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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
how is electrical current shared between cells
neuronal gap junctions
26
compare electrical and chemical synapses
27
what kind of synapse can be bidirectional?
electrical (neuronal gap junctions)
28
which synapse is wider electrical or chemical?
**chemical** (synaptic cleft can be 30-50nm apart) electrical (2-3 nm very small)
29
two types of Neurotransmitter receptors
ionotropic metabotropic
30
if an ion channel is inhibitory what will happen
cell becomes more negative (hyperpolarization) K+ will leave or Cl- will enter
31
if an ion channel is excitatory what will happen?
cell will become more positive (depolarization) Na+ or Ca2+ will enter cell
32
ligand gated ion channels
type of neurotransmitter receptor ionotropic receptor ion binds and opens channel
33
\_\_\_ is direct modulation of neuron excitability
ionotropic receptor | (ligand gated ion channel)
34
how do ionotropic receptors work?
neurotransmitter binds channel opens ions can flow in or out based on excitatory or inhibitory
35
\_\_\_ are G protein coupled receptors
metabotropic
36
how does metabotropic receptor work?
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
37
\_\_\_ will indirectly modulate neuron excitability by downstream regulation of ion channels
metabotropic receptors (G protein linked)
38
autoreceptors
•On presynaptic terminals **eithe**r ionotopic or metabotropic ## Footnote •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
criteria for neurotransmitter
in terminal Ca2+ dependent release subject to inactivation synaptic mimicry receptors exist on postsynaptic cell
40
what is the most common type of neurotransmitter
amino acid NT
41
90% of synapses involve what 4 amino acid transmitters?
glutamate, aspartate, GABA or glycine
42
what amino acids NT are excitatory?
Glutamate, Asparate
43
what amino acid NT are inhibitory
GABA and glycine | (make cell more negative)
44
what kind of receptors do amino acid NT use?
Most work through **ionotropic** (ion channel) receptors. Some use metabotropic receptors (*i.e.* linked to second messengers such as IP3 or cAMP).
45
how are amino acid NT inactivated
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
the major excitatory NT is \_\_\_
glutatmate
47
3 types of ionotropic receptors for glutamate
* NMDA (N-methyl-D-aspartate) * AMPA * Kainate
48
The ___ receptor is of great interest because it seems to be heavily involved in learning and memory.
ionotropic NMDA glutamate receptor (excitatory)
49
\_\_\_ is the major inhibitory NT in the CNS
GABA (γ-aminobutyric acid)
50
\_\_\_ is important in inhibitory control of interneurons
GABA
51
how to make GABA
52
if a cell has glutamic acid decarboxylase (GAD) what amino acid NT does it use?
GABA
53
two types of GABA receptors
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
Increasing overall ___ of CNS is useful for sedation, anesthesia, anxiolytics, and seizure control
inhibition
55
ketamine blocks ___ receptor for \_\_\_
NMDA receptor for glutamate which is excitatory blocking this will have inhibitory effect
56
Benzo and barbituates act to enhance what receptors \_\_\_
GABAa receptor for GABA which allows Cl- into the cell causing hyperpolarization or **inhibitory effect**
57
how to make acetylcholine
58
how does acetylcholine work as NT?
59
how is acetylcholine NT inactivated
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
can acetylcholine released into the synaptic cleft be reused?
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
what are some CNS functions of acetylcholine
Behavioral Arousal Attention REM sleep Memory Learning Aggression Grand Mal Seizures Sensory Perception Energy Conservation Mood Motor Coordination
62
\_\_\_ is a prominent neurotransmitter of the Autonomic Nervous System
Acetylcholine
63
neuromuscular junctions use ___ as a NT
acetylcholine
64
\_\_\_\_ are irreversible inhibitors of acetylcholinesterase inhibitors
organophosphates * Insecticides: malathion, acephate, diazinon. * Poisonous gases: Sarin and Soman.
65
Myasthenia gravis is an autoimmune disease with decreasing numbers of ___ receptors at neuromuscular junction
nicotinic
66
how to treat myasthenia gravis
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
tyrosine is the precursor to what type of monoamines?
catecholamines such as dopamine, norepinephrine and epinephrine
68
dopamine, norepinephrine and epinephrine are \_\_\_
catecholamines derived from tyrosine type of monoamines
69
tryptophan gives rise to what type of monoamine?
indoleamines serotonin and melatonin
70
serotonin and melatonin are \_\_
type of indoleamines derived from tryptophan type of monoamine
71
what is the precursor of histamine
histidine
72
what is the rate limiting step to make catecholamines?
73
how to make norephinephrine
tyrosine **(tyrosine5 hydroxylase)** → DOPA(aromaic amino acid decarboxylase)→ dopamine (dopamine-β-hydroxylase) →norephonephrine
74
how to make epinephrine
tyrosine **(tyrosine5 hydroxylase)** → DOPA(aromaic amino acid decarboxylase)→ dopamine (dopamine-β-hydroxylase) →norephonephrine (phenylethanolamine-*N*-methyl transferase) → epinephrine
75
compare catecholamine to (indoleamine) serotonin production
similar rate limiting step same enzyme for 2nd step
76
compare breakdown of catecholamine and indoleamines
serotonin is an indoleamine
77
Monoamine Oxidase breakdown \_\_
can break down both **indoleamines**(serotonin) and **catecholamines**(dopamine, norephinephrine, epinephrine)
78
•Serotonin, norepinephrine, and epinephrine mainly broken down by \_\_\_
MAO-A *Monoamine Oxidase*
79
•Dopamine broken down equally by \_\_\_
both MAO-A and MAO-B
80
MAO is a mitochondrial enzyme and is NOT the mechanism for removal of monoamines from\_\_\_
the synapse
81
how are catecholamine (such as dopamine) inactivated in the synaptic cleft?
rapid reuptake by specific transporters
82
how are catecholamine (such as norepinephrine) inactivated in the synaptic cleft?
rapid reuptake by specific transporters
83
how is serotonin inactivated?
84
what are two places dopamine NT are used in the brain?
ventral tegmental area sustantial nigra
85
function of dopamine
* 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
parkinson is the destruction of
dopaminergic neurons in the substantia nigra (which plays a major role in movement)
87
where is serotonin NT used in the body
* 90% present in the enterochromaffin cells of GI tract * 8% in platelets * 1-2% in CNS
88
function of norephinephrine
* 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
where in the CNS are serotonin NT?
raphe nuclei
90
serotonin function and location in the brain
91
how does prozac work?
blocks the reuptake of serotonin | (anti-anxiety medication)

22 spring: neurology (26 decks)

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