Action Potentials and Synaptic Transmission Flashcards

1
Q

what are key factors of AP

A

Self-propagating biochemical disturbance that generates an electric field or dipole
Successive APs can only be triggered following a brief recovery period, and finally
Absolute and relative refractory periods
All-or-none response
Naturally travel only in one (forward) direction

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2
Q

Describe an action potential generation

A

a neuron is depolarized to threshold
sodium ion channels open in response to changes in membrane potential (changes in voltage) (voltage gated ion channels)
since more positively charged sodium ions are outside the cell and inside the cell is more negative, opening of the channel allows sodium to rush in due to influence of diffusion and electrostatic forces
influx depolarizes the cell causing more voltage sodium channels to open leading to more depolarization (rising phase of an action potential)
potassium channels open and allow it to rush out along with potassium leak channels
signal moves down axon

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3
Q

what is the rising phase of an AP

A

the rapid change in membrane potential
when the influx of sodium causes depolarization in turn causing more voltage gated sodium ion channels to open leading to more depolarization

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4
Q

how does an ap come to an end?

A

once neuron membrane potential reaches its peak, voltage gated sodium channels begin closing
potassium moving out of a cell through potassium gated ion channels and leak channels helps repolarize the cell (back to resting membrane potential)
sodium potassium pump also helps to restore mp

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5
Q

how does an AP move down an axon

A

once depolarization occurs at one segment causes voltage gated sodium ion channels to open regenerating the ap in the next segment of the axon

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6
Q

lipid rich material that wraps around axons making propagation of ap down the axon faster and more efficient

A

myelin

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7
Q

How does myelin help propagations of ap go faster?

A

prevents current from leaking out of the axon
increases speed of propagation interruped by nodes of Ranvier (gaps in myelin)
these nodes are rich in voltage gated sodium channels causing inrushing of sodium and regeneration of AP (happens at each node) propelling the AP down the axon

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8
Q

saltatory conduction

A

regeneration of ap at nodes of ranvier and slowing at the myelinated regions between them (internodes) causes AP to appear as if its jumping down the axon

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9
Q

what is meant by all or none of an AP

A

refractory period makes rate of ap firing related to intensity of stimulation
AP don’t vary in size based on intensity of a stimulus, they either fire or they don’t
when they fire they’re consistent amplitude/size

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10
Q

more intense stimuli will cause ______ frequency firing of AP

A

more

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11
Q

why does a more intense stimuli will cause more frequency firing of AP?

A

they’re able to overcome relative refractory period in neurons

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12
Q

what happens after a RP depolarizes a receptor

A

connected axon can generate an AP
or after a receptor send NT across a synapse, the post-synaptic neuron will be triggered and if it is EXCITED postsynaptic potential (EPSP), the voltage change from the EPSP will start the AP

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13
Q

what are ligand-gated channels

A

alter their permeability as a function of the binding of chemicals/ligands to specific receptors as in the binding of a neurotransmitter to a post-synaptic cell
protein channel that allows an ion to pass through the membrane in response to the binding of a chemical messenger, like a neurotransmitter

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14
Q

what are mechanically or thermally gated channels

A

mechanically - open and close in response to mechanical vibration or pressure, such as sound waves or the pressure of touch
thermally - activated by temperature, voltage, pH, lipids, and agonists. usally calcium or magnesium channels

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15
Q

how long to voltage gated ion channels open for

A

10 milliseconds

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16
Q

where does voltage gated channel open at?

A

axon hillock

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17
Q

depolarization activates what

A

voltage gated potassium channels

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18
Q

gives rising phase

A

depolarization, influx of sodium

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19
Q

gives falling phase

A

repolarize, potassium leaving the cell

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20
Q

which channel stays open longer

A

potassium causing a prolonged outward K+ current

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21
Q

what is resting potential in mv

A

-70

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22
Q

how are ionic balances restored

A

sodium potassium pump

23
Q

what is absolute refractory period

A

time period after the threshold was reached (that caused the AP) until the sodium inactivation mechanism is reset which takes about 2 msec

24
Q

what is relative refractory period

A

after the sodium inactivation mechanism is reset and while there is still an outward potassium current
An AP can be generated but only by a stimulus that is stronger than what is usually required to reach threshold for an AP

25
Q

are AP travelling in one direction?

A

yes, The node or place that was just activated is still in a refractory period, but the node in the other direction is ready to fire so the AP propagates in only one direction
The AP is the same “full” strength at each occurrence so it does not degenerate or lose information on its way to or from the brain

26
Q

frequency of action potential firing rate

A

frequency modulated

27
Q

gentle pressure =

A

low frequency ap (slow)

28
Q

more pressure =

A

high frequency ap (faster)

29
Q

What happens at the synaptic cleft?

A

Chemical messengers carry info from one cell to another
AP reaches the terminal bouton of the axon
Ca++ channels are triggered and open = influx of Ca++
Triggers neurotransmitter vesicles to release NT into synaptic cleft
NT finds receptors sites on the next neuron and bind to have an action

30
Q

what are NTs?

A

amines, amino acids and neuropeptides

31
Q

what are the NTs of A/V system? (CNS)

A

glutamate +
aspartate +
GABAergic -
glycine -
acetylcholine efferent (olivocochlear bundle)

32
Q

what is NT at neuromuscular jxn (nerve to muscle) and in some areas of CNS?

A

acetycholine

33
Q

what are the efferent inhibitory NT of AVS?

A

noradrenaline

34
Q

what are the efferent excitatory NT of AVS?

A

acetycholine

35
Q

what are the afferent excitatory NT of AVS

A

glutamate
aspartate

36
Q

what are afferent inhibitory NT of AVS

A

GABA
glycine

37
Q

What are the Five Steps in Chemical Synaptic Transmission

A

1) Synthesis of NT in presynaptic endings and in soma
2) Concentration and packaging of NT in synaptic vesicles
3) Release of NT into synaptic cleft
4) Binding of NT to receptor molecules in postsynaptic membranes
5) Termination of NT action by uptake, degradation or diffusion

38
Q

How does termination of NT occur?

A

NT may diffuse away but this is slow
at most synpases NT is absorbed by the presynaptic ending or nearby glial cells or by the postsynaptic process
at some synapses, enzymes degrade the free NT
reabsorbed NT can by recycled for use again

39
Q

describe fast transmission

A

uses transmitter-gated (ligand-gated) ion channels
independent
ap reached terminal bouton
calcium goes in and causes vesicles to move to cell membrane and open and dump NT out
they will bind to receptor sites on next cell and the bounding opened the channel
chem ligand channel opening
sodium in potassium out and causes postsynaptic in next cell

40
Q

describe slow transmission

A

usually involves a second messenger after binding of the NT to postsynaptic receptors
caused some chemical to be the messenger
using helper system here
not as fast as the first one so the channels are slower at opening
electrical change reaches terminal bouton
stronger stimulus dumped NT at bottom but opens more vesicles and dumps it out on the sides
binds to sites and causes second messenger to open ion channels

41
Q

destinations of AP’s going from neuron to the next is the ascending info

A

goes to CNS: spinal cord, brainstem, cerebrum, cerebellum, etc

42
Q

antagonist

A

person who is blocking you, barrier, the problem
curare
beta-blocker

43
Q

agonist

A

the activator
el dopa - to mimic dopamine

44
Q

How does curare work

A

A molecule can bind to a receptor and prevents it from receiving a NT
paralyzes by blocking

45
Q

What is the resting potential of a cell?

A

-65-70mV
cell at rest is more neg inside than outside, and it is ready to be activated and receive information

46
Q

Define depolarization?

A

going from negative towards positive
polarizing = negative

47
Q

What is a receptor potential?

A

bioelectrical change in a receptor as a part of sensory transduction to code a stimulus (touch, vision, etcl.) into an electrical signal the CNS can
take some stimulus and code it into bioelectrical activity

48
Q

What is an action potential?

A

all or none, bioelectrical change that is self propagating in a forward direction to carry info from receptor sites to CNS or from A to B

49
Q

What is the sodium potassium pump?

A

maintains resting membrane potential
active pump that maintains balance of sodium and potassium for resting membrane potential and to reset it after there has been a receptor or active membrane potential
puts 3 sodium out and 2 potassium in
extracellular is high and sodium out and potassium in is low

50
Q

What is a synapse?

A

method of comm from one cell to another using a nt across a synaptic cleft

51
Q

what is a neurotransmitter

A

chemical or ligand used for synaptic transmission

52
Q

step by step of sensory transduction
Start with a stimulus and receptor
What happens at the receptor?
What triggers the AP?
How does the AP travel?
What happens at the terminal bouton?
What happens at the synaptic cleft?
What happens in the post-synaptic neuron?

A

at receptor sit at resting and stimulated by some force (mechanical, thermo, photo, etc.)
volt change from a receptor causes AP
AP travels in a self propagating, forward by soltatory conduction (jumping from node to node) if myelinated
prep for synaptic vesicles with NT to be dumped out onto SC
NT goes to next cell at synaptic cleft
NT at the next cell causes either EPSP or IPSP

53
Q

if there’s enough change or threshold is reached

A

an AP is activated