week 3 Flashcards

1
Q

diff bw GPs and APs in terms of…
a) location
b) channel types involved
c) ions involved
d) duration

A

GPs vs APs:
a) dendrites/soma/sensory receptors vs axon
b) ligand and mechanically-gated vs voltage-gated
c) Na+, Cl-, or K+ vs Na+ and K+
d) few msec to seconds vs 1-2 msec

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2
Q

phases of an AP (3)

A
  1. depolarization
  2. repolarization
  3. after-hyperpolarization
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3
Q

when do Na+ channels open?

A

once threshold is reached (~-55mV)

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4
Q

do VGSCs operate in a positive or negative feedback system?

A

positive

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5
Q

why does the peak depolarization of an AP only reach +30mV? why not reach the EP of Na+ (+60mV)?

A

because soon after the VGSCs open, they inactivate

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6
Q

what causes repolarization? (2)

A
  1. at rest, K+ leaks out of cell, so cell becomes more negative.
  2. VGPCs open (recall: EC of K+ = out).
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7
Q

which are faster: VGSC or VGPC?

A
  • VGSCs are faster.
  • this is why the repolarization phase (which depends on VGPCs) takes longer and overshoots (after-hyperpolarization).
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8
Q

do VGPCs operate in a positive or negative feedback system?

A

negative

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9
Q

review: at rest, is Na+ or K+ more permeable?

A

K+

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10
Q

what brings the membrane to threshold?

A

sum of the graded potentials

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11
Q

what restores resting membrane potential?

A

Na+/K+ pump

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12
Q

are the activation and inactivation gates open or closed at…
a) rest
b) depolarization
c) repolarization

A

a) rest: activation = closed, inactivation = open
b) depolarization: activation = open, inactivation = open
c) repolarization: activation = open, inactivation = closed

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13
Q

why are threshold and suprathreshold stimuli equal in size?

A

bc all-or-none principle

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14
Q

what is a refractory period? whats the diff bw absolute and relative refractory periods?

A

refractory period: decreased excitability following an AP because VGSCs are inactive until membrane potential is at rest.

absolute: ALL VGSCs are inactive. spans all of de and most of repolarization. second AP cannot occur.

relative: SOME VGSCs are inactive. last part of re and after-hyperpolarization. second AP may occur with stronger stimulus.

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15
Q

what is most common local anesthetic dentists use to “freeze” you and how does it work?

A
  • lidocaine
  • works as VGSC blocker, preventing APs (pain)
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16
Q

can you completely block membrane from generating AP?

A
  • yes
  • keep membrane depolarized above threshold to stop influx of sodium.
  • inject KCl to destroy concentration gradient for K+ (will keep inside of cell positive, keeping VGSC inactive).
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17
Q

if APs are all-or-none, how do we differentiate strong vs weak stimuli?

A
  • frequency coding
  • strong stimuli encoded in higher frequency of APs
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18
Q

what are the cons of an unmyelinated axon? (2)

A
  • leakage of ions
  • decreased conduction velocity
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19
Q

how does the propagation of APs work in unmyelinated axons?

A
  • A = depolarized
  • positive charge of A attracted to negative charge of B
  • B = depolarized
  • cycle continues
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20
Q

what makes the propagation of APs unidirectional?

A

absolute refractory period

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21
Q

what are the factors affecting propagation? (3)

A
  1. refractory period (makes it unidirectional)
  2. axon diameter (larger = faster)
  3. myelination (saltatory conduction = faster)
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22
Q

how does the propagation of APs work in myelinated axons?

A
  • high density of VGSC at nodes of ranvier
  • AP jumps from node-to-node
23
Q

in electrical synapses, neurons are linked together by ___. what do these contain?

A
  • gap junctions
  • contain connexins that allow ions to cross
24
Q

functions of electrical synapses in the nervous system? (5)

A
  1. rapid communication
  2. ions or second messengers
  3. usually bidirectional communication
  4. excitation and inhibition at same synapse
  5. identified in retina, cortex, brainstem (breathing), and hypothalamus (neuroendocrine neurons).
25
describe functional anatomy of chemical synapses (5)
1. presynaptic neuron releasing neurotransmitter 2. postsynaptic neuron accepting neurotransmitter 3. synaptic cleft 4. unidirectional communication 5. usually axodendritic, some axosomatic or axoaxonic
26
describe the anatomy of a synapse (7)
1. presynaptic axon terminal (AP arrives here) 2. neurotransmitter-containing vesicles 3. depolarization opens VG Ca2+ channels 4. neurotransmitter dropped into synaptic cleft 5. receptors 6. enzymes 7. reuptake molecules
27
how can leftover neurotransmitter be removed? (3)
1. enzymatic breakdown 2. diffusion 3. reuptake
28
what is synaptic delay? what is it caused by?
- 0.5–5 msec between arrival of AP and change in postsynaptic cell. - caused by changes in Ca2+ entry, vesicle docking, and release of neurotransmitter
29
what are the 2 types of receptors that allow signal transduction at chemical synapses?
1. channel-linked (ionotropic): ligand-gated, fast acting, close as soon as neurotransmitter leaves. 2. g-protein coupled (metabotropic): slow acting
30
describe the steps of... a) direct coupling b) second messenger systems
[discussing g-protein coupled receptors] a) neurotransmitter binds, activates g-protein, opens/closes ion channels. b) neurotransmitter binds, activates g-protein, activates/inhibits enzyme, produces second messenger, opens/closes ion channels or produces other cell responses.
31
whats a PSP?
change in membrane potential in response to receptor-neurotransmitter binding.
32
most common EPSP neurotransmitter? IPSP?
EPSP: glutamate IPSP: GABA
33
what makes an EPSP fast or slow?
whether channel-linked or g-protein coupled receptors are used
34
in inhibitory synapses, what happens if K+ channels open? Cl- channels?
K+: moves out = IPSP Cl-: moves in = IPSP (or stabilizes MP)
35
why are IPSPs more important than EPSPs? (3)
- more specific - more accurate - shape info
36
diff bw divergence and convergence?
divergence: axon of one neuron has several collaterals that communicate to several other neurons. convergence: many PREsynaptic terminals converge onto one postsynaptic neuron.
37
recall: temporal vs spatial summation
temporal = one stimulus, close times. spatial = multiple stimuli, same times.
38
more APs = more neurotransmitter released + ___ IPSP or EPSP in the next neuron.
greater
39
what is presynaptic modulation?
regulation of communication across a synapse on presynaptic neuron (axoaxonic)
40
what is presynaptic facilitation vs inhibition?
facilitation: modulating neuron results in modulated neuron releasing more neurotransmitter inhibition: modulating neuron results in modulated neuron releasing less neurotransmitter
41
diff between axoaxonic vs axodendritic/axosomatic ???
axoaxonic excites/inhibits one synapse and is selective others excite/inhibit postsynaptic neuron and is nonselective ("overall")
42
what is Ach used for and where is it found?
- muscular contractions - PNS and CNS (most abundant neurotransmitter in PNS)
43
how is Ach synthesized? broken down?
synthesis: Acetyl CoA + choline = acetylcholine + CoA (CAT = enzyme for synthesis) breakdown: Acetylcholine = acetate + choline (AChE = enzyme for degredation)
44
what is the Ach competitive agonist? what does it do?
- curare - blocks Ach, prevents voluntary movements
45
cholinergic receptors can be of what types? (2)
- nicotinic (ionotropic, EPSP) - muscarinic (metabotropic, EPSP or IPSP)
46
which type of cholinergic receptor is abundant in CNS?
metabotropic (muscarinic)
47
name the 5 biogenic amines
1. dopamine 2. epinephrine 3. norepinephrine tyrosine ^ 4. serotonin (tryptophan) 5. histamine (histidine)
48
serotonin (3)
- CNS (mainly brainstem) - regulates sleep + emotions - related directly to plasma concentration of tryptophan
49
histamine (3)
- CNS (mainly hypothalamus) - regulates wakefulness - commonly known for paracrine actions (allergies)
50
which amino acid neurotransmitters are at excitatory vs inhibitory synapses?
excitatory: glutamate, aspartate inhibitory: GABA, glycine
51
name the 6 neuropeptides
1. endogenous opioids 2. TRH 3. ADH 4. oxytocin 5. substance P 6. orexin
52
name one unique neurotransmitter. why is it uniqe?
- NO (gas) - unique bc cannot be stored; created on spot as needed.
53
is the effect determined by the receptors or the ligand for Ach?
receptor