Introduction to the neurone - L2 Flashcards

1
Q

do retinal receptors hyperpolarise in ight?

A

yeop

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2
Q

2 main categories of sen sory receptors?

A

short and long

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3
Q

describe long receptors

A

“long” receptors which send afferent axons to the CNS and fire action potentials,

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4
Q

describe short receptors

A

“short” receptors without an axon, which immediately synapse with a second-order cell for conduction to the CNS.

“Short” receptors often generate a graded potential instead of firing spikes, leading to graded changes in transmitter release at the synapse, and a graded generator potential in the second order cell, which modulates the rate of spike firing.

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5
Q

long vs short receptors$

A
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6
Q

In long receptors the magnitude of the stimulus is normally encoded as,,,,

A

In long receptors the magnitude of the stimulus is normally encoded as the frequency of action potential firing, as in this cutaneous sensory receptor.

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7
Q

describe sensory receptor adaptation

A

Sensory receptors normally adapt, leading to a diminution of firing frequency with time; this adaptation can take place over either a slow or a rapid time scale.

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8
Q

Cutaneous mechanoreceptors are the quintessential “___” receptors.

A

Cutaneous mechanoreceptors are the quintessential “long” receptors.

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9
Q

Special senses are mostly supplied with “____” receptors

A

short

The exception is the olfactory receptor, which sends axons directly to the olfactory bulb.

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10
Q

observe

A

noiocw

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11
Q

describe how mechano-receptors work

A

the transduction process is direct, involving the opening of stretch- sensitive channels coupled to the cytoskeleton or, for hearing, to more specialised structures.

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12
Q

direct vs indirect

A
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13
Q

Monosynaptic stretch reflex

A
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14
Q

If you inject a steady current into a spinal motor neuron to perturb its membrane potential and then stimulate the Group IA afferents, the EPSP changes sign at a potential of around zeromV. This implies that the excitatory post-synaptic current must reverse at this potential. This value does not correspond to the reversal potential of any single ion,

what does this imply

A

implying that this glutamate- gated channel must allow more than one ion to pass. In fact it is permeant to both Na+ and K+ ions, so the current reverses when the inward Na+ flux balances the outward flux of K+. In some cases, glutamate-gated channels in the CNS also allow Ca2+ to enter, with important implications for synaptic plasticity.

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15
Q

If, instead, you excite Group IA afferents from the antagonist muscle, then they inhibit the -motor neurons of the agonist, via inhibitory interneurons which release ____.

A

If, instead, you excite Group IA afferents from the antagonist muscle, then they inhibit the -motor neurons of the agonist, via inhibitory interneurons which release glycine.

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16
Q

The inhibitory post-synaptic potential in an alpha motor neuron reverses at –80mV. This reversal potential is made less negative by injecting __ ions from the recording electrode, indicating that it is due to an elevation in __ conductance.

Elsewhere in the CNS, inhibition may be achieved by either elevated ______ conductance via the central inhibitory transmitter GABA.

A

The inhibitory post-synaptic potential in an alpha motor neuron reverses at –80mV. This reversal potential is made less negative by injecting Cl- ions from the recording electrode, indicating that it is due to an elevation in Cl- conductance. Elsewhere in the CNS, inhibition may be achieved by either elevated Cl- or K+ conductance via the central inhibitory transmitter GABA.

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17
Q

you understadn that many IPSPs and EPSPs summate at the axon hilock right?

A

yep. good. they combine to produce a net effect

18
Q

3 places synapses can be located

A
19
Q

For example, a cortical pyramidal cell receives synapses …. where?

A

or example, a cortical pyramidal cell receives synapses on the soma, on the dendritic shaft and on dendritic spines.

20
Q

Type 1 and 2 synapses

A
21
Q

how do action potentials spread along nerves?

A

The action potential spreads along a nerve fibre by means of local circuit currents, which raise the nerve membrane to threshold ahead of the present location of the action potential.

22
Q

what is the space constant

A

at steady state the potential decays away exponentially with a space constant, , governed by the relative magnitudes of the membrane and longitudinal resistances.

23
Q

current decay in neurones

A
24
Q

splitting teh dendritic tree into many cables - and moddling EPSP decay is a start.

but are there booster mechanisms?

A

however recent evidence suggests that voltage-gated conductances (both to Na+ and Ca2+) are present in the dendrites of many neurons, serving to boost the decaying passively conducted dendritic signal.

25
Q

where is the AP initiated?

A

axon hillock

26
Q

what are the 2 main cable parameterS>?

A
27
Q

what are APS initiated at the axon hillock?

A

lowest threshold

28
Q

how do we know the AP is started at the axon hillock

A
29
Q

do APs spread back up the dentrits?

A

yep

30
Q

The extent to which a given synapse can influence the potential at the axon hillock depends on….

A

how far away from the cell body it is located along the dendritic tree.

31
Q

describe how the size (diameter) of the dentrite affects the influence of an supstream synapse?

A

Large = less impedance for potential

small = big impedance for potential

32
Q

The space constant of an unmyelinated nerve varies with the ……

A

The space constant of an unmyelinated nerve varies with the square root of its diameter.

33
Q

effect of dendritic diameter

A
34
Q

read and absorb

A
35
Q
A
36
Q

describe shunting inhibition

A

if the inhibitory synapse is located closer to the cell body on the same dendrite, then much of the excitatory current leaves before it can ever influence the cell body. Arithmetically, this is equivalent to division, and is called shunting inhibition

37
Q

The effectiveness of shunting inhibition explains ……

A

The effectiveness of shunting inhibition explains why most excitatory inputs are located further out on the dendrites, while inhibitory inputs are mostly close to the soma.

38
Q

what are Axo-axonic synapses

A

Axo-axonic synapses mediating presynaptic inhibition offer powerful control over synaptic transmitter release

often inhibition

39
Q

pre-synaptic inhibition

A
40
Q

describe pre-synaptic inhibtion

A
  • opening Cl- or K+ reduces the height of the action potential in the presynaptic terminal.
  • leading to a slight primary afferent depolarization, which partially inactivates Na+ channels.
  • This reduction in action potential height leads to reduced opening of voltage-gated Ca2+ channels.
  • Ca2+ channels can also be modulated directly by second messenger systems within the presynaptic terminal. The reduced Ca2+ influx leads to a reduction in transmitter release: since vesicle fusion depends steeply on Ca2+, a subtle change can result in a substantial decrease in release.
41
Q

how important in timing in pre-synaptic transmission?

A

The timing of inhibition needs to be precise, since it must arrive at virtually the same time as the action potential. This constraint is relaxed somewhat with peptide transmitters, which have slower neuromodulatory actions than ionotropic transmitters.

42
Q

fat

A

mamba