Exam 4: Nervous System: Impulse Conduction Flashcards

(62 cards)

1
Q

what type of event is conduction

A

electrochemical

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2
Q

formation of a charge differential on membrane

- the induction of an action potential through use of ion gradients

A

electrical conduction

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3
Q

manipulation of ion concentrations

using chemical signals to effect either excitatory or inhibitory potentials in target cells

A

chemical conduction

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4
Q

membrane potential

A

voltage difference across membrane

  • resting membrane potential = -70mV
  • salty banana: more Na out, more K in, Cl on outside
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5
Q

charge differential on membrane

  • formed by selective concentration of positive and negative charges
  • resting potential results in net pos charge otside, net neg charge inside
A

electrical gradient

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6
Q

ion concentrations set up by membrane pumps

  • sodium is concentrated outside, while K is concentrated inside cell
  • strictly concentration
A

chemical gradient

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7
Q

what are the main ions involved in membrane potentials

A

K and Na

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8
Q

voltage gated ion channels

A

need difference in charge on membrane to open

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9
Q

ligand gated ion channel

A

need something to bind ex: neurotransmitter

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10
Q

mechanically gated ion channel

A

distort the membrane

- poke it, vibrate it

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11
Q

ungated ion channel

A

like aquaporins - control if you put them on membrane

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12
Q

action potential

A
  • neuron at resting potential, stimulus is applied, mechanically gated Na channels open, Na rushes into cell
  • once threshold reached -55, Na channels open, if not they reset and no action potential
  • depolarization causes Na channels to close and K channels to open , K rushes in
  • repolarization occurs, charge reset
  • hyperpolarization
    K channels close
    reset to resting potential
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13
Q

absolute refractory period

A

in repolarization

cannot send another signal no matter how strong stimulus is

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14
Q

relative refractory period

A

in hyperpolarization

need super strong signal

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15
Q

factors that affect excitability

-blocking gated channels or altering gradients

A

caine drugs
serum Ca2+ levels
shifting of K levels

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16
Q

caine drugs effects on excitability

A

block Na channels preventing depolarization of neuron

- cannot send pain signals hence numb feeling - novacaine, cocaine

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17
Q

serum Ca levels effect on excitability

decrease

A

less channels blocked, neuron may have small Na channels opening, can reach threshold - hyperexcitability

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18
Q

serum Ca levels effect on excitability

increase

A

more channels blocked
cardiac muscle - needs external Ca, when raised will not contract as rapidly
- initially the inc riases heart rate bc depolarizing to get more contraction, but as it goes up you get inverse effect - problems with nerve impulses, cardiac irregularities
- harder to depolarize

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19
Q

shifting K levels effect on excitability

A

releasing K can cause problems, screw up the ion balance making it harder to depolarize the cell
- if acidosis - bring in H but releasing K

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20
Q

what dose is fatal for saxitoxin

A

0.2 mg

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21
Q

what dose is fatal for tetrodotoxin

A

1 mg

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22
Q

what does the dosage amount indicate regarding binding affinities?

A

saxitoxin has a higher affinity for saxitoxin bc it is lower dosage to be fatal

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23
Q

presynaptic vs postsynaptic cell

A

presynaptic cell: sends impulse

postsynaptic cell: target cell, receiving

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24
Q

cells separated by synaptic cleft, do not directly touch

requires release of neurotransmitter to the target

A

chemical synapse

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25
cells connected by gap junctions, no neurotransmitter required found in hippocampus, retina, cerebellum (equilibrium) rapid, NOT modulated
electrical synapse
26
synaptic vesicles hold the same amount of neurotransmitter, what is this amount called?
quanta
27
same amount per vesicle, the release is directly proprtional to what?
strength of signal you are sending | - stronger depolarization, the longer it will last
28
in chemical synapses what are all of the receptors?
ligand gated
29
what determines if the effect will be excitatory or inhibitory?
the type of ion channel
30
depolarization of the end terminals opens...
voltage gated Ca channels, lets in Ca to do exocytosis via the SNARE complex
31
opening Na channels results in... | opening K channels or Cl channels results in...
Na - EPSP stimulates target cell | K/Cl - IPSP
32
ionotropic receptors
binding to receptor directly opens ion channels
33
metabotropic receptors
indirect opening of channels via second messengers, G protein - dissociation of G protein is what causes channel to open
34
4 possible cascades of second messengers
Gs, Gi, Gq, Gt
35
Gs cascade
stimulates adenylyl cyclase inc cAMP EPSP
36
Gi cascade
inhibits adenylyl cyclase dec cAMP IPSP
37
Gq
activates phospholipase C splits PIP2 into IP3 and DAG EPSP
38
Gt
transducin to dec cGMP in retina | inhibits dark current - get bleaching of an image onto the eye
39
how do you make acetylcholine (Ach)
acetyl CoA and choline - can not make sufficient amount of choline so get from diet - make Ach and store in synaptic vesicle
40
when you depolarize cell you release Ach, what happens?
it hits cholinergic receptor - never enters postsynaptic cell - does its work on the surface - once bound, acetylcholinesterase snaps it apart the acetyl group is gone and the choline gets recycled
41
Where is Ach found?
- both pre-ganglionic and post-ganglionic parasympathetic divisions - pre-ganglionic sympathetic only - some CNS - the ONLY neurotransmitter in somatic division!!!! ONLY neurotransmitter to interact with skeletal muscle!!
42
Ach role in the functioning of the CNS?
helps memory processing and formation - hippocampus
43
nicotinic cholinergic receptors
ionotropic EPSP somatic CNS all preganglionic (both symp and parasymp) when neurotransmitter hits it opens Na and depolarizes cell
44
muscarinic cholinergic receptors
``` post ganglionic (parasympathetic) CNS - reward, memory formation metabotropic M1-5 some muscle movement ```
45
which muscarinic cholinergic receptors are excitatory?
M1, M3, M5
46
which muscarinic cholinergic receptors are inhibitory?
M2 and M4
47
M1
EPSP glands - inc secretions - salvation, digestion, sweating, mucous production
48
M2
IPSP cardiac - lowers HR, you are relaxed so do not need a pounding HR
49
M3
EPSP smooth muscle - inc peristalsis - lungs : more contracted in resting state, do not need dilated bronchioles when relaxed
50
M4
IPSP brain - muscle movement - more relaxed muscles
51
M5
EPSP brain - reward center - easier to recall memories, learn
52
Pesticide poisoning: what happens to Ach concentartion in synapse if you are blocking acetylcholinesterase?
will not be able to breakdown Ach so get a build up of Ach, inc binding of Ach to receptors in post synaptic cel, over stimulation!
53
what is a drug that blocks ACH activity at muscarinic receptors?
atropine
54
what are catecholamines derived from | 3 examples of catecholamines
tyrosine | norepinephrine, epinephrine, dopamine
55
when NE removed from adrenergic receptor, what 2 enzymes can break it down?
MAO, COMT | usually recycled or in bloodstream and the liver will break it down liver has MAO and COMT
56
all adrenergic receptors are...
metabotropic
57
Alpha 1 adrenergic receptors
Gq cardiovascular, vasconstriction inc BP - if in fight or flight situation you want BP up
58
Alpha 2 adrenergic receptor
Gi self regulatory lowers NE (negative feedback, modulation), lowers anxiety helps you think of an action instead of becoming frozen in fear
59
all beta receptors are...
stimulatory
60
Beta 1 adrenergic receptors
heart: gives faster, stronger HR kidneys: inc pressure of blood going into kidneys increase BP bc heart is pumping faster
61
Beta 2 adrenergic receptors
opposite effect inc cAMP in beta 2 cell dec Ca in muscle, so not strong contraction - in lungs get bronchodilation and vasodilation - better blood flow for oxygenation, opens air ways
62
Beta 3 adrenergic receptors
adipose fat cells lipolysis release lipids from fat cells to have alternate energy source