Nervous Coordination Flashcards

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1
Q

structure of a motor neurone

A

-cell body: contains usual organelles and high proportion of RER- associated with the production of proteins and neurotransmitters
-dendrons: branches into dendrites, which carry nerve impulses towards cell body.
-axon: long unbranched fibre carries nerve impulses away from cell body

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2
Q

additional features of a myelinated motor neuron

A

-schwann cells: wrap around the axon many times
-myelin sheath: made of myelin-rich membranes of shwann cells
-nodes of ranvier: very short gaps between neighboring shwann cells where there is no myelin sheath

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3
Q

3 processes shwann cells are involved in

A

-phagocytosis
-nerve regeneration
-electrical insulation

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4
Q

functions of the different neurones

A

-sensory neurone: transmits nerve impulses from receptor to a relay neurone
-relay neurone: transmits impulses between neurones
-motor neurone: transmits nerve impulses from a relay neurone to an effector, such as a muscle or gland

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5
Q

resting potential

A

potential difference across neuron membrane when not stimulated- -65mV in humans

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6
Q

how is resting potential estabilished

A

-sodium-potassium pump actively transports 3Na+ out of cell for every 2K+ into the cell.
-esabilishes an electrochemical gradient as cell contents more negative than extracellular environment
-sodium begins to diffuse back naturally into axon, while potassium diffuses out
-however most of the sodium ion channel gates are closed, whereas gates for potassium ions remain open

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7
Q

action potential

A

a temporary reversal of the charges across the axon membrane which increase from -65mv to +40mv

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8
Q

stages of generating an action potential

A

depolarisation
repolarisation
hyperpolarisation
return to resting potential

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9
Q

depolarisation

A

-stimulus is detected, permeability of membrane for sodium ions increases.
-sodium ion channels open-allows facilitated diffusion of Na+ into cell down electrochemical gradient.
-cell membrane depolarises- p.d across membrane becomes more positive
-if membrane reaches threshold potential (-55mV), voltage gated sodium channels open
-causes influx of Na+ ions into cell-p.d reaches +40mV.

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10
Q

repolarisation

A

-voltage gated Na+ channels close, voltage gated K+ channels open
-K+ ions diffuse out of cell down their electrochemical gradient
-p.d. across membrane becomes more negative

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11
Q

hyperpolarisation

A

-p.d. overshoots slightly as K+ ions diffuse out-p.d. more negative than resting potential
-refractory period: no stimulus is large enough to raise membrane potential to threshold
-voltage gated K+ channels closes, sodium-potassium pump re-establishes resting potential

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12
Q

importance of refractory period

A

no action potential can be generated in hyperpolarised sections of membrane:
-ensures unidirectional impulse
-ensures discrete impulses
-limits frequency of impulse transmission

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13
Q

‘all or nothing’ principle

A

any stimulus that causes the membrane to reach threshold potential will generate action potential
action potential is the same size, regardless of the size of stimulus

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14
Q

factors that affect speed of conductance

A

myelin sheath
axon diameter
temperature

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15
Q

how does axon diameter affect speed of conductance

A

greater diameter=faster
-less resistance to flow of ions (depolarisation and repolaristaion)
-less leakage of ions (easier to maintain membrane potential)

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16
Q

how does temperature affect speed of conductance

A

higher temperature=faster
-faster rate of diffusion (depolarisation repolarisation)
-faster rate of respiration (enzyme-controlled)= more ATP produced for active transport to re-establish resting potential

temperature too high=membrane proteins denature

17
Q

how action potential passes along unmyelinated axon

A

-stimulus leads to influx of Na+ ions. First section of axon membrane depolarised
-localised electrical currents cause sodium voltage-gated channels further along membrane to open.
-section behind, sodium voltage-gated channels channels close, potassium voltage-gated channels open=begins to repolarise
-sequential wave of depolarisation
-

18
Q

how action potential passes along myelinated axon

A

-in myelinated axons, fatty sheath of myelin acts as an electrical insulator, preventing depolarisation- action potential from forming
-action potentials therefore take place at intervals of 1-3mm (nodes of ranvier
-action potentials move through saltatory conduction
-as a result of saltatory conduction, action potential moves along the axon faster

19
Q

saltatory conduction

A

impulse ‘jumps’ from one node of Ranvier to another.

20
Q

synapse

A

the junction between two neurones or a neurone and an effector cell.
synapses transmit information, but not impulses,from one neurone to another by neurotransmitters.

21
Q

structure of synapse

A

presynaptic neuron: releases neurotransmitters, ends in synaptic knob
-contains many mitochondria, endoplasmic reticulum & vesicles of neurotransmitter
synaptic cleft: 20-30nm gap between neurons
postsynaptic neuron: has complementary receptors to neurotransmitters

22
Q

cholinergic synapse

A

a synapse in which the neurotransmitter is acetylcholine.
can be excitory or inhibitory
located at:
-peripheral NS
-neuromuscular junctions (between neurones and muscles)

23
Q

transmission across cholinergic synapse

A
  1. action potential arrives at end of presynaptic neurone
    2.this depolarises membrane & stimulates voltage-gated calcium ion channels to open- influx of Ca2+ ions enter synaptic knob by facilitated diffusion
  2. influx of Ca2+ ions causes synaptic vesicles containing ACh to fuse with presynaptic membrane releasing ACh into the cleft through exotysosis.
  3. ACh diffuses across the cleft and binds to receptor sites on sodium ion protein channels in membrane of postsynaptic membrane, causes a slight delay in impulse
  4. Na+ ion channels open and an influx of sodium depolarises postsynaptic membrane=generates new action potential
24
Q

what happens to ACh from synaptic cleft

A

Acetylcholinesterase (AChE) hydrolyses ACh into choline and ethanoic acid (acetyl), which diffuses back into presynaptic cleft
ATP released by mitochondria used to recombine choline and acetyl to reform acetylcholine which is stored in synaptic vesicles for future use.
- sodium ion protein channels close in absence of ACh in receptor sites.

25
Q

importance of AChE

A

-enables acetyl and choline to be recycled
-prevents ACh from continuously generating new action potential in postsynaptic neurone, so leads to discrete transfer of information across synapses.

26
Q

features of synapse

A

-unidirectionality: synapses only pass neurotransmitters from the presynaptic knob through the cleft to receptors on post synaptic membrane
-summation: low-frequency action potentials often lead to release of insufficient concentrations of neurotransmitter to trigger an action potential in post synaptic neuron
-inhibition: inhibitory synapses make it less likely that the new action potential will be created

27
Q

2 types of summation

A

-spatial summation: a number of different presynaptic neurones collectively release enough neurotransmirrer altogether to exceed the threshold value (-55mv) in post-synaptic neurone.
-temporal summation: single presynaptic neurone releases neurotransmitter many times over a very short period, i.e. frequency action potentials

28
Q

what happens in inhibitory synapse

A

-the presynaptic neurone releases neurotransmitter (GABA) that binds to Cl- protein channels on the postsynaptic neurone.
-Cl- ions move into the postsynaptic neurone by facilitated diffusion
-binding of neurotransmitter causes the opening of nearby K+ protein channels
-K+ ions move out postsynaptic neurone into synapse
-causes membrane potential to decrease to as much as -80mV: hyperpolarisation
-makes it less likely that new action potential will be created

29
Q

how drugs can increase synaptic transmission

A

inhibit AChE
mimic shape of neurotransmitter

30
Q

how drugs can decrease synaptic transmission

A

-inhibit release of neurotransmitter
-decrease permeability of postsynaptic membrane to ions
hyperpolarise postsynaptic membrane