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22 spring: neurology > test 1: lecture 4 and 5 > Flashcards

test 1: lecture 4 and 5 Flashcards

1
Q

___ neuroanatomical structure that permits communication between a neuron and its target cell.

A

synapse

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2
Q

____ is the physical “gap” between neuron and target organ

A

synaptic cleft

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3
Q

axodendritic

A
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4
Q

axiosomatic synapse

A
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5
Q

axoaxonix

A
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6
Q

neurotransmitters are stored in ___

A

vesicles

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7
Q

three reasons to use vesicles to store neurotransmitters

A

quantal release (release entire payload into the synaptic cleft)

protect NT from degradation

storage- many NT are recycled

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8
Q

how does AP influence voltage gated N-type Calcium channels near synapse?

A

depolarization (+ charge) will cause Ca+ channels to open and Calcium will flood into the axon

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9
Q

How do NT get into synaptic vesicles

A

proton pump pushes H into vesicle

transmitter transporters will use the energy of returning H to the outside of the vesicle to bring NT into the vesicle

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10
Q

___ causes the release of vesicle from cytoskeleton

A

voltage gated Ca open

Calcium floods into cell

calcium-dependent phosphorylation of synapsin (Ca2+/calmodulin kinase)

calcium binds with synapsin and synapsin lets go

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11
Q

SNARES

A

Soluble N-ethylmaleimide-sensitive fusion protein attachment receptor

Vesicular (v-SNARE) vs Terminal (t-SNARE)

help vesicle bind to plasma membrane

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12
Q

2 types of V-snares

A

synaptobrevin

synaptotagmin

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13
Q

two types of t-SNARES

A

syntaxin

SNAP-25

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14
Q

___ regulates the assembly of SNAREs that tether the vesicle to the presynaptic membrane

A

SNAP-25 (a t SNARE)

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15
Q

___ is a Ca2+ sensor and catalyzes membrane fusion and NT unloading

A

Synaptotagmin

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16
Q

tetanus toxin damages what SNARE?

A

synaptobrevin (v-SNARE)

has to do with SNAP-25 (a t-SNARE) binding the vesicle to syntaxin(t-SNARE)

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17
Q

what toxin damages t-SNARES

A

botulinum

C1→ syntaxin and SNAP 25

A and E → SNAP-25

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18
Q

what SNARE will botulinum B,D,F,G and tenatus attack?

A

synaptobrevin (v-SNARE

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19
Q

C. botulinum bacterium grows in the intestinal tract and produces toxins. This happens most often in foals and is also called “___” Human correlate can happen by feeding honey to infants (< 1 years old).

A

shaker foal syndrome.

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20
Q

INGESTION OF PREFORMED TOXIN: Occurs when animals ingest feed that has been contaminated with ___ toxin, such as hay or silage that has been improperly produced or stored, or that has been contaminated by an animal that has died of botulism. This form can affect animals of any age

A

botulinum

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21
Q

where are ion channels found in mammalian CNS

A

–Vestibular nucleus

–Nucleus of trigeminal nerve

–Inferior olivary nucleus

(rare)

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22
Q

ion channels are formed by ___-

A

connexins

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23
Q

neuronal gap junctions

A

direct connection of one cell to another that allows ions to flow (share electrical current from cell to cell)

rare

formed by connexins

allow synchronous firing (fire one- fire them all)

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24
Q

Gap junctions allow for rapid ___ stimulation.

A

excitatory

can fire one and it will fire all that are directly connected

•Used to respond with high frequency (µsec) in nerve cells.

Stay open for seconds to minutes.

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25
Q

how is electrical current shared between cells

A

neuronal gap junctions

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26
Q

compare electrical and chemical synapses

A
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27
Q

what kind of synapse can be bidirectional?

A

electrical (neuronal gap junctions)

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28
Q

which synapse is wider electrical or chemical?

A

chemical

(synaptic cleft can be 30-50nm apart)

electrical (2-3 nm very small)

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29
Q

two types of Neurotransmitter receptors

A

ionotropic

metabotropic

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30
Q

if an ion channel is inhibitory what will happen

A

cell becomes more negative (hyperpolarization)

K+ will leave or Cl- will enter

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31
Q

if an ion channel is excitatory what will happen?

A

cell will become more positive (depolarization)

Na+ or Ca2+ will enter cell

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32
Q

ligand gated ion channels

A

type of neurotransmitter receptor

ionotropic receptor

ion binds and opens channel

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33
Q

___ is direct modulation of neuron excitability

A

ionotropic receptor

(ligand gated ion channel)

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34
Q

how do ionotropic receptors work?

A

neurotransmitter binds

channel opens

ions can flow in or out based on excitatory or inhibitory

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35
Q

___ are G protein coupled receptors

A

metabotropic

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36
Q

how does metabotropic receptor work?

A

neurotransmitter binds to receptor, this triggers change in G protein

alpha subunit will go off and cause secondary messangers

gamma and beta subunit will go off and cause downstream regulation of ion channels

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37
Q

___ will indirectly modulate neuron excitability by downstream regulation of ion channels

A

metabotropic receptors (G protein linked)

38
Q

autoreceptors

A

•On presynaptic terminals either ionotopic or metabotropic

•Regulates transmitter release,

INHIBITS FURTHER NT RELEASE

•Can be a different subtype compared to postsynaptic receptors

POTENTIAL FOR SPECIFIC DRUGS TO CONTROL NT RELEASE

39
Q

criteria for neurotransmitter

A

in terminal

Ca2+ dependent release

subject to inactivation

synaptic mimicry

receptors exist on postsynaptic cell

40
Q

what is the most common type of neurotransmitter

A

amino acid NT

41
Q

90% of synapses involve what 4 amino acid transmitters?

A

glutamate, aspartate, GABA or glycine

42
Q

what amino acids NT are excitatory?

A

Glutamate, Asparate

43
Q

what amino acid NT are inhibitory

A

GABA and glycine

(make cell more negative)

44
Q

what kind of receptors do amino acid NT use?

A

Most work through ionotropic (ion channel) receptors.

Some use metabotropic receptors (i.e. linked to second messengers such as IP3 or cAMP).

45
Q

how are amino acid NT inactivated

A

rapid re-uptake by energy dependent channels that will place amino acid into vesicles or into pool of amino acids

glial cells will also reuptake AA

46
Q

the major excitatory NT is ___

A

glutatmate

47
Q

3 types of ionotropic receptors for glutamate

A
  • NMDA (N-methyl-D-aspartate)
  • AMPA
  • Kainate
48
Q

The ___ receptor is of great interest because it seems to be heavily involved in learning and memory.

A

ionotropic NMDA

glutamate receptor (excitatory)

49
Q

___ is the major inhibitory NT in the CNS

A

GABA

(γ-aminobutyric acid)

50
Q

___ is important in inhibitory control of interneurons

A

GABA

51
Q

how to make GABA

A
52
Q

if a cell has glutamic acid decarboxylase (GAD) what amino acid NT does it use?

A

GABA

53
Q

two types of GABA receptors

A

A: ion channel: Allow Cl- ions into neuron resulting in membrane _hyper_polarization

B: G-protein coupled, several subtypes cloned- Connected to K+ channels to cause membrane _hyper_polarization

GABA is an inhibitory NT

54
Q

Increasing overall ___ of CNS is useful for sedation, anesthesia, anxiolytics, and seizure control

A

inhibition

55
Q

ketamine blocks ___ receptor for ___

A

NMDA

receptor for glutamate which is excitatory

blocking this will have inhibitory effect

56
Q

Benzo and barbituates act to enhance what receptors ___

A

GABAa

receptor for GABA which allows Cl- into the cell causing hyperpolarization or inhibitory effect

57
Q

how to make acetylcholine

A
58
Q

how does acetylcholine work as NT?

A
59
Q

how is acetylcholine NT inactivated

A

there is acetylcholinesterase on the postsynaptic cell that breaks acetylcholine into acetate and choline

choline can be reabsorbed and used to make more acetylcholine

60
Q

can acetylcholine released into the synaptic cleft be reused?

A

no they are broken down into choline and acetate, the cell has to make new ones every time

but choline can be reabsorbed and used to make more acetylcholine

61
Q

what are some CNS functions of acetylcholine

A

Behavioral Arousal

Attention

REM sleep

Memory

Learning

Aggression

Grand Mal Seizures

Sensory Perception

Energy Conservation

Mood

Motor Coordination

62
Q

___ is a prominent neurotransmitter of the Autonomic Nervous System

A

Acetylcholine

63
Q

neuromuscular junctions use ___ as a NT

A

acetylcholine

64
Q

____ are irreversible inhibitors of acetylcholinesterase inhibitors

A

organophosphates

  • Insecticides: malathion, acephate, diazinon.
  • Poisonous gases: Sarin and Soman.
65
Q

Myasthenia gravis is an autoimmune disease with decreasing numbers of ___ receptors at neuromuscular junction

A

nicotinic

66
Q

how to treat myasthenia gravis

A

give short acting reversible AChE inhibitor such as edrophonium chloride

myasthenia gravis is when receptors for ACh (nicotinic receptors) are low or damaged by blocking enzyme that breaks down ACh it allows more ACh to attach to the ACh receptors that are there

67
Q

tyrosine is the precursor to what type of monoamines?

A

catecholamines such as dopamine, norepinephrine and epinephrine

68
Q

dopamine, norepinephrine and epinephrine are ___

A

catecholamines derived from tyrosine

type of monoamines

69
Q

tryptophan gives rise to what type of monoamine?

A

indoleamines

serotonin and melatonin

70
Q

serotonin and melatonin are __

A

type of indoleamines derived from tryptophan

type of monoamine

71
Q

what is the precursor of histamine

A

histidine

72
Q

what is the rate limiting step to make catecholamines?

A
73
Q

how to make norephinephrine

A

tyrosine (tyrosine5 hydroxylase) → DOPA(aromaic amino acid decarboxylase)→ dopamine (dopamine-β-hydroxylase) →norephonephrine

74
Q

how to make epinephrine

A

tyrosine (tyrosine5 hydroxylase) → DOPA(aromaic amino acid decarboxylase)→ dopamine (dopamine-β-hydroxylase) →norephonephrine (phenylethanolamine-N-methyl transferase) → epinephrine

75
Q

compare catecholamine to (indoleamine) serotonin production

A

similar rate limiting step

same enzyme for 2nd step

76
Q

compare breakdown of catecholamine and indoleamines

A

serotonin is an indoleamine

77
Q

Monoamine Oxidase breakdown __

A

can break down both indoleamines(serotonin) and catecholamines(dopamine, norephinephrine, epinephrine)

78
Q

•Serotonin, norepinephrine, and epinephrine mainly broken down by ___

A

MAO-A

Monoamine Oxidase

79
Q

•Dopamine broken down equally by ___

A

both MAO-A and MAO-B

80
Q

MAO is a mitochondrial enzyme and is NOT the mechanism for removal of monoamines from___

A

the synapse

81
Q

how are catecholamine (such as dopamine) inactivated in the synaptic cleft?

A

rapid reuptake by specific transporters

82
Q

how are catecholamine (such as norepinephrine) inactivated in the synaptic cleft?

A

rapid reuptake by specific transporters

83
Q

how is serotonin inactivated?

A
84
Q

what are two places dopamine NT are used in the brain?

A

ventral tegmental area

sustantial nigra

85
Q

function of dopamine

A
  • Hypothalamic regulation of hormones (anterior pituitary)
  • Substantia nigra to basal ganglia play major role in movement.
  • Midbrain projections to cortex & limbic system involved in schizophrenia, central “reward” pathway, working memory.
86
Q

parkinson is the destruction of

A

dopaminergic neurons in the substantia nigra (which plays a major role in movement)

87
Q

where is serotonin NT used in the body

A
  • 90% present in the enterochromaffin cells of GI tract
  • 8% in platelets
  • 1-2% in CNS
88
Q

function of norephinephrine

A
  • A role in attention (vigilance).
  • Involvement with control of feeding (stimulatory).
  • Connection to mood (depression)
  • Cell bodies of NE neurons reside in pons and medulla
  • Locus coeruleus (LC), lateral tegmental area (LTA), and dorsal medullary (DM).
89
Q

where in the CNS are serotonin NT?

A

raphe nuclei

90
Q

serotonin function and location in the brain

A
91
Q

how does prozac work?

A

blocks the reuptake of serotonin

(anti-anxiety medication)

22 spring: neurology (26 decks)

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