pre midterm 1 Flashcards

1
Q

resting membrane potential

A

constant voltage across a membrane when the cell is at rest (-40 to-90 mV, usually -60)

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2
Q

receptor potential:

A

change in membrane potential when sensory neurons are stimulated.

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3
Q

passive vs active flow in an axon

A

passive conduction decays over distance and active conduction is constant over distance.

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4
Q

K, Na, Cl, and Ca concentrations inside and outside the cell? what does this mean?

A

K: high inside, low outside
Na- low inside, high outside
Cl- low inside high outside
Ca- low inside high outside.
this means there is a slow potassium leak from the cell.

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5
Q

hodgekin and huxley

A

used a squid giant axon to study neurobiology. found when potassium concentration was changed, the membrane potential changed therefore potassium drives membrane potential.

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6
Q

voltage gated sodium channels and APs.

A

sodium channels don’t open until the threshold potential is reached. sodium channels open quickly during depolarization during the rising phase. they inactivate for the absolute refactory period. then the channels must be de-inactivated to generate another AP.

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7
Q

voltage gated potassium channels and AP

A

channel is sensitive to voltage changes and subunits undergo shape conformation to open the pore with depolarization. there is a 1 ms delay.

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8
Q

key properties of action potentials (repeat card until i understand)

A
  1. membrane voltage is at threshold when sodium channels open.
  2. during the rising phase membrane voltage is negative and Na influx leads to depolarization
  3. overshoot phase causes membrane voltage to rise above 0mV and approach the equilibrium for Na
  4. falling phase: Na channels inactivate and the K channels open with a delay and K efflux causes the membrane voltage to be negative.
  5. undershoot phase: when membrane voltage approaches equilibrium for K, there is hyperpolarization until K channels close.
  6. absolute refractory period: Na channels inactivate.
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9
Q

active and passive flow in action potentials

A

active: local inward movement of Na, outward movement of K. depolarization and hyperpolarization
passive: movement of current produced in active phase

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10
Q

tetrodotoxin

A

blocks Na channels and inhibits depolarization

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11
Q

alpha toxins

A

prolong action potentials and scramble information flow

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12
Q

beta toxins

A

cause Na channels to open at lower potentials causing uncontrolled action potential firing

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13
Q

dendrotoxin

A

blocks K channels

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14
Q

ion slectivity

A

each ion channel has a sleectivity filter that allows a particular ion to travel through. acheived by amino acids at the mouth of the pore.

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15
Q

voltage gated ion channels

A

larger than other channel types
transmembrane structures have structures with oppisite charges to their ion that act as voltage sensors.
depolarization pushes sensors outwards openening the channel and hyperpolarization pushes the sensors inwards closing the channel

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16
Q

ligand gated ion channels

A

respond to chemical signals, less selective that voltage gated,

17
Q

electrical vs chemical synaptic transmission

A

electrical: direct neuron-neuron current flow, is passive, bidirectional, and uses gap junctions as ion channels
chemical: signals are mediated by neurotransmitters at the synapse. are slower, unidirectional, and use neuriotransmitters and their receptors.

18
Q

where is electrical synaptic transmission found and why is it used

A

found in areas where neuron activity is highly synchronized in mammalian CNS. in non-neuronal cells like epithelial and heart muscle ceclls. 6 connexin units form 1 connexon channel and pores allow for bidirectional ion flow. the generation of AP in one neuron results in the synchronized firing of AP in the adjacent neuron, stimulating entire tissues at once.

19
Q

presynaptic structures that guide neurotransmitter

A

pools of vesicles, voltage gated calcium channels, SNARE proteins to bring vesicle and membrane together.

20
Q

postsynaptic structures for neurotransmitter purpose

A

help to anchor postsynaptic receptors in their membrane. prevent lateral diffusion of receptors, involved in synaptic plasticity.

21
Q

neurotransmitter release

A

depolarization causes voltage gated calcium channels to open causing calcium influx. calcium causes vesicles to fuse with the presynaptic membrane and release neurotransmitter into synaptic cleft

22
Q

postsynaptic path of neurotransmitter

A

transmitter binds to receptor molecules in the postsynaptic membrane. polysynaptic channels will either open (depolarize) or close (hyperpolarize). neurotransmitter either has excitatory or inhibitory effect on the postsynaptic neuron.

23
Q

criteria for classical neurotransmitter

A
  1. substance exists in presynaptic neuron
  2. substance is released in response to presynaptic depolarization and mediated by calcium.
  3. specific receptors for the substance exist in the postsynaptic cell
24
Q

what is the clinical significance of the neuromuscular junction? what is it?

A

neuromuscular junctions are synaptic junctions outside the brain or spinal chord. neuron-muscle. fast and reliable transmission and a large synapse size make there junctions pharmacologically significant.

25
voltage clamp method: calcium BAD CARD DONT STUDY YET
voltage clamp the presynaptic neuron and record from the postsynaptic, if you depolarize the neuron there is a calcium influx into the presynaptic membrane. the postsynaptic neuron depolarizes. if you put a calcium channel blocker, the presynaptic
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calcium indicator
flourescent dye
27
inject calcium into presynaptic cell experiment
causes neurotransmitter release
28
injection of BAPTA effect/what is BAPTA
binds a bunch of calcium so calcium cannot connect with a receptor, postsynaptic response from neurotransmitter is lost
29
how are calcium vesicles recycled
intracellular endosomes take the empty vesicles and refill them and send them back out.
30
important proteins in membrane fusion for neurotransmitter release
synapsin, SNAPs, NSFs, SNAREs.
31
SNARE proteins in SNARE complex
synaptobrevin, syntaxin, SNAP-25, synaptotagmin. these all form the snare complex and bring the vesicle and membrane together to fuse. synaptotagmin fuses with the snare complex and binds to calcium, this causes the membrane to bulge and and the vesicles move towards it. the vesicles move due to synaxin and synaptobrevin exert a force by a sweeping motion.
32