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How Nerves Work Flashcards

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1
Q

Subdivisions of the nervous system

A

the brain
the spinal cord
the peripheral nerves

the somatic nervous system
the autonomic nervous system
the enteric nervous system

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2
Q

The brain

A
  • Meninges
  • Gyrus vs sulcus
  • Cerebellum
  • Cerebrum
  • Diencephalon
  • Brainstem
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3
Q

cerebrum contains

A
  • frontal lobe
  • temporal lobe
  • parietal lobe
  • occipital lobe
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4
Q

diencephalon contains

A
  • thalamus

- hypothalamus

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5
Q

brainstem contains

A
  • midbrain
  • pons
  • medulla oblongata
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6
Q

frontal lobe is

A

the front half bit of the brain

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7
Q

temporal lobe is

A

under the frontal and parietal lobe and above the cerebellum. It touches the occipital lobe perpendicularly.

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8
Q

parietal lobe is

A

between the frontal and occipital lobe and above the temporal lobe.

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9
Q

occipital lobe is

A

the very end of that touches the temporal lobe perpendicularly and also touches the back end of the cerebellum

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10
Q

the forebrain contains

A
  • cerebrum

- diencephalon

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11
Q

The spinal cord

A 
31 pairs of spinal (plus 12 pairs of cranial) nerves
8 cervical (7 vertebrae)
- neck, shoulders & arms
12 thoracic (12 vertebrae)
- chest & abdomen
5 lumbar (5 vertebrae)
- hips & legs
5 sacral (5 fused vertebrae)
- genitalia & gastrointestinal  tract
1 coccygeal (4 fused vertebrae)
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12
Q

very mobile vertebrae

A
  • cervical (neck)
  • lumbar (hips and legs)

discs between lumbar vertebrae are most susceptible to wear and tear over time - cumulative strain

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13
Q

discs

A
  • promote flexibility of spine
  • act as shock absorber by preventing jarring
  • reduce friction
  • act as spacer between vertebrae
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14
Q

afferenet is

A

sensory and on the dorsal root

note: s in dorsal means its sensory

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15
Q

efferent is

A

motor and on the ventral root

note: no s in ventral so its motor

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16
Q

ganglion is between

A

dorsal root and dorsal horn

note: dorsal also means posterior (both have s in them meaning they are sensory)

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17
Q

Neurones

A 
Cell body (soma)
Dendrites
- receive information
Initial segment (axon hillock )
- triggers action potential
Axon
- sends action potential
Axon (presynaptic) terminals
- release transmitter
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18
Q

Afferent (sensory) neurones send signals they receive to

A

Interneurones

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19
Q

Interneurones are found in the

A

Central nervous system

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20
Q

Interneurones send signals to

A

Efferent (motor) neurones

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21
Q

Efferent (motor) neurones are found in the

A

Peripheral nervous system

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22
Q

Afferent (sensory) neurones are found in the

A

Peripheral nervous system

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23
Q

the axon terminal can cause a reaction to occur in

A

muscle, gland or neuron

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24
Q

Glia

A
  • Comprise 90% of cells in the CNS
  • Astrocytes
  • Oligodendrocytes
  • Microglia
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25
Q

Astrocytes

A
  • maintain the external environment for the neurones

- surround blood vessels & produce the blood brain barrier

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26
Q

Oligodendrocytes

A
  • form myelin sheaths in the CNS
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27
Q

Microglia

A
  • phagocytic hoovers mopping up infection
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28
Q

Gross structure of the spinal cord

A
  • grey (inside) vs white matter (outside)
  • dorsal vs ventral horn
  • dorsal root ganglion
  • spinal nerves
  • spinal tracts
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29
Q

Action potentials

A

transmit signals over long distances - big all or none things that self propagate over potentially infinite distances.

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30
Q

Graded potentials

A

decide when an action potential should be fired

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31
Q

Resting membrane potential

A

keeps cell ready to respond

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32
Q

the equilibrium potential is

A

the membrane potential at which the electrical gradient is exactly equal and opposite to the concentration gradient pushing the K out.
ie- the concentration gradient determines the equilibrium potential

If the concentration gradient was higher it will develop a bigger electrical potential before it is matched and so the equilibrium potential will be higher.

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33
Q

Higher [K+]

A
  • Reduces concentration gradient
  • Sustains a smaller electrical gradient at equilibrium
  • RMP is reduced (ie cell depolarises) fires action potential
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34
Q

The blood brain barrier

A
  • Capillaries of the brain are especially “tight”
  • Due to astrocytes & tight junctions between endothelial - cells
  • This protects the brain from changes in plasma [K+]

The heart is not so lucky and therefore hyperkalemia causes ventricular fibrillation as there is no heart blood barrier to stop the K reaching excitable cells in the heart.

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35
Q

ventricular fibrillation

A

s a heart rhythm problem that occurs when the heart beats with rapid, erratic electrical impulses. This causes pumping chambers in your heart (the ventricles) to quiver uselessly, instead of pumping blood around the body.

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36
Q

why is RMP close to K equilibrium

A

At rest there is lots of open K channels.

There is also some open Na and open Cl channels but because permeability is lower they have a smaller effect on RMP.

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37
Q

if you poison the Na/K pump,

A

cells only depolarise a few mV. You have to wait for concentration gradient to run down before you lose the RMP.

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38
Q

The RMP is dominated by the

A

resting permeability to K which is why the RMP is close to the K equilibrium potential. This in turn depends on the K concentration gradient that has been set up by the Na/K pump.

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39
Q

Open (more) K channels and

A

and K flows out and cell hyperpolarises.

This happens as there is less K outside the cell due to the Na/K pump. Think of the “leaky” K channels that are concentration gradient of K.
The electrical gradient is opposite to this as k is positive and cell is negative but concentration wins.

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40
Q

Open Na channels and

A

Na flows in and cell depolarises.

This happens as there is less Na inside the cell due to the Na/K pump. Opening Na channels means passive transport and so more Na goes inside cell.
The electrical gradient is same as this as Na is positive and cell is negative.

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41
Q

Open Cl channels and

A

Cl flows in and cell hyperpolarises.

This happens as there is less Cl inside the cell.
Opening Cl channels means passive transport and so more Cl goes inside cell.
The electrical gradient is opposite to this as Cl is negative and cell is also negative but concentration wins.

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42
Q

Open Ca channels and

A

Ca flows in and cell depolarises.

This happens as there is less Ca inside the cell.
Opening Ca channels means passive transport and so more Ca goes inside cell.
The electrical gradient is same as this as Na is positive and cell is negative.

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43
Q

Hyper means

A

over

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44
Q

hypo means

A

under

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45
Q

depolarisation

A

Anything towards zero

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46
Q

overshoot

A

Over zero

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47
Q

repolarisation

A

Back to original

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48
Q

hyperpolarisation

A

Below resting membrane potential

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49
Q

Potassium increase causes

A

neurons to depolarise

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50
Q

what makes a neurones decide to fire an action potential

A

the resting membrane potential has to be depolarised to a magic threshold - about -55mV.

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51
Q

what makes it depolarise?

A

External stimuli acting on specific sets of ion channels to create graded potential where the size of the potential is related to the size of the stimulus.

52
Q

Junction between two neurones - the synapse - where Action Potential releases

A

transmitter molecules, they activate (pharmacological) receptors on second cell which open ion channels and create another graded potential.
It could:
- try and make the cell fire = EPSP (excitatory post-synaptic potential)
- stop it reaching threshold = IPSP (inhibitory post-synaptic potential)

53
Q

Graded potentials could occur

A

out in the terminals of sensory nerves - say in response to pressure on the skin. Called a generator potential (Vander calls it a receptor potential – confusing).
If the graded potential is big enough it will reach threshold and make the cell fire an action potential (or more)

54
Q

At neuromuscular junction,

A

motoneurone depolarises the muscle to threshold by evoking a graded potential = endplate potential

55
Q

Examples of graded potentials

A
  • Generator potentials
  • Postsynaptic potentials
  • Endplate potentials
  • Pacemaker potentials
56
Q

Generator potentials

A
  • at sensory receptors
57
Q

Postsynaptic potentials

A
  • at synapses
58
Q

Endplate potentials

A
  • at neuromuscular junction
59
Q

Pacemaker potentials

A
  • in pace maker tissues
60
Q

Graded potentials

A

determine when an action potential is fired

61
Q

Graded potentials are also known as

A
  • electrotonic potentials
  • decremental potentials
  • non-propagated potentials
  • local potentials
62
Q

some local stimulus (could be pressure on a touch receptor or a neurotransmitter on a postsynaptic membrane) causes channels to open. Let’s say they are Na channels.
what happens?

A

Current flows across membrane and creates a potential difference (V=IR, membrane potential, draw it). That current leaks out along the rest of the membrane.
As you go further away, more current has already leaked out so you get a smaller and smaller membrane potential (draw it). In that sense they are decremental and non propagated. They can only operate very locally.
For long distance transmission you need the action potentials that come later.

63
Q

Graded potentials are graded therefore

A

can signal stimulus intensity in their amplitude.
If there is a stronger stimulus at the beginning (bigger pressure or more neurotransmitter) you get more channels opened, bigger current flow, and therefore a bigger potential.

64
Q

Graded potentials can be

A
  • depolarising
  • hyperpolarising

Firing an action potential depends on reaching a firing threshold and therefore graded potentials can excite or inhibit a cell.

65
Q

Hyperpolarising postsynaptic potentials

A

Opens Cl- channels - or open even more K+ channels.
Takes them away from threshold and so is inhibitory.
Hence called IPSPs.
And this is what GABA and Glycine do.

Cl entering cell causes fast IPSP.
K leaving cell causes slow IPSP.

66
Q

Depolarising postsynaptic potentials

A

To depolarise cells, transmitters tend to open the type of channels permeable to Na and K (= non-specific monovalent cation channels), but more Na gets in than K gets out, so it depolarises. Causes fast EPSP.

Or block some of those leaky K channels. Causes slow EPSP.
If glutamate was released it would bind and cause another channel to open.

67
Q

ligand-gated ion channels

A

Postsynaptic potentials are produced by a neurotransmitter opening or closing ion channels

68
Q

voltage-gated ion channels

A

Actions potentials are produced by depolarisation of the membrane potential opening ion channels

69
Q

Graded potentials are important in synaptic integration as they can

A

summate (add to each other).
This whole process is called integration - just means looking at all the inputs (synapses or physical stimuli) and deciding whether or not to send one of those long distance signals (an action potential).

70
Q

temporal summation.

A

One stimulation on its own does this. Stimulate it again quickly and the next EPSP adds on to it.

71
Q

spatial summation.

A

Or you can do the same with two stimulation, eg- red and blue.

72
Q

If initial segment reaches threshold,

A

cell fires an action potential.

73
Q

EPSP is

A

decremental so it gets smaller as it travels

74
Q

imagine this, a is further away from axon hillock so it decays more than b.
Neither on its own reaches threshold.
Stimulate b twice, what will happen?

A

temporal summation that reaches threshold.

75
Q

Imagine this, a is further away from axon hillock so it decays more than b.
Neither on its own reaches threshold.
If you stimulate a and b, what will happen?

A

spatial summation that reaches threshold.

76
Q

spatial summation cannot happen without

A

temporal summation

77
Q

Synaptic integration

A

The process of summing all inputs in space and time, to determine whether or not the initial segment reaches threshold.

78
Q

Anything closer to the axon hillock have

A

a bigger EPSP than those that are far away as the EPSP is decremental and so gets smaller as it travels.

79
Q

And you also get IPSPs that

A

tend to stop the cell reaching threshold.

80
Q

EPSP and IPSP are ___ _______

A

pre-synaptic

81
Q

if an IPSP directly touches the dendrite area then it can

A

inhibit all input as it is non-specific. eg- if someone has already eaten then why buy the sandwich

82
Q

if an IPSP indirectly touches the dendrite area (by touching one EPSP) then it can

A

inhibit just that one input as it is specific. eg- sandwich contains everything a person likes except tomatoes.

83
Q

EPSPs act by

A
  • opening Na+/K+ channels

- closing K+ channels

84
Q

IPSPs:

A
  • opening Cl- channels

- opening K+ channels

85
Q

action potential steps

A
  • RMP sitting at -70mV, reaches threshold for some reason - usually about -55mV.
  • Sudden massive depolarsiation and overshoot to +30. - - - Only last about 1 msec, then rapid repolaristion beyond resting level.
  • After repolarising it will hyperpolarise and go back to stable state

note: its much bigger, but shorter lasting than most graded potentials

86
Q

Ionic basis of the action potential

A

At RMP:
- Na permeability is very low, K is higher because of those leaking channels.

During depolarisation:
- Voltage dependent Na channels open almost immediately, Na floods in and depolarises cell. Massive increase in permeability = decrease in resistance.
Example of positive feedback

During repolarisation:

  • K+ permeability slowly rises as more K+ channels (this time the voltage dependent ones) open.
  • Cause repolarisation and after hyperpolarisation.
  • Eventually they shut and we are back to where we started.
87
Q

Absolute refractory period

A

The voltage gated channels need some time to rest.

88
Q

Voltage gated potassium channels are

A

slower to open and close and so stay open longer

89
Q

voltage gated sodium channels

A

are quicker to open and close and so stay open for a short period of time.

90
Q

Poisoning the pump produces a

A 
delayed effect. It takes time for the gradients to run down.
Local anaesthetics (procaine/lidocaine) block those voltage dependent Na channels. So APs cannot be transmitted.
91
Q

Properties of action potentials

A
  • They have a threshold
  • They are all or none
  • They cannot encode stimulus intensity in their amplitude, only in their frequency
  • Self propagate
92
Q

Self-propagation of APs

A

Action potentials have a threshold and therefore are all or none. They cannot encode stimulus intensity in their amplitude but can do this in their frequency of action potentials fired.

Local current flow also spreads back, but this does NOT evoke a new AP because those channels are in their refractory state - hence the depolarisation (the action potential) can only keep sweeping forward down the axon and so on - until the electrical signal gets to the end of the axon where it may make a muscle twitch or another neurone do something

93
Q

Properties of action potentials

A
  • mediated by voltage-gated channels
  • have a threshold
  • are all-or-none
  • can only encoded stimulus intensity in their firing frequency, not amplitude
  • are self-propagating
  • have a refractory period
  • travel slowly
    • conduction velocity can be improved by big axons or
    • myelination
94
Q

large axons increase conduction velocity as

A

A bigger axon has a lower axial resistance – that means the depolarisation evoked at one channel can spread further – it does this passively, but VERY quickly.
That means you can spread you Na+ channels out further and the depolarisation from one will still be big enough by the time it gets to its neighbour to reach threshold and make its neighbour open.

It is the opening of the voltage gated channels that takes the time – so the less of that and the more of the passive spread you can have, the better it is.
Big fibres are good, but if you have may of them you have nerves the size of tree trunks.

95
Q

what forms myelin?

A

Folds of membrane from:
- Schwann cells (in PNS)
- Oligodendrocytes (in CNS)
form the myelin sheath

Gaps = nodes of Ranvier

96
Q

Graded potentials summate (integrate) trigger

A

an AP at the axon hillock/initial segment by reaching threshold.
Na channels are only present at the nodes, so it cannot propagate as normal, but because myelin increases resistance of membrane it allows the AP to spread like a local current, to the next segment, with little decrement.
Evokes a new AP there.
And the next, and the next.

97
Q

The signal (AP) cannot go back because of the

A

refractory period (recovery period).

98
Q

Absolute refractory period is when

A

the neuron cannot be excited to generate a second action potential (no matter how intense the stimulus)

99
Q

Relative refractory period is when

A

a stronger than normal stimulus is needed to initiate a new action potential.

100
Q

Saltatory conduction (to hop or leap) is the

A

propagation of action potentials along myelinated axons from one node of Ranvier to the next, increasing the conduction velocity of action potentials.

101
Q

Effect on myelination on APs:

The depolarisation evoked by voltage-gated Na channels at one node of Ranvier spreads as a

A

local circut and while this is decremental (i.e. non- propagated), it travels further than in an un-myelinated axon because less current is wasted leaking out of the membrane or charging up the capacitance. This means it is still big enough by the time it reaches the next node to reach threshold and trigger another action potential.

And you can tell how important it is because of the effects of de-myelinating diseases – e.g. multiple sclerosis (problems with vision, arm or leg movement, sensation or balance)

102
Q

Effect on demyelination on APs:

A
  • Big local current decays quicker
  • Does not depolarise to next node to threshold.
  • And conduction fails.

eg

  • Multiple sclerosis
  • Guillain-Barre syndrome
103
Q

compound action potential

A

Mammals have small and large unmyelinated and small and large myelinated axons. Therefore extracellular recording from a bundle of axons (a nerve trunk) evokes a “compound” action potential

104
Q

Fibres vary in sensitivity to pressure

A

Big ones go first ie A>B>C

that is why you arms goes numb and useless when you sleep on it - but it does not necessarily hurt.

105
Q

And in their sensitivity to anaesthetics

A

small ones go first which is handy.

106
Q

There is another classification system that originated in sensory nerve fibres:

A

Ia muscle spindle annulospiral ending = A alpha
Ib golgi tendon organ = A alpha
IIb muscle spindle flower spray ending = A beta
III pain and cold = A delta
IV pain and heat = C

107
Q

Action potentials:

A
  • mediated by voltage-gated channels
  • Encode stimulus intensity by frequency
  • Cannot summate so are are all-or-none
  • Evoked at threshold
  • Refractory period
  • Self-propagating
  • Depolarising
  • Sends electrical signal over long distances
  • have a refractory period
  • travel slowly
  • conduction velocity can be improved by big axons or by myelination
108
Q

Graded potentials:

A
  • Graded
  • Encode stimulus intensity by amplitude
  • Can summate
  • Has no threshold
  • No refractory period
  • Decremental (signal can decay)
  • De- or hyper-polarising
  • Ligand-gated channels
  • “Decides” if a cell will fire an action potential
109
Q

Ionic basis of the action potential is

A

mediated by voltage-gated channels

110
Q

But how does AP in neurone evoke contraction in muscle?

A

Contraction is triggered by AP in sarcolemma.

111
Q

The neuromuscular junction (first half that happens in the sarcolemma):
Action potential in motor neurone

A
  • Opens voltage-gated Ca2+ channels in presynaptic terminal
  • Triggers fusion of vesicles
  • Acetylcholine (ACh) released
  • Diffuses across synaptic cleft
  • Binds to ACh (nicotinic) receptors
  • Opens ligand-gated Na+/K+ channels
  • Evokes graded (local) potential (end plate potential)
  • Always depolarises adjacent membrane to threshold
  • Opens voltage-gated Na+ channels - evokes new AP
  • ACh removed by acetylcholinesterase
112
Q

The neuromuscular junction:

tetrodotoxin

A

blocks Na+ channels and so blocks the action potential

113
Q

The neuromuscular junction:

joro spider toxin

A

blocks Ca2+ channels and so stops transmitter release

114
Q

The neuromuscular junction:

botulinum toxin

A

disrupts the release machinery and so blocks transmitter release

115
Q

The neuromuscular junction:

curare

A

blocks Ach receptors and so prevents the end plate potential

116
Q

The neuromuscular junction:

anticholinesterases

A

block ACh breakdown and so increase trasnmission at the NMJ

117
Q

Central nervous system synapses:

Action potential reaches axon terminal

A
  • Opens voltage-gated Ca2+ channels in presynaptic terminal
  • Calcium enters axon terminal and to active zone
  • neurotransmitter release and diffusion
  • neurotransmitter binds to postsynaptic receptors
  • neurotransmitter removed from synaptic cleft
118
Q

Central nervous system synapses:

Range of neurotransmitters

A
  • Acetylcholine
  • Norepinephrine
  • Dopamine
  • Serotonin (5HT)
  • Histamine
  • Glutamate
  • GABA
  • Glycine
  • Peptides
  • ATP
  • Adenosine

each have several receptors

119
Q

Central nervous system synapses:

Range of postsynaptic potentials

A
  • Fast EPSPs (ionotropic)
  • Slow EPSPs (metabotropic)
  • Fast IPSPs
  • Slow IPSPs

Enables complex synaptic integration

120
Q

NMJ postsynaptic potentials

A

big endplate potential

121
Q

Central nervous system synapses:

Anatomical arrangement of synapse

A
  • Axo-somatic
  • Axo-dendritic
  • Axo-axona

this has significant effects on their function.

122
Q

Anatomical arrangement of NMJ

A

does not change.

123
Q

Central nervous system synapses:

Synaptic connectivity

A
  • convergence
  • divergence
  • feedback inhibition
  • monosynaptic vs polysynaptic pathways (Polysynaptic pathways are much more open to modulation at each synapse)

note: Stick an inhibitory interneurone in the polysynaptic chain and the effect changes entirely.

124
Q

Synaptic connectivity of NMJ

A

always motorneurone-muscle cell – a bit of divergence to make a motor unit, but otherwise that is it.

125
Q

CNS more complex than NMJ because:

A
  • Range of neurotransmitters
  • Range of postsynaptic potentials
  • Small potentials (hence synaptic integration)
  • Variations on anatomical arrangement
  • Variations on “connectivity” of neurones
126
Q

NMJ as a simple synapse

A

presynaptic vesicle, Ca2+-dependent ACh release, postsynaptic receptors, endplate potential, “safe” transmission, acetylcholinesterase

127
Q

Comparison with CNS synapses

A

recognise why CNS synapses are so much more complicated; ie range of transmitters & receptors, fast and slow PSPs, EPSPs and IPSPs, small PSPs, synaptic integration, types of synapse, neuronal connectivity

Science for Medicine (16 decks)

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