does the hypothalamus consider?

Back 218

1. contextual information-cerebral cortex, amygdale, hippocampal formation
2. sensory inputs-visceral and somatic sensory pathways, chemosensory and humoral signals
3. after comparing these inputs to the biological set points and undergoes visceral motor, somatic motor, neuroendocrine, behavioral responses

Front 219

What are cholinergic symptoms (as seen with organophosphate/pesticide poisoning, for example)?

Back 219

“SLUDGE” syndrome (salivation, lacrimation, urination, defecation, GI distress (abdominal cramps), emesis (vomiting)

Front 220

What are anti-cholinergic symptoms (seen with exposure to atropine, for example)?

Back 220

mad as a hatter=seizures, hallucinations
blind as a bat=papillary dilation
hot as a hare=no sweating
dry as a bone=no secretions
red as a beet=flushing (as in with exercise, not parasympathetic flush with blushing)

Front 221

Describe the receptor potential.

Back 221

channel opens in response to mechanical pressure, has a small response (compared to AP), graded (harder pressure evokes a larger response) and not conducted very far, a passive response

Front 222

Describe the synaptic potential.

Back 222

channels open in reponse to a neurotransmitter, response is small (compared to AP), graded (more neurotransmitter evokes a larger response) and not conducted very far, passive response

Front 223

What is the purpose of gap junctions in between cells?

Back 223

connect cells to be electrically coupled, gives the two cells the same membrane potential, gap junctions allow ions to move between the cells

Front 224

Describe what bi-directional conduction was.

Back 224

very fast conduction between two coupled hippocampal neurons, they are nearly perfectly synchronized, it is good for coordinating electrical activity of a population of cells (particular CNS neurons (hormone-secreting cells in hypothalamus), cardiac muscle and smooth muscle)

Front 225

What are synaptic vesicles?

Back 225

membrane bound organelles in the presynaptic terminal contain one or several different neurotransmitters

Front 226

What are synaptic clefts?

Back 226

a relatively wide space separating the pre and post-synaptic neurons

Front 227

What are the steps found in neurotransmission?

Back 227

1. synthesize neurotransmitter and load vesicle
2. AP
3. and 4. open calcium channels, Ca2+ influx
5-8. vesicles fuse, neurotransmitter is released, diffuses into cleft, binds to receptors, receptors do whatever they do
9. postsynaptic neurons responds
9.5. inactivate or remove the neurotransmitter
10. vesicular membrane retrieved

Front 228

What drugs disrupt the steps found in neurotransmission?

Back 228

1. lidocaine-blocks the AP
2. conotoxin-blocks the Ca2+ influx
3. BoTX-block the vesicle release
4. curare-block the receptor (ACh)
5. physostigmine, prozac-block inactivation/uptake of neurotransmitter

Front 229

What is the role of Ca2+ in a voltage-change across the membrane triggers a biochemical event?

Back 229

voltage activates voltage-gated Ca2+ channels in the presynaptic membrane provide Ca2+ to trigger the release of neurotransmitter, if extracellular Ca2+ is removed or Ca2+ entry is blocked there will be no release (Ca2+ removal is done in the lab, block of Ca2+ entry is done clinically)

Front 230

What is co-transmission?

Back 230

the ability of all neurons to release several to many neurotransmitters

Front 231

What types of vesicles hold small-molecule neurotransmitters and neuropeptides?

Back 231

small-moleculare neurotransmitter in small clear-core vesicles, neuropeptide in large dense-core vesicles

Front 232

Describe low-frequency stimulation.

Back 232

a small number of AP raises Ca2+ only near the membrane, releasing the clear core vesicles, sustained stimulation will mobilize the release of the neuropeptides

Front 233

Describe high-frequency stimulation.

Back 233

a high number of AP raises the Ca2+ throughout the entire synaptic terminal, the neuropeptides are released as well

Front 234

What is the model for vesicle recycling?

Back 234

1. vesicles bud from the endosome and fill with transmitter
2. vesicles dock at release site (being primed to undergo exocytosis)
3. vesicles fuse into the plasma membrane (exocytosis, in response to INC Ca2+)
4. vesicle membrane retrieved by endocytosis (through clathrin coated pits)
5. vesicles return to the endosome

Front 235

What is the “kiss-and-run” model?

Back 235

a model for vesicle fusion, states that vesicle fusion seems to be incomplete and that only part of the vesicle touches the membrane, releases its contents, then closes back up, some vesicles are competent for the kiss and run method while others are not

Front 236

What are the more important proteins involved in vesicle release discussed in class?

Back 236

SNARES, synaptotagmin and Ca2+ channel

Front 237

What is the purpose of the Ca2+ channels?

Back 237

they release Ca2+ for this system, into the presynaptic bulb

Front 238

What is the purpose of synaptotagmin?

Back 238

it is the Ca2+ sensor on the vesicle

Front 239

What are some examples of SNARES?

Back 239

synaptobrevin (on the vesicle), syntaxin (on the membrane), SNAP-25 (which is not a SNAP, found on the membrane and regulates the assembly of two other SNARES)

Front 240

What is the molecular mechanism for vesicle binding?

Back 240

1. vesicle docks with the three types of SNARES, synaptotagmin and the Ca2+ channels not interacting with each other
2. Ca2+ enters and binds to synaptotagmin
3. SNARE complexes form to pull membranes together
4. Ca2+ bound synaptotagmin catalyzes membrane fusion

Front 241

Why is it important to study the details of the release of neurotransmitters?

Back 241

it is a target for drug action, new methods are revealing new facets of the process

Front 242

Why is permeability important for determining membrane potential?

Back 242

the contribution of an ion gradient to the membrane potential is weighted by the permeability of the cell membrane to that ion, if Pk is large, Em is close to Ek, Pna is large, Em is close to Ena, see GHK equation

Front 243

What are three rules that govern the effect of the ion gradient on membrane potential?

Back 243

1. each ion gradient contributes a gradient o the membrane potential
2. permeability has an effect on the gradient
3. permeability is controlled by opening and closing of ion channels

Front 244

Describe the effect on nonselective channels on the membrane potential.

Back 244

nonselective channels are channels that open that allow both Na+ and K+ through the membrane, both Pna and Pk will INC and the membrane potential will move toward a potential in between Ena and Ek, use GHK equation, makes the membrane potential less negative (depolarization)

Front 245

What happens when the membrane potential is set to different values and nonselective channels are opened?

Back 245

if set to a positive value (+65), then the membrane potential will become more negative (move toward 0), if set to 0 mV, then the membrane potential will not change staying at 0 mV

Front 246

Describe the reversal potential (Erev).

Back 246

it is the target potential associated with the opening of a particular channel, for a highly selective channel, Erev is the Nernst equilibrium potential of the chosen ion, for a non-selective channel, Erev will be between the Nernst equilibrium potentials of the ions that pass through the channel

Front 247

What is the general rule for how Erev works?

Back 247

the general rule is that the action of a neurotransmitter drives the postsynaptic potential toward Erev for the particular ion channels being activated

Front 248

Describe the main channels that generate receptor potentials.

Back 248

the main channels activated by neurotransmitters are selective for Cl- or Ca2+ or are nonselective for monovalent cations, rarer channels are selective for K+ and Na+, this is different from the channels that generate the AP (which are usually highly selective for Na+ or K+ or Ca2+

Front 249

What type of potential is Erev if it is positive to threshold?

Back 249

the event is an excitatory postsynaptic potential (EPSP)

Front 250

Describe EPSPs.

Back 250

the EPSP caused by a single presynaptic AP in a single axon typically does not reach Erev or threshold and would not fire an AP, if multiple EPSPs are triggered by multiple presynaptic APs then it may reach threshold

Front 251

What type of potential is Erev if it is negative to threshold?

Back 251

the event is an inhibitory postsynaptic potential (IPSP), especially if it is negative to resting potential, if it is more positive than the resting potential, but lower than threshold, opening these channels (usually Cl- channels) stabilizes the membrane potential near Erev making it harder to get to threshold, therefore it is possible to get an IPSP that is depolarizing the membrane potential

Front 252

What type of potential do Ca2+ or nonselective for cations channels mediate?

Back 252

EPSPs

Front 253

What type of potential do K+ channels mediate?

Back 253

IPSP

Front 254

What type of potential do Cl- channels mediate?

Back 254

IPSPs unless Ecl is positive to threshold, where it would be an EPSP, Cl- can sometimes be excitatory

Front 255

Describe summation of the various inputs that a neuron receives

Back 255

for summation, location and timing are very important, if a neuron receives a combination of EPSPs and IPSPs, just sum the value of all the potentials (that occur at the same time, those that occur later are not summed if the previous potential has already passed) to calculate the total potential

Front 256

What triggers an EPP (end plate potential)?

Back 256

at the NMJ, one AP in the motor neuron evokes an EPP that triggers one AP in the muscle fiber, EPPs are huge (about 15 mV) and will take you to threshold, if it doesn’t then it is pathological

Front 257

what triggers EPSPs and IPSPs?

Back 257

at neuron to neuron synapses, APs in the presynaptic neurons typically evoke EPSPs or IPSPs that INC or DEC, respectively, the likelihood that the postsynaptic neurons will fire an AP (whether or not threshold is reached)

Front 258

Describe retrograde signaling.

Back 258

allows for postsynaptic neurons to signal back to the presynaptic neuron, for example, activation of glutamate receptors raises [Ca2+]i generating a retrograde signal, some other examples of retrograde transmitters include NO, CO, cannabinoids and prostaglandins

Front 259

How are presynaptic receptors responsible for regulating release?

Back 259

neurotransmitters release from the presynaptic terminal can come from the neuron itself or other neurons and it is common for a neurotransmitter to inhibit its own release

Front 260

What are the different families of receptors?

Back 260

ligand-gated ion channels (ionotrophic receptors), G-protein coupled receptors (metabotropic receptors), receptor tyrosine kinases

Front 261

Descirbe the ligand-gated ion channels (ionotrophic receptors).

Back 261

the response of this channel type is limited to the channel opening or closing unless the ion is Ca2+, thousands of different receptor types are made by mixing and matching subunits (potentially)

Front 262

Describe the G-protein coupled receptors.

Back 262

binding of the neurotransmitter activates trimeric G-proteins that directly and/or indirectly influence the opening and closing of ion channels (along with a thousand other activities), there are only a few (<10) receptor types (monomers), have an unlimited response mediated by G-proteins, Ca2+, kinases, phosphatases

Front 263

Describe the mechanism of the G-protein coupled receptors.

Back 263

1. neurotransmitter binds
2. G-protein becomes activated
3. G-protein subunits or intracellular messengers modulate ion channels
4. ion channel opens
5. ion flows across membrane

Front 264

Describe the receptor tyrosine kinases and there mechanism of action.

Back 264

binding of the ligand activates a tyrosine kinase that directly and/or indirectly influence the opening and closing of ion channels (along with a thousand other activities), when the signal binds, the enzyme becomes activated and the enzyme generates a product

Front 265

What is the difference between inotrophic and ionotrophic?

Back 265

inotrophic is related to the force of contraction of a muscle (cardiac electrophysiology) while ionotrophic is a type of channel that lets ions through channels

Front 266

What are the necessary criteria for a molecule to be considered a neurotransmitter?

Back 266

1. present (or made quickly) presynaptically
2. Ca2+-dependent release (or generation)
3. postsynaptic receptors
4. application mimics release
5. blockers prevent action

Front 267

What are some examples of small molecule neurotransmitters?

Back 267

1. amino acids-glutamate, aspartate, GABA, glycine
2. biogenic amines-catecholamines (norepinephrine and epinephrine), serotonin (5-HT) and histamine
3. purines-ATP, ADP, adenosine

Front 268

Describe the properties of the small molecule neurotransmitters.

Back 268

are synthesized in the presynaptic terminal, necessary enzymes are made in the cell body, transported down to the presynaptic terminal (slow axonal transport), where the enzymes are made and work, packed in small clear-core vesicles usually

Front 269

Describe the properties of the neuropeptides

Back 269

there are a lot of these and they are not easily summarized, are large neurotransmitters, most of which are found in the GI system, synthesized and processed into vesicles in the cell body, fast axonal transport to the terminal, packaged in dense-core vesicles

Front 270

what is an example of a neuropeptide?

Back 270

an example is gastrin releasing peptide (GPR) and it plays a role in creating memory of fearful situations, mutants that lack receptors for GPR have trouble forgetting scary experiences

Front 271

what are some unconventional neurotransmitters

Back 271

endocannabinoids, NO, CO, hydrogen sulfide

Front 272

What are the postsynaptic effects, precursors, rate-limiting step in synthesis, removal mechanism and type of vesicle for ACh?

Back 272

1. postsynaptic effect-excitatory
2. precursor-choline + acetyl CoA
3. rate-limiting step-CAT
4. removal mechanism-AChEase
5. type of vesicle-small, clear

Front 273

What are the postsynaptic effects, precursors, rate-limiting step in synthesis, removal mechanism and type of vesicle for glutamate?

Back 273

1. postsynaptic effect-excitatory
2. removal mechanism-transporters
3. type of vesicle-small, clear

Front 274

What are the postsynaptic effects, precursors, rate-limiting step in synthesis, removal mechanism and type of vesicle for GABA?

Back 274

1. postsynaptic effect-inhibitory
2. removal mechanism-transporters
3. type of vesicle-small, clear

Front 275

What are the postsynaptic effects, precursors, rate-limiting step in synthesis, removal mechanism and type of vesicle for glycine?

Back 275

1. postsynaptic effect-inhibitory
2. removal mechanism-transporters
3. type of vesicle-small, clear

Front 276

What are the postsynaptic effects, precursors, rate-limiting step in synthesis, removal mechanism and type of vesicle for catecholamines (epinephrine, norepinephrine, dopamine)

Back 276

1. postsynaptic effect-excitatory
2. precursor-tryosine
3. rate-limiting step-tyrosine hydroxylase
4. type of vesicle-small, dense-core, or large irregular dense-core

Front 277

What are the postsynaptic effects, precursors, rate-limiting step in synthesis, removal mechanism and type of vesicle for serotonin?

Back 277

1. postsynaptic effect-excitatory
2. removal mechanism-transporters (MAO
3. type of vesicle-large, dense-core

Front 278

What are the postsynaptic effects, precursors, rate-limiting step in synthesis, removal mechanism and type of vesicle for histamine?

Back 278

1. postsynaptic effect-excitatory
2. removal mechanism-transporters
3. type of vesicle-large dense core

Front 279

What are the postsynaptic effects, precursors, rate-limiting step in synthesis, removal mechanism and type of vesicle for ATP?

Back 279

1. postsynaptic effect-excitatory
2. precursor-ADP
3. removal mechanism-hydrolysis to AMP and adenosine
4. type of vesicle-small, clear

Front 280

What are the postsynaptic effects, precursors, rate-limiting step in synthesis, removal mechanism and type of vesicle for neuropeptides?

Back 280

1. postsynaptic effect-excitatory and inhibitory
2. precursor-amino acids (protein synthesis)
3. removal mechanism-proteases
4. type of vesicle-large, dense-core

Front 281

What are the postsynaptic effects, precursors, rate-limiting step in synthesis, removal mechanism and type of vesicle for endocannabinoids?

Back 281

1. precursor-membrane lipids
2. rate-limiting step-enzymatic modification of lipids
3. type of vesicle-none

Front 282

What are the postsynaptic effects, precursors, rate-limiting step in synthesis, removal mechanism and type of vesicle for NO?

Back 282

1. precursor-arginine
2. rate-limiting step-NO synthase
3. removal mechanism-spontaneous oxidation
4. type of vesicle-none

Front 283

Describe ACh as a neurotransmitter.

Back 283

the transmitter at the NMJ, in the autonomic ganglia, post-ganglionic neurons in parasympathetic branch in many CNS neurons, inactivated by acetylcholinesterase, acts via ionotropic and metabotropic receptors, transported in vesicle transporters, use Na+/choline transporter to bring choline back into the presynaptic terminal after ACh is broken down by acetylcholinesterase

Front 284

What enzyme is used in the synthesis of ACh?

Back 284

choline acetyl-transferase, put together acetyl-CoA + choline

Front 285

Describe the nicotinic receptors.

Back 285

are a type of ACh receptor, is composed of a pentamer with alpha, beta, gamma, delta and epsilon subunits, ACh, nicotine, curare and bungarotoxin binding sites are on the alpha1 subunits and are specific for skeletal muscle nicotinic nAChR, while hexamethonium is specific for neuronal nACh receptors, can mix and match different subunits giving each different pharmacologies

Front 286

What is the significance of the torpedo fish?

Back 286

gives off an electrical current, used in studying summation, has modified muscle cells that generate electricity, can deliver a current of 60 amp at 80 V as a result of series and parallel summation of many of these specialized muscle cells

Front 287

Describe the muscarinic receptors.

Back 287

a type of ACh receptor, there are M1-M5 types coupled to various types of G-proteins regulating multiple cellular processes including the opening and closing of ion channels, the same receptors are found in muscle and nerve (as opposed to that found in nicotinic) but they are coupled to different processes

Front 288

Describe glutamate as a neurotransmitter.

Back 288

it is the principle fast excitatory neurotransmitter in the nervous system, half of the synapses in the brain are glutamatergic, there are ionotropic and metabotropic receptors, some ionotropic receptors can pass Ca2+ to trigger Ca2+ dependent events

Front 289

What enzyme is responsible for the formation of glutamate?

Back 289

glutaminase catalyzes the reaction glutamine -> glutamate

Front 290

What is the mechanism involved in the removal and inactivation of glutamate?

Back 290

glial cells are very active in removal and inactivation of glutamate, EAATs (excitatory amino acid transporter) collect glutamate (and turns it into glutamine via glutamine synthetase) while VGLUT loads the vesicles with glutamate

Front 291

What are the three types of ionotropic glutamate receptors?

Back 291

these are pharmacological agonists (activators), can mix and match different subunits to give different receptors, a tetramer
1. NMDA (N-methyl-D-aspartate) receptors
2. AMPA (alpha-amino-3-hydroxyl-5-methyl-isoxazole-proprionate) receptors
3. Kainate receptors (Kainic acid)

Front 292

Describe the NMDA receptor.

Back 292

the pore of this receptor passes Na+, K+ and Ca2+ (that acts as a 2nd messenger), this produces depolarization and activation of Ca2+ dependent processes (a twofer)

Front 293

What is the role of Mg2+ in the NMDA receptor?

Back 293

blocks the receptor, the block is very strong at normal resting potential such that activation of NMDA receptors alone might not evoke much depolarization, it is weaker if the neuron is depolarized such that activation of NMDA and AMPA receptors will result in big depolarization and Ca2+ entry, if Mg2+ is absent then there is a big current at all potentials, if Mg2+ is present, then there is a tiny current at the resting potential, but a bigger current at the depolarized potential

Front 294

How does long-term potentiation affect the glutamate receptor?

Back 294

the power of a glutamate synapse is adjustable, after high frequency (tetanus) stimulation of a pathway, stimulation of that pathway results in a larger EPSP, LTP requires strong depolarization, this depolarization relieves the block of NMDA channels by Mg2+ letting Ca2+ enter, Ca2+ activates kinases (CaM kinase II specifically) setting off a cascade resulting in more AMPA receptors and larger EPSPs, so when another stimulation comes there are lots of AMPA receptors leading to a bigger EPSP

Front 295

What is the importance of the coincidence detector in Ca2+ entry?

Back 295

the combination of activation of both AMPA and NMDA receptors (coincidence detector) is required for Ca2+ entry, this allows for long-term potentiation (or even long-term depression

Front 296

Describe what excitotoxicity is.

Back 296

many brain injuries result in maintained high levels of extracellular glutamate that can kill neurons with glutamate receptors, the mechanism of this killing is under investigation and elevations of [Ca2+]i are important, block of glutamate receptors can reduce cell death experimentally

Front 297

Describe the metabotropic receptors for glutamate.

Back 297

there are mGluR1-GluR8 types, coupled to various types of G-proteins regulating multiple cellular processes including the opening and closing of ion channels, there are these types of receptors on astrocytes too

Front 298

Describe GABA as a neurotransmitter.

Back 298

GABA is a major inhibitory neurotransmitter, it synthesized from glucose via the TCA cycle by glutamic acid decarboxylase

Front 299

How is GABA inactivated?

Back 299

it is inactivated by uptake (GATs) and breakdown in the mito

Front 300

What are the different types of GABA receptors?

Back 300

1. ionotropic receptors-2 types, GABAa and GABAc, they are Cl- channels and usually mediate IPSPs, benzodiazepines (Valium and Librium) activate GABAa receptors
2. metabotropic receptors-GABAb do the usual things, are G-protein coupled receptors

Front 301

Describe Glycine as a neurotransmitter.

Back 301

classified as the other inhibitory neurotransmitter that activates ionotropic Cl- channels

Front 302

Describe the biogenic amines as neurotransmitters.

Back 302

implicated in a range of behaviors (homeostasis, attention, movement, psychiatric disorders) in the CNS and in the ANS, include the catecholamines, histamine and serotonin

Front 303

Describe the synthesis of catecholamines.

Back 303

starts with tyrosine and uses tyrosine hydroxylase (as the rate limiting step) to produce norepinephrine and epinephrine, the enzymes presence in a neuron is a strong indicator that catecholamines are important, inhibition reduces synthesis of all catecholamines

Front 304

Describe norepinephrine as a neurotransmitter.

Back 304

is the neurotransmitter released by sympathetic post-ganglionic neurons, important in the CNS, inactivated by norepinephrine transporter (NET) that also transports dopamine and is inhibited by amphetamines

Front 305

What are the receptors for norepinephrine?

Back 305

are metabotropic alpha and beta-adrenergic receptors

Front 306

Describe epinephrine as a neurotransmitter.

Back 306

it is a transmitter in the CNS, inactivation mechanism is uptake but the transporter is not identified yet

Front 307

What are the receptors for epinephrine?

Back 307

are metabotropic alpha and beta-adrenergic receptors

Front 308

Describe dopamine as a neurotransmitter.

Back 308

dopaminergic neurons projecting from substantia nigra to corpus striatum are important coordinating movements (Parkinson’s Disease), motivation, reward, reinforcement, addiction, inactivation by Na+-dependent uptake (DAT) is inhibited cocaine

Front 309

Describe the receptors for dopamine.

Back 309

they are metabotropic receptors, consists of D1A, D1B, D2-D4 subtypes, they are coupled to various types of G-proteins regulating multiple cellular processes including opening and closing of ion channels

Front 310

Describe histamine as a neurotransmitter

Back 310

it is a neurotransmitter in the CNS, it mediates the allergic responses in the periphery

Front 311

How is histamine synthesized and inactivated?

Back 311

it is synthesized from histidine by histidine decarboxylase, it is inactivated by uptake but the transporter is not identified yet

Front 312

Describe serotonin as a neurotransmitter.

Back 312

serotonergic pathways in the CNS are involved in psychiatric disorders, serotonin is also huge in the periphery including the GI tract

Front 313

How is serotonin synthesized and inactivated?

Back 313

it is synthesized form tryptophan by trytophan-5-hydroxylase, it is inactivated by a specific serotonin transporter (SERT) that is inhibited by anti-depressant drugs (Prozac)

Front 314

What are the receptor types for serotonin?

Back 314

they are metabotropic receptors 5-HT 1, 5HT 2, 5HT 4-5HT 7, they do the usual things, there are also ionotropic receptors (5HT 3) that are nonselective cation channels

Front 315

Describe the purines (ATP, ADP, AMP, adenosine) as neurotransmitters.

Back 315

ATP is released along with all the other neurotransmitters (co-transmission) and there are important purinergic receptors with different sensitivities to each of the purines, extracellular ecto-5’ nucleotidases convert ATP to a soup of purines, thus one has a mix of purines hitting a mix of receptors, purinergic transmission is important in the periphery (smooth muscle) and in the CNS (mechanosensation and pain)

Front 316

What are the different types of purinergic receptors?

Back 316

there are P2X1-P2X7 subunits that mix and mtach to make up ionotropic receptos, these are nonselective channels, there are also P2Y1-P2Y8 that are metabotropic receptors that do the usual things, and there are also A1-A3 types that are metabotropic that also do the usual things

Front 317

Describe the synthesis of the large neurotransmitters (neuropeptides).

Back 317

genes encoding neuropeptides have a signal sequence that targets the pre-propeptides to the ER and golgit, these are processed to produce more than one neuropeptide

Front 318

What are the different types of neuropeptides?

Back 318

brain/gut peptides (including substance P-is a hypotensive agent, GI motility, CNS, pain) and the opioid peptides (including endorphins, enkephalins, dynorphins), there are also pituitary peptides, hypothalamic peptides

Front 319

Describe the different types of neuropeptide receptors.

Back 319

virtually all receptors are metabotropic receptors that do the usual things

Front 320

What are some rules that have emerged concerning neuropeptides?

Back 320

neuropeptides can travel to affect distant neurons, the effects of neuropeptides are characteristically slow and long lasting

Front 321

Describe endocannabinoids as neurotransmitters and their receptors.

Back 321

two have been identified (anandamide and 2-arachidonylglcerol) produced by Ca2+-dependent enzymatic degradation of membrane lipids, cannabindoid receptors are G-protein coupled receptors and act as retrograde messengers

Front 322

Describe NO as neurotransmitters and their receptors.

Back 322

it is generated by Ca2+ activated NO synthase, it is freely diffusible but with a short half-life, activates guanylyl cyclase and may have other actions, it is a retrograde messenger

Front 323

Describe neurotrophic factors as neurotransmitters.

Back 323

they are not routinely thought of as neurotransmitters, there receptors are tyrosine kinases