Week Ii - More Nervous System Basics

Front 1

Which cranial nerves have components that lie outside the CNS?

Back 1

III, VII, IX and X

Front 2

List the three connective tissue sheaths found in a peripheral nerve from the outside in.

Back 2

1. Epineurium-surrounds nerve
2. Perineurium - surrounds nerve fascicle
3. Endoneurium - surrounds individual exon

Front 3

Which CT layer of the nerve behaves like a blood-nerve barrier?

Back 3

The Perineurium

Front 4

Do the CT sheaths surrounding the nerve have a blood supply or are they avascular?

Back 4

They have a blood supply

Front 5

There are two distinct areas seen in a myelinated axon. name them and describe which cellular side they are on.

Back 5

1. major dense line - cytoplasmic side (dark due to squished proteins in cell)
2. intraperiod line - extracellular side

Front 6

What are the 2 main proteins found in myelin of peripheral nerves?

Back 6

1. MBP (myelin basic protein)
2. Po

Front 7

Charcot-Marie-Tooth disease is a mutation of what? (mutated thing pertains to myelin)

Back 7

mutation of the Po protein

Front 8

What is the analog of Po in the CNS? What about MBP?

Back 8

PLP (proteolipid protein)
MBP has no analog; it is present as itself in the CNS

Front 9

define the following nerve-nerve synapses: axodendritic, axosomatic, axoaxonic, dendrodendritic

Back 9

axodendritic: axon synapses on dendrite
axosomatic: axon synapses on soma (cell body)
axoaxonic: axon synapses on another axon
dendrodendritic: dendrite synapses on another dendrite

Front 10

List the 3 types of ganglia

Back 10

1. sensory
2. sympathetic
3. parasympathetic

Front 11

There are 2 types of sensory ganglia. What are they?

Back 11

dorsal root ganglia
cranial ganglia

Front 12

autonomic ganglia are characterized by _________ (multi/uni/pseudouni polar) neurons.

Back 12

multipolar

Front 13

In what type of ganglia are neuron-neuron synapses found?
In what type of ganglia are no neuron-neuron synapses found?

Back 13

Found in autonomic ganglia
not found in sensory ganglia

Front 14

* What type of nerve cell damage results in cell death?
* What type of nerve cell damage results in regeneration?

Back 14

* Damage to the perikaryon results in cell death
* Damage to the axonal processes can result in regeneration

Front 15

What are the three findings observed with perikaryon damage?

Back 15

1. chromatolysis
2. eccentric nucleus
3. perikaryon swells

Front 16

Define primary and secondary degeneration. Where does this occur?

Back 16

occurs in the axon after damage.
1. primary degeneration - degeneration of axon proximal to cut. (minor)
2. secondary degeneration - degeneration of axon distal to cut (complete)

Front 17

T/F: Schwann cells do not degenerate when the axon they are associated with degenerates.

Back 17

FALSE. Schwann cells degenerate along with the axon.

Front 18

What happens to the endoneurium after axonal damage? Why is this critical for regeneration?

Back 18

The endoneurium remains as a hollow tube and is now called the endoneurial tube. Schwann cells eventually proliferate and fill the tube.

Front 19

What are Bugner Bands? What is their function?

Back 19

endoneurial tubes filled with Schwann cells. Axon sprouts grow along these bands.

Front 20

Distinguish between inter- and intra- cellular signalling.

Back 20

intercellular - between cells
intracellular - within cells (from one end to another)

Front 21

What are the advantages of utilizing electrical intracellular transport vs. the other types of transport?

Back 21

FAST transmission
MODIFIABLE - can increase or decrease signal very easily
diffusion and transport are slow mechanisms and are not modified easily.

Front 22

neuronal electrical potentials are dependant on 2 things:

Back 22

1. DIFFERENT ION CONC. on the inside and outside
2. SELECTIVE PERMEABILITY of the plasma memb. to different ions

Front 23

the electrochemical gradient is formed by two separate forces. what are they?

Back 23

1. concentration gradients
2. electrical charges

Front 24

when determinig the voltage potential of a neuron, what is the reference point?

Back 24

the outside of the neuron is assumed to have a charge of 0.

Front 25

*What is the resting membrane potential for most neurons?
*What does this mean in regards to charge differences across the membrane?

Back 25

-60 to -75 mV
*the inside of the cell is more negative than the outside.

Front 26

what is the difference between an ion channel and an ion transporter?

Back 26

*ion channel - passive, specific; ions flow down concentration gradient
*ion transporter - active, specific; ions move against concentration gradient & create gradients

Front 27

which ion is responsible for maintenance of the resting membrane potential?

Back 27

K+ (flows out of the cell leaving the inside very negative)

Front 28

At RMP: which ions are very permeable? which ions are not?

Back 28

Very permeable: K+, Cl-
Not: Na+, Ca++
* K+ and Cl- follow concenration gradient

Front 29

T/F: at electrochemical equilibrium K+ is moving outside of the cell

Back 29

FALSE: by the time electrochemical equil. is reached the [K+] on the inside and outside are equal.

Front 30

the equilibrium potential of K+ is -120 mV. Why is the RMP of a neuron only -60 mV?

Back 30

This is due to a slight influx of Na+ that makes the RMP more (+)

Front 31

What is the neuron membrane potential of Na+?

Back 31

+56 mV

Front 32

What are two types of graded potentials (which are a subcategory of slow potentials)?

Back 32

1. Spatial
2. Temporal

Front 33

Which ion has the greatest influence on the RMP? How about the AP?

Back 33

RMP -> K+
AP -> Na+

Front 34

in an AP, what phases does Na+ control and what phases does K+ control?

Back 34

Na+ controls: rising phase and overshoot phase
K+ controls: undershoot phase and termination

Front 35

What [exactly] is the factor that initiates the AP?

Back 35

an increase in Na+ permeability; hence Na+ rushes into the cell

Front 36

Describe the membrane permeability changes throughout the AP.

Back 36

Rising and Overshoot phases -membrane very permeable to Na+
Undershoot phase - Na+ permeability turned off, K+ perm. increased
Termination phase - K+ permeability decreases and cell returns to resting state

Front 37

Describe the changes in the voltage gated ion channels during an AP.

Back 37

1. RMP - both closed
2. early depolarization - Na+ channels open
3. later depolarization and early hyperpolarization - Na+ channels inactivated; K+ channels open
4. later hyperpolarization - both closed, return to RMP

Front 38

Why is there a refractory period after an AP?

Back 38

Na+ channels take a while to "reset."

Front 39

What is essential for neurons to maintain RMP?

Back 39

ATP to run their Na+/K+/ATPases

Front 40

T/F: an AP degrades as it moves along an axon.

Back 40

FALSE: an AP does not degrade as it moves down the axon. An AP in one area induces an AP in another area, kind of like passing a baton in a relay race.

Front 41

Why does an AP not spread in both directions down the axon?

Back 41

The refractory period from where the AP just came from prevents that.

Front 42

in what part of a neuron does the AP usually start?

Back 42

the axon hillock

Front 43

is passive current flow fast or slow?

Back 43

fast: it is almost instantaneous and is used between the nodes of Ranvier.

Front 44

Which is faster: saltatory conduction or sequential conduction?

Back 44

saltatory conduction. sequential conduction occurs in an unmyelinated axon.

Front 45

List the 3 types of ion channels.

Back 45

1. voltage gated (only open within a certain voltage range)
2. ligand gated (ion channel opened by specific chemical signal)
3. stretch & heat activated (sensory receptors that generate receptor potentials)

Front 46

What are the two active transporters that return a cell to RMP?

Back 46

ATPase pumps
Ion Exchangers

Front 47

Why are myelinated axons more energy efficient than unmyelinated axons?

Back 47

myelinated axons have fewer ATPases (only at nodes of Ranvier), therefore they use less ATP.

Front 48

There are two types of electrical synapses: what are they and how does each type work?

Back 48

1. Ephatic transmission (ion flow in one axon influences other axons)
2. Gap junctions (pores that connect adjacent cells)

Front 49

What are the special structures (2) for chemical neurotransmission called and where is each found?

Back 49

1. terminal boutons (at axon terminal)
2. en passant boutons (along the axonal length)

Front 50

which is slower: chemical or electrical synapses?

Back 50

chemical synapses are slower (neurotransmitter must cross synaptic cleft and act on receptors). electrical synapses are virtually instant

Front 51

Which ion is essential for presynaptic transmission?

Back 51

Ca++ (rushes into neuron and causes vesicles to fuse w/plasma membrane)

Front 52

What happens once the neurotransmitter binds to its postsynaptic receptor?

Back 52

Ion channels open, ions flow in and alter membrane potential in postsynaptic cell. (this may initiate or inhibit an AP here)

Front 53

in a neuromuscular junction: what is the presynaptic neuron and what is the postsynaptic cell?

Back 53

presynaptic neuron: a-motor neuron
postsynaptic cell: skeletal muscle

Front 54

What neurotransmitter is used exclusively by the NMJ and is it (+) or (-)?

Back 54

ALWAYS Acetylcholine
ALWAYS (+)

Front 55

Where are neuron-neuron chemical synapses found? Are they (+) or (-)

Back 55

In both the CNS and PNS. May be either (+) or (-)

Front 56

What is a postsynaptic potential? Is it (+) or (-)

Back 56

a slow potential that sums temporally and spacially to sometimes form a postsynaptic AP. Can be either (+)EPSP or (-)IPSP

Front 57

EPSPs are due to the influx of what ion?
What about IPSPs?

Back 57

EPSPs: due to influx of Na+ or Ca++ (depolarize)
IPSPs: due to influx of Cl- (hyperpolarize)

Front 58

T/F: EPSPs and IPSPs can sometimes cancel eachother out.

Back 58

TRUE. When an EPSP and an IPSP occur at the same time the net effect is 0. (they cancel eachother out)

Front 59

what is presynaptic inhibition of a postsynaptic potential?

Back 59

when presynaptic axon terminals are inhibited there is no terminal depolarization: therefore no postsynaptic depolarization

Front 60

Mini end plate potentials sum up to form ___________, which are a form of postsynaptic potential.

Back 60

end plate potentials

Front 61

what is the result of a miniature end plate potential?

Back 61

results in a spontaneous release of one synaptic vesicle worth of neurotransmitter (1 quantum)

Front 62

What is the difference between secretory vesicles and synaptic vesicles?

Back 62

secretory vesicles: contain neuropeptides, open anywhere along axon
synaptic vesicles: contain neurotransmitters, open only at terminal or passant boutons.

Front 63

What is a docking complex?

Back 63

a specialization in the presynaptic membrane that binds synaptic vesicles.

Front 64

T/F: synaptic vesicles are recycled. Why/why not?

Back 64

TRUE - this cuts down on time (otherwise vesicles have to come from neuronal soma)

Front 65

What determines the number of vesicles released during one AP?

Back 65

amount of Ca++ influx into cell

Front 66

What 2 proteins prime the vesicle for fusion to the docking complex of the presynaptic membrane?

Back 66

NSF and SNAP

Front 67

SNAP and NSF regulate ___________.

Back 67

the assembly of SNAREs (SNAP receptors)

Front 68

what is the name of the protein that binds Ca++ upon its influx into the presynaptic terminal? What is it's other function?

Back 68

synaptogogmin: also senses Ca++ levels and triggers vesicle fusion

Front 69

Name the 3 protiens involved in vesicle recycling. what are their specific functions?

Back 69

1. clathrin - buds recycled vesicles from plasma membr.
2. dynamin - pinches off membranes after budding
3. synapsin - keeps vesicles tethered to cytoskeleton for a reserve pool.

Front 70

define: neurotransmitter

Back 70

neural signalling molecules that can act alone

Front 71

what is the difference between a neurotransmitter and a neuromodulator/neuroeffector?

Back 71

neurotransmitters act alone (primary signaling molecule)
neuromodulators are secondary neurotransmitters as they modify the signal of the primary neurotransmitter

Front 72

Give an example of:
1. a neurotransmitter and
2. a neuromodulator/effector.

Back 72

1. acetylcholine
2. neuropeptides

Front 73

Give an example of:
1. a small molecule neurotransmitter
2. a neuropeptide
3. a gas neurotransmitter

Back 73

1. classic transmitters: Ach, glutamate, aspartate, GABA, glycine, ATP, DA, NE
2. any peptide 3-26 aa long
3. NO, CO

Front 74

small neuropeptides are synthesized in ____________, whereas peptide neurotransmitters are synthesized in ___________.

Back 74

neuron terminals
cell body

Front 75

What are the 3 ways a neurotransmitter is removed from the synaptic cleft?

Back 75

1. diffusion
2. reuptake in neuron or glia
3. degradation

Front 76

When would a cotransmitter be observed?

Back 76

when a neuron makes and releases more than 1 neurotransmitter

Front 77

What decides the neurotransmitter action (whether the AP is (+) or (-))?

Back 77

type and location of neurotransmitter receptors.

Front 78

what is the difference between:
1. cell-permeant (intracellular) receptors
2. cell-impermeant (transmembrane) receptors?

Back 78

1. A lipophilic neurotransmitter crosses the p.m. to access the receptors inside.
2. neurotransmitter binds to receptors found on the membrane.

Front 79

What are 3 types of transmembrane (cell-impermeant) receptors?

Back 79

1.ionotropic(channel-linked)
2.enzyme linked - alters intracellular target proteins
3. metabotropic (G-protein coupled), initates GTP-mediated cascade.

Front 80

which receptor is faster: an ionotropic or metabotropic receptor?

Back 80

ionotropic - msec response
(vs. metabotropic, sec->min response)

Front 81

what is the advantage of a metabotropic receptor?

Back 81

these receptors can amplify signals by activating signal transduction: signal is also long lasting

Front 82

What is the basic pathway through a metabotropic receptor (binding to eventual physiological response)

Back 82

NT binds,(+) G-protein,(+) 2nd messenger, this (+) enzymes that alter the phosphorylation of protiens, which alters RNA and protein synthesis.

Front 83

give an example of 4 second messengers used by metabotropic receptors.

Back 83

1. Ca++
2. cAMP, cGMP
3. IP3, DAG
4. NO

Front 84

Regarding Ach:
1. where found?
2. Precursor?
3. Removal mechanism?
4. classes of receptors?

Back 84

1. NMJ, glands, (+) in CNS
2. acetyl CoA & choline
3. AchE(acetylcholinesterase)
4. nicotinic, muscarinic

Front 85

nicotinic receptors:
1. type?
2. usually (+) or (-)
3. Agonist?
4. Antagonist?

Back 85

1. ligand-gated
2. (+) because open to all cations
3. nicotine
4. curare

Front 86

muscarinic receptors:
1. type (class)
2. two kinds of muscarinic receptors, name&where found?
3. Agonist?
4. Antagonist?

Back 86

1. metabotropic, in CNS & PNS
2. M1-CNS, M2-peripheral
3. muscarine, pilocarpine
4. atropine, scopolamine

Front 87

Neurotransmitter used by 95% of ecitatory neurons in brain?

Back 87

Glutamate

Front 88

glutamate:
1. where made?
2. precursor?
3. types (classes) of receptors?

Back 88

1. nerve terminals
2. glutamine (from glia), or glucose (via TCA cycle)
3. both ionotropic and metabotropic

Front 89

Does glutamate cross the BBB?

Back 89

NO (therefore it must be synthesized in within the CNS)

Front 90

PCP and ketamine are antagonists at which receptors? What neurotransmitter normally binds here?

Back 90

*NMDA receptors
*glutamate normally binds to NMDA receptors

Front 91

What are the two major inhibitory neurotransmitters of the CNS and, more specifically, where are they found?

Back 91

GABA (brain)
Glycine (spinal cord)

Front 92

why is strichnine toxic?

Back 92

b/c it blocks glycine receptors

Front 93

catecholamines, seratonin and histamine can all be classified as _____________.

Back 93

biologic amines

Front 94

Where is NE made in the CNS?
what is the precursor?

Back 94

in the locus ceruleus (precursor - tyrosine)

Front 95

What are the 2 enzymes that remove catecholamines?
Where are they found?

Back 95

MAO-B
COMT
Both found in neurons & glia

Front 96

what type of receptors do catecholamines use?

Back 96

metabotropic receptors (that are G protein coupled)

Front 97

what type of receptors do histamines use?

Back 97

metabotropic (H1-H4)

Front 98

which H receptor do antihistamines and anti-nausea medications work against?

Back 98

H1

Front 99

1. Where is seratonin made?
2. Precursor?
3. what is the name of the only ionotropic seratonin receptor?

Back 99

1. main Raphe nucleus
2. tryptophan
3. 5-HT3

Front 100

what type of receptors are 5-HT1 and 5-HT2 receptors? function?

Back 100

*metabotropic seratonin receptors
*implicated in higher functions and motor behaviors

Front 101

What is the source of ATP, AMP and adenosine in the CNS?

Back 101

comes from mitochondrial oxidative phosphorylation and glycolysis

Front 102

Purines have what type of receptors?

Back 102

both ionotropic(+) and metabotropic(-)

Front 103

how does coffee work?

Back 103

blocks adenosine metabotropic(-) receptors in the CNS; therefore stimulates

Front 104

morphine and other narcotics are _________ neurotransmitters. (class) They act at __________ receptors.

Back 104

peptide
metabotropic

Front 105

m-opiod receptors are what type of receptor? The fact that morphine can act at such a low concentration classifies it as_________ action.

Back 105

matabotropic
paracrine

Front 106

T/F: peptides can be found & released anywhere along an axon. Release is slow

Back 106

TRUE
slow release, however, do not need docking complexes to coordinate exocytosis.

Front 107

What are the 5 terminal branches of CN VII?

Back 107

temporal
zygomatic
buccal
mandibular
cervical

Front 108

what three muscles make up the "nasal group?"

Back 108

1. nasalis
2. procerus
3. depressor septi

Front 109

name the four deep muscles of the face

Back 109

1. buccinator
2. levator anguli oris
3. depressor labii inferiorus
4. mentalis

Front 110

Name the 8 superficial muscles of the face.

Back 110

orbicularis oris, zygomaticus major and minor, levator labii superioris, levator labii superioris aleque nasi, depressor anguli oris, platysma, risorius

Front 111

what muscle is found in the temporal fossa?

Back 111

temporalis

Front 112

Where are the branches of the anterior division of the mandibular branch of CN V going?

Back 112

motor: to temporalis, masseter, lateral and medial pterygoids
sensory: buccal

Front 113

What are the branches of the posterior division of the mandibular branch of CN V?

Back 113

motor: to mylohyoid and ant. belly of digastric
sensory: auriculotemporal n., lingual n, inferior alveolar n.