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DPT 503 > Neural Communication > Flashcards

Neural Communication Flashcards

(59 cards)

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1
Q

what is a synapse?

A

where a neuron and postsynaptic cell communicate

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2
Q

what are the components of a synapse?

A

a presynaptic terminal, postsynaptic membrane, and a synaptic cleft b/w the 2

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3
Q

axodendritic synapse

A

pre=axon
post=dendrite

most common synapse found in the body

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4
Q

axosomatic synapse

A

pre=axon
post=soma

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5
Q

axoaxonic synapse

A

pre and post=axon

axon terminal can synapse on distal axon or extreme distal axon near the terminal

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6
Q

dendrodendritic synapse

A

pre and post=dendrite

dendrite of one neuron synapsing on the dendrite of another neuron

not very common-only localized in certain areas for the brain

may be bidirectional signaling

may occur in diseased state where axodendritic synapses are damaged

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7
Q

what are the 2 forms of synaptic transmission?

A

electrical and chemical synapses

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8
Q

electrical synapses

A

gap junctions enable rapid and synchronized activity of many neurons

pore connections allow AP though pre and post

beneficial in cardiac muscle and its neurons

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9
Q

chemical synapses

A

key feature: synaptic vesicles filled with NTs

complex=slower but more flexible

  1. AP reaches presynaptic terminal and vesicles are brought down to terminal membrane
  2. Ca2+ enters presynaptic terminal through voltage gated Ca2+ channels bc inside has become more positive
  3. Ca2+ binds to docking proteins (SNARE) and vesicles fuse to membrane
  4. exocytosis: NT released into cleft
  5. NT binds to receptors on postsynaptic membrane and opens ion channels (ligand gated)
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10
Q

what are the effects of Botox

A

snips proteins that make up SNARE complex=no ACh into the cleft=no muscle contraction

no exocytosis of ACh

muscle paralytic

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11
Q

what happens to a NT after it’s used?

A

NT have to be inactivated/removed from receptors

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12
Q

what are the 3 mechanisms to eliminate NTs?

A

reuptake, degradation, diffusion

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13
Q

how does reuptake get rid of used NTs?

A

the NT is taken up, repackaged, and recycled

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14
Q

how does degradation get rid of used NTs?

A

when a NT is unbound and just existing in the cleft, an enzyme comes and deactivates it

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15
Q

how does diffusion get rid of used NTs?

A

the NT just diffuses away after it has done its job

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16
Q

what is an excitatory postsynaptic potential?

A

when the ion channel opens, makes the inside more positive, and depolarizes

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17
Q

how does the sodium channel result in an EPSP?

A

there is more sodium outside the cell, so when the channel opens, sodium will flow in making the inside more positive causing a depolarization

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18
Q

what is an inhibitory postsynaptic potential?

A

when the ion channel opens, makes the inside more negative, and depolarizes/hyperpolarizes

inhibits APs

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19
Q

how does the chloride channel result in an IPSP?

A

there is more chloride outside the cell, so when the channel opens, chloride flows in making the inside more negative causing a depolarization/repolarization

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20
Q

summation of postsynaptic potentials

A

one excitatory potential=depolarization

2 excitatory potentials=larger depolarization

inhibitory potential=some hyperpolarization

excitatory and inhibitory potential=depolarization if depolarization amplitude is greater than the inhibitory amplitude

2 excitatory and inhibitory potentials=depolarization larger than 1 excitatory and inhibitory but smaller than just 2 excitatory

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21
Q

what is presynaptic facilitation

A

a neuron excites the presynaptic neuron increasing transmission resulting in a large depolarization (EPSP)

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22
Q

what is presynaptic inhibition?

A

a neuron inhibits the presynaptic neuron decreasing transmission resulting in a smaller depolarization or hyperpolarization (IPSP)

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23
Q

what is presynaptic facilitory modulation of NT release?

A

an excitatory neuron increases the amount of NT released from the presynaptic neuron

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24
Q

what is presynaptic inhibitory modulation of NT released?

Study These Flashcards
A

action of an inhibitory neuron on an axon decreases the amount of NT released from the presynaptic neuron

not every receptor is occupied so the response is decreased

25
what is a real world example of presynaptic modulation of NT released?
pain perception: when you think about a cut more it hurts more bc more NT is released when you think about a cut less, it hurts less bc less NT is released
26
what are the modulations of receptors?
down regulation and upregulation
27
what is downregulation?
internalization decreases the number of receptors inactivation/desensitization decreases the number of active receptors
28
what is upregulation?
when the number of receptors increase or the receptors become hypersensitive
29
are upregulation and downregulation reversible?
yes!
30
what are the 2 types of transmission speeds?
fast transmission and slow transmission
31
what is another name for fast transmission?
ionotropic
32
what is another name for slow transmission?
metabotropic
33
what is fast (ionotropic) transmission?
ligand-gated channels a NT binds to the receptors, channels open, and ions flow through the channels
34
what is slow (metabotropic) transmission? what are the 2 types? what do they in
more steps involved makes it slower and more flexible G-protein coupled receptors: - a protein is embedded in the membrane - NT binds to the receptor, conformational changes occur, G-protein is activated, subunits float somewhere else volume transmission: - extrasynaptic release - neuronal communication at variable distances - NT not released into the cleft - no particular target tissue
35
how long does fast (ionotropic) transmission occur?
a millisecond to a minute
36
how long does slow (metabotropic) transmission occur?
100s of milliseconds to days
37
cholinergic
ACh
38
glutamatergic
glutamate
39
GABAergic
GABA
40
glycinergic
glycine
41
(nor)adrenergic
norepinephrine/epinephrine
42
dopaminergic
dopamine
43
serotonergic
serotonin
44
histaminergic
histamine
45
how are neurons classified?
by the NT they produce, release, or respond to
46
ACh
excitatory nicotinic - ionotropic - NMJ and CNS - Alzheimers muscarinic - metabotropic - CNS and PNS - parasympathetic
47
glutamate
excitatory ionotropic development, learning, and memory formation non-NMDA - AMPA and Kainate receptors - sodium in=depolarization NMDA: - glycine acts a agonist - magnesium block moved by depolarization of non-NMDA, then sodium and calcium can move in and potassium out
48
GABA
inhibitory CNS GABAa - ionotropic - ligand-gated Cl- channels open and allow Cl- in making the inside more negative leading to a hyperpolarization GABAb - metabotropic pathology: seizure, involuntary contraction, anxiety (over excitation of the brain)
49
glycine
Inhibitory BS and SC one of the most abundant inhibitory NTs learning and memory ligand-gated Cl- channels open allowing Cl- in making the inside more negative causing a hyperpolarization involved in NMDA receptor activation pathology: (not enough) involuntary contractions
50
dopamine
excitatory or inhibitory motor control, cognition, reward mechanism, motivation metabotropic all throughout brain pathology: addiction, Parkinson's disease, schizophrenia
51
norepinephrine (NE)
inhibitory or excitatory attention and arousal sympathetic: increased HR, BP, resp rate, vasodilation, vasoconstriction metabotropic too much=panic disorder, PTSD epinephrine closely resembles NE
52
serotonin
inhibitory ionotropic and metabotropic sleep, arousal, cognition, motor function, mood, pain perception pathology-depression (lack of serotonin)
53
amines
redundancy complicates treatment bc it's hard to know which NT is contributing to symptoms the most NE, serotonin, and dopamine
54
opioid peptides
inhibitory endorphins, enkephalin, dynorphin inhibit pain perception SC, hypothalamus, BS
55
substance P
excitatory released by injured tissue and stimulates nerve endings at site of injury CNS: - relays pain signal from SC to brain - hypothalamus and cerebral cortex - pathology-pain syndrome one of the most common neuropeptides in the body nociceptive neurons volume transmission-metabotropic
56
nitric oxide
excitatory gasotransmitter acts through diffusion so it doesn't require a receptor or membrane vasodilation long-term potentiation seizure disorder
57
co-transmission
multiple neurons released at the same synapse or from the same neuron increased stimulus strength pain info depolarization=release of glutamate and substance P slow pain and fast pain
58
what are NT agonists
bind to receptors and has the same effects of the normal NT same affinity and effects
59
what are NT antagonists
bind to receptors and impedes the effects prevents release of NT ACE inhibitor, NMDA blocker, Botox

DPT 503 (22 decks)

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