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Anatomy and Physiology I > Exam 4: Nervous System: Impulse Conduction > Flashcards

Exam 4: Nervous System: Impulse Conduction Flashcards

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
Q

cells connected by gap junctions, no neurotransmitter required
found in hippocampus, retina, cerebellum (equilibrium)
rapid, NOT modulated

A

electrical synapse

26
Q

synaptic vesicles hold the same amount of neurotransmitter, what is this amount called?

A

quanta

27
Q

same amount per vesicle, the release is directly proprtional to what?

A

strength of signal you are sending

- stronger depolarization, the longer it will last

28
Q

in chemical synapses what are all of the receptors?

A

ligand gated

29
Q

what determines if the effect will be excitatory or inhibitory?

A

the type of ion channel

30
Q

depolarization of the end terminals opens…

A

voltage gated Ca channels, lets in Ca to do exocytosis via the SNARE complex

31
Q

opening Na channels results in…

opening K channels or Cl channels results in…

A

Na - EPSP stimulates target cell

K/Cl - IPSP

32
Q

ionotropic receptors

A

binding to receptor directly opens ion channels

33
Q

metabotropic receptors

A

indirect opening of channels via second messengers, G protein
- dissociation of G protein is what causes channel to open

34
Q

4 possible cascades of second messengers

A

Gs, Gi, Gq, Gt

35
Q

Gs cascade

A

stimulates adenylyl cyclase
inc cAMP
EPSP

36
Q

Gi cascade

A

inhibits adenylyl cyclase
dec cAMP
IPSP

37
Q

Gq

A

activates phospholipase C
splits PIP2 into IP3 and DAG
EPSP

38
Q

Gt

A

transducin to dec cGMP in retina

inhibits dark current - get bleaching of an image onto the eye

39
Q

how do you make acetylcholine (Ach)

A

acetyl CoA and choline

  • can not make sufficient amount of choline so get from diet
  • make Ach and store in synaptic vesicle
40
Q

when you depolarize cell you release Ach, what happens?

A

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
Q

Where is Ach found?

A
  • 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
Q

Ach role in the functioning of the CNS?

A

helps memory processing and formation - hippocampus

43
Q

nicotinic cholinergic receptors

A

ionotropic
EPSP
somatic
CNS
all preganglionic (both symp and parasymp)
when neurotransmitter hits it opens Na and depolarizes cell

44
Q

muscarinic cholinergic receptors

A 
post ganglionic (parasympathetic)
CNS - reward, memory formation
metabotropic 
M1-5 
some muscle movement
45
Q

which muscarinic cholinergic receptors are excitatory?

A

M1, M3, M5

46
Q

which muscarinic cholinergic receptors are inhibitory?

A

M2 and M4

47
Q

M1

A

EPSP
glands
- inc secretions - salvation, digestion, sweating, mucous production

48
Q

M2

A

IPSP
cardiac
- lowers HR, you are relaxed so do not need a pounding HR

49
Q

M3

A

EPSP
smooth muscle
- inc peristalsis
- lungs : more contracted in resting state, do not need dilated bronchioles when relaxed

50
Q

M4

A

IPSP
brain - muscle movement
- more relaxed muscles

51
Q

M5

A

EPSP
brain - reward center
- easier to recall memories, learn

52
Q

Pesticide poisoning: what happens to Ach concentartion in synapse if you are blocking acetylcholinesterase?

A

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
Q

what is a drug that blocks ACH activity at muscarinic receptors?

A

atropine

54
Q

what are catecholamines derived from

3 examples of catecholamines

A

tyrosine

norepinephrine, epinephrine, dopamine

55
Q

when NE removed from adrenergic receptor, what 2 enzymes can break it down?

A

MAO, COMT

usually recycled or in bloodstream and the liver will break it down liver has MAO and COMT

56
Q

all adrenergic receptors are…

A

metabotropic

57
Q

Alpha 1 adrenergic receptors

A

Gq
cardiovascular, vasconstriction
inc BP - if in fight or flight situation you want BP up

58
Q

Alpha 2 adrenergic receptor

A

Gi
self regulatory
lowers NE (negative feedback, modulation), lowers anxiety
helps you think of an action instead of becoming frozen in fear

59
Q

all beta receptors are…

A

stimulatory

60
Q

Beta 1 adrenergic receptors

A

heart: gives faster, stronger HR
kidneys: inc pressure of blood going into kidneys
increase BP bc heart is pumping faster

61
Q

Beta 2 adrenergic receptors

A

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
Q

Beta 3 adrenergic receptors

A

adipose fat cells
lipolysis
release lipids from fat cells to have alternate energy source

Anatomy and Physiology I (17 decks)

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