6. ET: neurons Flashcards

(56 cards)

1
Q

name the features of the neuron and their functions

A

dendrites - receives electrical signals
cell body - contains nucleus and organelles, passively conveys signals
axon hillock - trigger zone for action potentials
axon - propagates axon potentials
axon terminal - releases chemical signals

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2
Q

what is the RMP’s value and the meaning of this

A

~ -70mV; charge inside the cell is ~70mV more negative than outside

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3
Q

differences in intracellular and extracellular Na+ and K+ concentration in neurons

A

Na+ 10 fold greater outside, K+ 20 fold greater inside

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4
Q

explain leak channels and relative permeability of each Na+ and K+

A

K+ has many leak channels mediating flow outwards, while Na+ has less leak channels that mediate flow inwards
at rest, P K+: P Na+ = 40:1

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5
Q

what is the equilibrium potential

A

an intracellular potential at which the net flow of an ion is zero, according to its electrochemical gradient

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6
Q

equilibrium potential K+

A

-80 mV

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7
Q

equilibrium potential Na+

A

+60mV

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8
Q

what is the nernst equation

A

calculates EP for a singular permeant ion based on concentrations
E(ion) = 61.5 x log (ion conc outside)/ (ion conc inside)

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9
Q

what is the goldman equation

A

calculates RMP based on permeability of multiple permeant ions
RMP = 61.5mV log x (permeability ions outside)/(permeability ions inside)

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10
Q

amplitude of action potential is: (voltage and features)

A

constant, doesn’t depend on intensity of stimulus ~100mV

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11
Q

what is hyper polarisation

A

when the membrane potential becomes more negative

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12
Q

what is depolarisation

A

when the membrane potential becomes more positive

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13
Q

define an action potential

A

brief fluctuation in membrane potential caused by a transient opening of voltage-gated ion channels which spreads along an axon

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14
Q

what is ‘threshold’ in neurons

A

~ -55 mV

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15
Q

what occurs prior to an action potential

A

a slow graded depolarisation is evoked by a stimulus, which can be physical, chemical, and affects a ligand or mechanically gated ion channel

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16
Q

name the three steps of an action potential

A
  1. depolarisation
  2. repolarisation
  3. after hyperpolarisation
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17
Q

describe the depolarisation stage of an AP with respect to changes in ion permeability and MP

A

if MP reaches threshold, a fast depolarisation to around +30mV occurs due to rapid opening of voltage-gated Na+ channels
which increases permeability of Na+ to 20:1 (Na+:K+)

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18
Q

describe the repolarisation stage of an AP with respect to changes in ion permeability and MP

A

MP is becoming more negative
as Na+ channels close due to closing of inactivation gate (Na+) decreasing
and K+ channels open as delayed response to AP, P (K+) increasing

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19
Q

describe the after hyperpolarisation stage of an AP with respect to changes in ion permeability and MP

A

MP briefly overshoots/becomes more depolarised/more negative
Na+ channels are back to resting state w activation gate closed
K+ channels are open
permeability = K+:Na+ 100:1

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20
Q

what is the absolute refractory period

A

the period after an AP is generated (depolarisation and repolarisation) when a new AP cannot be fired, as voltage-gated Na+ channels are temporarily unexcitable

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21
Q

what is the relative refractory period

A

the stage where an action potential can be generated, but stimulus must be bigger than usual due to MP being more negative than usual, as membrane is in after hyperpolarisation state

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22
Q

why does influx of Na+ stop in an AP

A
  1. the electrical gradient for influx decreases as more Na+ comes in, making the inside of neuron more positive
  2. the channels deactivate quickly, due to the inactivation gate
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23
Q

explain the structure and function of the two Na+ channel gates

A
  1. activation gate -
    extracellular side
    closed at rest
    opens first and quickly upon depolarisation
    closes during AHP (starts closing in repolarisation)
  2. inactivation gate:
    intracellular side
    open at rest
    closes second, starts in repolarisation
    reverts to resting state in AHP
24
Q

what ions does cathode attract, what charge aggregates at the membrane adjacent, what movement of ions occurs, what happens to MP

A

cations, positive charge, ions move from outside to inside, membrane depolarises

25
what ions does anode attract, what charge aggregates at the membrane adjacent, what movement of ions occurs, what happens to MP
anions, negative charge, ions move outside to inside, membrane hyper polarises
26
how are APs evoked internally/physiologically
APs generate at the axon hillock at the top of the axon and spread down the axon in one direction, as the Na+ channels behind them are in the refractory period
27
what are the two paths for current to flow in external AP generation, and what are their differences?
outside the axon from anion to cation - path of least resistance, most current moves this way across the membrane, inside the axon - only this path changes RMP/generates AP
28
diameter of myelinated axons vs myelinated axons
5-10 uM, ~1 uM
29
what is passive spread of charge described as
the natural tendency for positive charges to move towards negative charges
30
what happens on the outside of the axon
positive charge moves backward towards depolarised area, to balance/complete the circuit
31
passive can occur in one or both directions, and typically lasts for how long?
both directions, and less than 1 uM
32
speed of conduction in myelinated axons
20-100 m/s
33
glial cells involved in myelination
oligodendrocytes CNS schwann cells PNS
34
speed of conduction in myelinated axons
1 m/s
35
how does myelination increase efficiency/speed of conduct
myelin is insulting, so prevents dissipation of passive current along the axon. therefore APs don’t need to be regenerated at every part of the membrane, rather are only generated at the nodes of ranvier.
36
pattern of AP generation in myelinated vs unmyelinated axons
saltatory (in big leaps) vs continuous
37
benefits and difficulties of myelination
less passive current loss, faster conduction, less energy required for maintenance of ion concentrations as Na+/K+ ATPase has to work less hard to regenerate concentrations but myelination requires space and energy
38
what neurons are in the peripheral nervous system
afferent sensory neurons, and efferent motoneurons
39
how is information about strength of stimulus conveyed by sensory neurons
strength/amplitude of the receptor potential, and frequency of APs
40
what is the receptor potential
a graded depolarisation from non-voltage gated ion channels in response to chemical or mechanical stimulus, triggering an AP that spreads along the axon to the CNS
41
what is the presynaptic terminal
the end of a transmitting axon, where the electrical signal (the action potential) is converted into a chemical signal (neurotransmitter release)
42
describe synaptic transmission in 6 steps, starting with 1. AP travels down the...
1. ... presynaptic axon to the presynaptic terminal 2. AP triggers opening of Ca2+ channels 3. Ca2+ triggers release of neurotransmitters via exocytosis 4. neurotransmitters diffuse across the synaptic cleft and react with postsynaptic receptors 5. causing ligand-gated ion channels to open in postsynaptic neuron, causing a local depolarisation 6. AP is triggered in postsynaptic neuron
43
what is a neuromuscular junction
the synapse where a motor neuron communicates with a muscle fibre
44
what is the end plate potential (EPP)
the local depolarisation of a muscle fibre at the neuromuscular junction caused by release of Ach, and causing opening of non-selective cation channels, triggering an AP along the muscle fibre.
45
what is an IPSP, incl ion channels involved and neurotransmitters
inhibitory postsynaptic potential: graded hyperpolarisation of the postsynaptic membrane, making it less excitable/likely to fire APs. caused by transient opening of K+ channels neurotransmitters usually GABA and glycine
46
what is an EPSP, incl ion channels involved and neurotransmitters
excitatory postsynaptic potential: graded depolarisation of the postsynaptic membrane, making it more likely to fire APs. caused by transient opening of K+, Na+, sometimes Ca2+ neurotransmitters usually Ach and glutamate
47
name and compare the two main classes of neurotransmitters
classical/small molecule: small act directly on channels in postsynaptic membranes action is fast (milliseconds) neuropeptides/neuromodulators: larger act indirectly/metabotropic modulatory action action is slower (seconds-mins_
48
what is long term potentiation
increasing number of receptors/strength of synpase/sensitivity of neuron to stimulus caused by repeated use
49
factors affecting speed of synaptic transmission
type of neurotransmitter transmitted type of neurotransmitter receptor/channel complex in postsynaptic membrane
50
what is glutamate, what receptors does it have
classical neurotransmitter; primary excitatory neurotransmitter in CNS. has 3 receptors: AMPA - causes fast synaptic response in PS neuron NMDA - slow synaptic response in PS neuron Kainate - longer duration modulatory action
51
what is long term depression
decrease in strength of synapse/number of receptors due to stimulation of a neuron frequently in certain way
52
3 methods of neurotransmitter inactivation
1. diffusion of neurotransmitter away from synaptic cleft 2. enzymatic degradation in the synaptic cleft - e.g acetylcholine esterase 3. reuptake - involves specific neurotransmitter transporters in the presynaptic membrane. beneficial as doesn't require regeneration.
53
what is the idea of 'integration of synaptic inputs'
each neuron forms thousands of synapses, all of which translate to very small PSPs at the axon hillock (0.1mV). neurons must integrate thousands of these through summation to fire an AP
54
describe two types of summation for synaptic integration
temporal summation: neuron is stimulated with increased frequency in order to build up amplitude spatial summation: multiple presynaptic neurons stimulate one postsynaptic neuron in order to build up amplitude
55
what is excitotoxicity
neurotoxic process in which excessive release of excitatory (glutamate) neurotransmitters/ excessive stimulation of the receptors leads to accumulation of Ca2+, activating enzymes leading to cell damage/death
56
how does excitotoxicity damage the cell and cause cell death
mitochondrial dysfunction, oxidative stress from reactive oxidative species, apoptosis.