Neuro 3000 Exam #2 (Ntrans Systems 1 And 2)

Front 1

in the presynaptic axon terminal

Back 1

where are these located: Ntrans synthesizing enymes, synaptic vesicle trasnporters, reuptake transporters, degradative enzymes

Front 2

in the postsynaptic dendrite

Back 2

where are these strucures located:

trasnmitter gated channels

Gprotein coupled factors

g proteins

g-protein gated ion channels

second messenger cascades

Front 3

cholinergic

Back 3

cells that produce and release acetylcholine (ACh) are called this

Front 4

noradrenergic, GABAergic, glutamergic,peptidergic

Back 4

cells that make/release: noreprinephrine, GABA, glutamate, and peptides

Front 5

must have a neuron that makes it, must be released/controlled, and must have postsynaptic receptors for it

Back 5

to e classified as a ntrans, these three things must be true

Front 6

immunocytochemistry

Back 6

make antibodies to specific ntrans or enzymes which synthesize the ntrans

Front 7

in-situ hybridization

Back 7

detects RNA expression using a specific probe, labeled with radioactivity or colored flourescent product

Front 8

transmitter release

Back 8

can be difficult to study, though fluid near axons or cells can be tested for substance after stimulation and chemically anaylzed

Front 9

CNS

Back 9

in _______ many synapses using different ntrans arein close proximity, can't stimulate a single population of synapses

Front 10

in-vitro slice

Back 10

can stimulate a single nueron or group of cells in this, high K +and Ca+ dependency to characterize transmitter character

Front 11

loewi, ACh

Back 11

this experimenter identified this neurotransmitter by taking fluid out of the heart by the vagus nerve (helps keeps beat slower) and put it in a heart with no vagus nerve ---> the heart beat slowed

excitatory ntrans

Front 12

optogenetics

Back 12

can be used to control signaling in individual neurons, loops used to enhance cAMP, IP3, other secondary messengers etc

exploits cations that are sensitive to light (opens channels)

Front 13

different

Back 13

each ntrans can bind to _____ subtype(s)

Front 14

cannot

Back 14

two different ntrans (can/cannot) bind to the same receptor

Front 15

neuropharmacology

Back 15

uses agonists and antagonists to classify receptor subtypes, (ie, ACh, glutamate, NE (alpha and beta) and GABA -A and B

Front 16

muscarinic and nicotinic

Back 16

ACh is agonist for these 2 receptors

Front 17

nicotinc

Back 17

nicotine agonist for this receptor (s)

Front 18

muscarinic

Back 18

muscarine is an agonist for this receptor (s)

Front 19

curare

Back 19

antagonist for nicotinic receptor

Front 20

atropine

Back 20

antagonist for the muscarinic receptor

Front 21

AMPA, NMDA, kainate receptors

Back 21

glutamate is agonist for these three receptor types (plus subfamilies related to each receptor type)

Front 22

ligand binding

Back 22

type of receptor that uses ligands to bid specifically to receptors (label a ligand that binds)

Front 23

ligands

Back 23

can be the ntrans, agonist, antagonist

can be toxic

Front 24

cloning of many receptor cDNAs, protein sequencing

Back 24

methos used to analyze ntrans receptors

Front 25

amino acids

Back 25

most ntrans are this type

Front 26

dales principle

Back 26

neuron has only one ntrans

found to not be accurate, peptide containing neurons and other recently found neuron violate the idea

Front 27

ACh

Back 27

ntrans at neuromuscular junction, made by all motor neurons in spinal cord and brain

Front 28

basal forebrain, dorsalateral tegmentum of pons

Back 28

two major places with cholineric neruons in the brain

Front 29

basal forebrain

Back 29

neurons here take part in learning. memory, alzheimers

most are cholinergic

Front 30

dorsalateral tegmentum of pons

Back 30

place with lots of cholinergic neurons

involved in forebrain activity in sleep, wakefulness

Front 31

ChAT (choline transferase)

Back 31

required for synthesis, good marker for cholinergic cells

Front 32

choliergic systems

Back 32

system fairly widespread in the cortex

Front 33

acetyl CoA from glycolsysis and crebs cycle, choline made from blood

Back 33

ACh synthesis, primary reactants

Front 34

vesicular transporters

Back 34

help load ACh into the vesicle once it is synthesized

Front 35

choline (taken up again by choline transporter) and acetic acid (diffuses away)

Back 35

ACh breaks down to this

Front 36

choline

Back 36

uptake of this is the rate limiting step, treatments for some diseases such as alzheimers involve increasing these levels

Front 37

acetylcholinesterase

Back 37

ACh is degraded by _________ in the synaptic cleft 5000/sec

also made by some noncholinergic neurons, nerve gas and some insecticides

Front 38

choline transporter

Back 38

Na and Cl dependent transporter protein on the synaptic membrane, rate limiting step in ACh synthesis, regulated by protein kinase C and phosphatases

Front 39

13 times

Back 39

choline transporter winds in and out of the membrane ______ times

lots of places to be modified

Front 40

H+ gradient powered by H+-ATPase (2H+/ACh)

Back 40

fillling of the vesicular acetylcholine transporter (VAChT) driven by this

Front 41

catecholamines

Back 41

fairly important ntrans type: includes dopamine, noreprinephrine, and epinephrine

Front 42

catecholeminergic neurons

Back 42

neurons that are involved in mood, attention, and autonomic functions (fight or flight), all contain tyrosine hydroxylase (good marker)

end product inhibition

synthesized from tyrosine

Front 43

dopaminergic systems

Back 43

not as widespread in the cortex as cholinergic systems, important in motor control and parkinsons

from substantia nigra to caudate nucleus

Front 44

dopa

Back 44

amount of dopamine made depends on the amount of _____ available, basis for parkinsons treatment

Front 45

catecholamines

Back 45

these are not degraded in the synaptic cleft like ACh, but are transported back into the terminal by specific Na+ dependent transporters

Front 46

amphetamines and cocaine

Back 46

these two drugs block catecholamine degradation

Front 47

monoamine oxidase (MAO)

Back 47

catecholamines can be reloaded into the vesicle after upake or degraded by ______ in mitochondria

Front 48

adrenergic neurons

Back 48

present in noradrenergic neurons, in synaptic vesicles, not in cytosol

Front 49

PMNT

Back 49

adrenergic neurons contain ___________ which synthesizes epinephrine (adrenaline)

in the cytosol, NE made in the vesicle then released into the cytosol, the epinephrine taken back up into vesicles

Front 50

adrenaline

Back 50

used as ntrans in the brain and systematically released from the adrenal gland

Front 51

noreprinephrine

Back 51

major group of neurons with this in locus coeruleus which project to numerous structures including cortex, hipp, and hypothalamus

taken back up by specific transporter

Front 52

noradrenergic neurons

Back 52

modulates attention, feeding behavior, and sleep

Front 53

noreprinephrine

Back 53

ntrans with a different distribution but very widespread through the brain

Front 54

dopamine

Back 54

transported by vesicular transporter

removed from synapse and destroyed

Front 55

epinephrine

Back 55

present at lower level then other catecholamines

present in fewer neurons, function in CNS not known

Front 56

medulla

Back 56

major groups of adrenergic cells in this brain structure

Front 57

epinephrine

Back 57

not as widespread, mostly in the lower brain structures (not cortex)

Front 58

serotonin

Back 58

does NOT ONLY go through g protein coupled receptor, is both trasnmitter/ligand gated as well as g protein coupled

Front 59

serotonin

Back 59

neurons with this not in as many neurons, but is fairly widespread

regulates sleep, mood, emotional behavior, aggression

Front 60

raphe region of pons and upper brainstem

Back 60

place in the brain where there is a lot of serotonin

Front 61

raphe nucleus

Back 61

these neurons regulate pain signaling

Front 62

tryptophan

Back 62

sythesis of serotonin regulated by amount of ________ in extracellular fluid, brain _________ comes from the blood

Front 63

serotonin

Back 63

precursor to melatonin in the pineal gland

Front 64

MAO (monoamine oxidase)

Back 64

serotonin transported back into terminal, reloaded or degraded by _______

Front 65

amino acid neurotransmitters

Back 65

glutamate, GABA, glycine

in the CNS synapses

Front 66

glutamate transporters

Back 66

loads glutamate into synaptic vesicles

Front 67

GABA

Back 67

synthesized from glutamate by L-glutamic acid-1-decarboxylase (GAD)

glutamate is the precursor

Front 68

GAD (glutamic acid decarboxylase)

Back 68

not present in glutamatergic neurons or glia

in about 1/3 of all synapses in the brain, only there for the ones that express GABA

Front 69

GABA

Back 69

made only in neurons which use it

Front 70

GABAergic neurons

Back 70

major inhibitory system in the nervous system

present in many areas of the brain

Front 71

specific transporters

Back 71

AA transmitters (glutamate, glycine, GABA) taken up by the nerve terminal by _________

Front 72

glutamate

Back 72

in 1/2 of all synapses

involved in many circuits including learning and memory and motor functions

most excitatory neurons use this

long term potentiation and depression

involved in many, if not all, disorders

Front 73

glutamate

Back 73

________packed by vesicular ______ transporter

Front 74

excitatory amino acid transporters (EAAT)

Back 74

glutamate taken up (into glia or cell) by different types of transporters known as this type

Front 75

glutamate

Back 75

this ntrans does not cross the blood-brain barrier

Front 76

glutamate

Back 76

synthesized from glutamine or glucose and alpha-ketoglutarate

Front 77

Na dependent EAAT

Back 77

glutamate removed from cleft into nerve terminals or astrocytes by __________

3 and 4 are neuronal

1 and 2 are on glia

differentially expressed in the CNS

Front 78

vesicular

Back 78

_______ form of the transporter and all have somewhat similar structure

surface ones similar to surface ones

Front 79

GABA, glycine

Back 79

____________ does most inhibition in the CNS and __________mediates inhibition everywhere else

Front 80

GABA-A and glycine

Back 80

these receptors are Cl gated channels, structures are similar to the nAChR

Front 81

GABA (gamma aminobutyric acid)

Back 81

major inhibitory neurotransmitter

neurons with this present in many areas of the brain (1/3 of all synapses) and spinal cord

mostly present in local circuit interneurons, but some can be projection neurons

NOT present in peripheral tissues or nerves

Front 82

GABA

Back 82

involved in many diseases bc so widespread

Front 83

GABA

Back 83

signaling deficits of this molecule associated with Huntington's, Parkinson's, schizophrenia, senile dementia

Front 84

barbiturates

Back 84

modulators of GABA receptors, used to treat epilepsy

Front 85

vesicular inhibitory amino acid transporter

Back 85

GABA packaged into synaptic vesicles by ________

Front 86

GABA

Back 86

removal by high affinity transporters into neuron and glia, broken down in mitochondria

Front 87

vitamin B6

Back 87

this vitamin required as cofactor for sythesis, dietary deficiency lowers GABA synthesis, can lead to seizures

Front 88

GABA-A, GABA-B, GABA-C

Back 88

three types of GABA receptors,

Front 89

ionotropic

Back 89

GABA A and C receptors are this type

gate Cl- and are inhibitory

Front 90

metabotropic

Back 90

GABA-B is this type of receptor

Front 91

glycine

Back 91

half of inhibitory synapses in spinal cord are this ntrans

Front 92

glycine

Back 92

synthesized from serine by serine hydroxymethyltransferase

Front 93

vesicular inhibitory amino acid transporter

Back 93

glycine is loaded into vesicles by _____________

Front 94

glycine receptors

Back 94

these receptors are ligand gated Cl channels, similar in structure to GABA-A receptors

cys loop family member

Front 95

strychnine

Back 95

antagonist for glycine receptors

overstimulation of spinal/motor neurons and end up seizing

blocks inhibition and leaves to over-excitation

Front 96

ATP

Back 96

another ntrans that opens cation channel (nucleotide receptor)

Front 97

endocannabinoids

Back 97

ntrans that participates in retrograde signaling, not in vesicles, membrane permeable, bind to CB1 receptors, inhibits presynaptic Ca2+ channels

Front 98

ATP

Back 98

excitatory ntrans in sensory and autonomic ganglia and in motor neurons

Front 99

ATP and adenosine receptors

Back 99

these receptors are widespread

Front 100

adenosine

Back 100

not packaged into vesicles

is a breakdown product of ATP and can act as ntrns after breakdown of ATP

Front 101

purine receptor families

Back 101

two families of this

one ligand gated family (Pzx1-P2x7)

two transmembrane domains

have 2 gprotein coupled receptor families (A type, P type)

Front 102

retrograde

Back 102

this type of signaling is involved with endocannabinoids

this signal decreases the opening of presynaptic Ca channels (neg feedback loop that stops Ca channels from opening after there are a lot of ntrans released

Front 103

peptides

Back 103

1/3 of all ntrans are these

ALL are g protein coupled

processed more like proteins than classical small ntrans

can be more than one kind in a vesicle

often coreleased with small molecule ntrans

Front 104

peptide ntrans

Back 104

this type of ntrans include: endorphins, enkephalins, dynorphin, substance P

Front 105

nitric oxide

Back 105

ntrans sunthesized from arginine, released by some postsynaptic neurons, is a retrograde signal, permeable

a GAS so not packed into vesicles

enhance ntrans release in presynaptic side and prolong its time in the cleft

Front 106

carbon monoxide

Back 106

can act as a second messenger

tiny amount in the brain, can act as a signaling molecule

Front 107

transmitter gated channel

Back 107

the model for this is the nicotinic AChR from skeletal muscle

first ones to be discovered

Front 108

nicotinc AChR

Back 108

five subunits, four types (alpha, beta, gamma, delta)

each subunit has a unique sequence, but are similar

each subunit has 4 hydrophobic alpha-helical membrane spanning regions (transmembrane regions) these can go through the bilayer

Front 109

glutamate receptors

Back 109

exception to the rule that transmitter gated receptors has 5 subunits with 4 transmembrane regions

Front 110

nicotinic receptors

Back 110

these receptors have different properties with different subunit makeups

about 10-15 have been identified, all are transmitter gated

can be heteromeric(mix of alpha and beta) or homomeric

has a pocket that can be seen

Front 111

receptor channel

Back 111

specifc amino acids control the gating of this

at opening have negatively charged AAs the help cations go through

ring of pos charged AAs help the chlorine get through

Front 112

resting state

Back 112

ACh receptors are in this state when the channels are closed

low affinity binding

Front 113

active

Back 113

ACh receptors are in this state when the channel is open

low affinity binding

Front 114

desensitization

Back 114

this occurs to ACh receptors when ntrans bound for too long and not removed from the synapse, the channel may become inactive after long term ____________

high affinity bonding

Front 115

alpha 7 receptor

Back 115

genetic relationships exist among ACh receptor types, this type is most likely the common ancestor

Front 116

brain regions

Back 116

receptors have specificity to certain brain regions

Front 117

amino acid gated channels

Back 117

mediate fast synaptic transmission in CNS

involved in many systems and diseases

Front 118

glutamate receptors

Back 118

examples of this type of receptors include: AMPA, NMDA, kainate

Front 119

AMPA

Back 119

glutamate receptor permeable to Na+ and K+, NOT Ca2+

activation causes Na+ entry and depolarization, coexist with NMDA receptors

Front 120

NMDA

Back 120

glutamate receptor

permeable to Ca2+

inward current is voltage dependent

Ca2+ entry important to many actions

Front 121

Mg2+

Back 121

NMDA receptor can be blocked by this ion

blocks the hole at -65mV

-------> no learning if receptor blocked

Front 122

AMPA

Back 122

these receptors are NOT blocked by Mg2+

can open up and depolarize the cell

Front 123

benzodiazapines

Back 123

(ie, valium)

modulate GABA-A and glycine receptors to increase frequency of opening

Front 124

barbiturates

Back 124

modulate GABA-A and glycine receptors to increase channel open time

Front 125

common themes in ligand gated ion channels

Back 125

1.) multiple subtypes

2.) each subtype has distinct pharmacology properties

3.) 4 transmembrane regions

4.) ligand binding sites at subunit interfaces

5.) each subtype with distinctive expression pattern

6.) 5 subunits

Front 126

g protein coupled receptors

Back 126

have 7 transmembrane regions

extracellular loops form binding site for the ligands

bind to some of the intracellular loops and are activated upon transmitter binding

100+ types are known

metabotropic receptor

Front 127

conformational change

Back 127

where the ntrans binds to the g protein coupled receptor signals a _____________

Front 128

g proteins

Back 128

guanosine triphosphate (GTP) binding proteins

20 kinds

three subunits (alpha, beta, gamma)

when activated, splits into G-alpha + GTP and G-beta/gamma

can stimulate or inhibit

activates effector systems, G-alpha converts GTP to GDP, stopping action

different ones can have different effects

Front 129

GDP

Back 129

bound to G-alpha on the inside of the membrane

Front 130

g protein coupled systems

Back 130

shortcut pathway-when activated, binds to ion channel, 30-100 milisecond timescale, localized

Front 131

second messenger cascades

Back 131

part of g protein coupled systems

multiple steps, activation of enzymes

takes several seconds to do something

kinases and phosphatases involved in many cascades (work in opposite ways)

Front 132

multiple pathways

Back 132

activated g proteins can stimulate ________

Front 133

signal cascades

Back 133

slow

amplification

many control points

longer range signaling

long lasting effects

Front 134

signal amplification

Back 134

can occur on the timescale of seconds

one ntrans can activate may channels

can be upregulated or down regulated