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A2 Biology > Chapter 15: Nervous coordination (Part I) > Flashcards

Chapter 15: Nervous coordination (Part I) Flashcards

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1
Q

what are the two main forms of communication in animals?

A

the nervous system

the hormonal system

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2
Q

give one example of a nervous coordination and a hormonal coordination

A

hormonal: control of blood glucose conc
nervous: reflex action

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3
Q

compare and contrast the hormonal and nervous systems

A 
hormonal:
communication by chemicals: hormones
transmission by blood system
transmission relatively slow 
hormones travel all over body, but only target cells respond 
response is widespread 
response is slow 
response is often long-lasting 
effect may be permanent/irreversible
nervous:
communication by nerve impulses
transmission by neruones 
transmission is very rapid 
nerve impulses travel to specific parts of body 
response is localised 
response is rapid 
response is short-lived 
effect usually temporary/reversible
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4
Q

role of sensory neurons in the nervous system

A
  • transmit nerve impulses from receptor to intermediate or motor neuron
  • has 1 dendron (often long), it carries impulses towards cell body and 1 axon that carries it away from cell body
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5
Q

role of motor neurons in the nervous system

A
  • transmit nerve impulses from intermediate neuron to effector (e.g. gland/muscle)
  • has long axon and many short dendrites
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6
Q

role of intermediate/relay neurons in the nervous system

A
  • transmit impulses between neurons

- has numerous short processes (axons and dendrites)

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7
Q

describe the general structure of a motor neuron

A

cell body: contains organelles and high proportion of RER, also associated w/ production of proteins and neurotransmitters

dendrons: extensions of cell body that branch into dendrites which carry impulses towards cell body
axon: long, unbranched fibre carries nerve impulses away from cell body.

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8
Q

describe the additional features of a myelinated motor neuron

A

● Schwann cells: wrap around axon many times (so layers build up)
● Myelin sheath: made from myelin-rich membranes of Schwann cells.
● Nodes of Ranvier: very short gaps between neighbouring Schwann cells where there is no myelin sheath.

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9
Q

state (2) role(s) of schwann cells

A
  • surround axon to protect it and provide electrical insulation
  • carry out phagocytosis and play a part in nerve regeneration

(schwann cells have membranes rich in fatty substances called myelin)

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10
Q

state three main functions of the myelin sheath

A

1 - acts as an electrical insulator for the neurone - it prevents electrical impulses travelling through the sheath.

2 - The sheath prevents the movement of ions into or out of the neurone/ it prevents depolarisation.

3 - speeds up conduction/ transmission of electrical impulse in the neurone - impulses cannot travel through the sheath instead, impulses ‘jump’ from a gap in the myelin sheath to another gap (it jumps from one Node of Ranvier to another Node). This is a process called Saltatory Conduction.

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11
Q

role of nodes of Ranvier

A

periodic gaps in myelin sheath on axon of certain neurons, that assist rapid conduction of nerve impulses

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12
Q

what is myelin sheath formed from in the CNS and PNS?

A
  • formed by Schwann cells in the peripheral nervous system (PNS)
  • oligodendrocytes in the central nervous system (CNS)
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13
Q

list three ways in which a response to a hormone differs from a response to a nerve impulse [ 3 MARKS ]

A
  • hormone response is slow, wide-spread and long-lasting

- nervous response is rapid, localised and short-lived

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14
Q

define a nerve impulse

A
  • self propagating wave of electrical activity that travels along the axon membrane
  • temporary reversal of electrical potential difference
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15
Q

what is an action potential?

A
  • rapid changes in charge across the membrane that occur when a neuron is firing
  • occurs in three stages: depolarisation, repolarisation and refractory period
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16
Q

what does the resting potential mean?

A
  • the difference in electrical charge across neurone membrane while neurone is not stimulated (i.e. at rest)
  • (-50 to -90 mV, usually about -70 mV in
    humans) .
  • maintained through action of the sodium-potassium pump
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17
Q

name three processes schwann cells are involved in

A

● electrical insulation
● phagocytosis
● nerve regeneration

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18
Q

name three ways resting potential is maintained across the axon membrane (i.e. neuron is polarised)

A
  • phospholipid bilayer of axon plasma membrane prevents Na+ and K+ ions diffusing across
  • channel proteins (they have gates), some remain open so Na+ and K+ move freely through them by facilitated diffusion
  • sodium-potassium pump moves Na+ ions out of axon (and K+ in) creating an electrochemical gradient
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19
Q

what does it mean for a neuron to be polarised?

A
  • neuron not stimulated therefore its membrane is polarised
  • being polarised means that electrical charge on outside of membrane is positive while electrical charge on inside of membrane is negative (resting potential = 70mv)
  • therefore generates a potential difference
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20
Q

why is the resting potential of a neurone -70mV?

A
  • net movement of positive ions out of the cell making the inside of the cell negatively charged, relative to the outside
  • this charge is the resting potential of the cell and is about -70mV
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21
Q

Describe the action of the membrane in maintaining the resting potential of the neurone

A
    • Na+/K+ pumps move (3) Na+ ions out of the neurone but membrane isn’t permeable to Na+ so they can’t diffuse back in
  • creates Na+ electrochemical gradient because more positive Na+ ions outside cell than inside
  • Na+/K+ pumps also move (2)K+ ions into the neurone down their electrochemical gradient but membrane is permeable to K+ so they diffuse back out through potassium ion channels by FD
  • which makes outside positively charged compared to inside (bc results in net loss of 1 +ve charge each time)
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22
Q

during the resting membrane potential there are:

A

more sodium ions (Na+) outside than inside the neuron

more potassium ions (K+) inside than outside the neuron

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23
Q

Explain how the resting potential of –70 mV is maintained in the sensory neurone when no pressure is applied (i.e. no action potential generated)

A
  1. Membrane more permeable to potassium ions and less permeable to sodium ions;
  2. Sodium ions actively transported/pumped out and potassium ions in;
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24
Q

Explain why K+ and Na+ can only pass through membrane through proteins.(2)

A
  • Cant pass through phospholipid bilayer

- As water soluble/ not lipid soluble/ CHARGED

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25
Q

why is there no net movement of K+ ions during the resting potential

A
  • bc they diffuse back out of membrane bc membrane is more permable to them (sodium channels blocked)
  • electrochemical gradient moves K+ back in bc repelled by +ve charges out of channel

(two electrochemical gradients counteract each other and there’s no net movement of K+)

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26
Q

Name the stages in generating an action potential.

A
  1. Depolarisation
  2. Repolarisation
  3. Hyperpolarisation
  4. Return to resting potential
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27
Q

What happens during depolarisation?

A
  1. energy from stimulus→ causes some Na voltage-gated channels in axon membrane to open and so Na+ ions diffuse down their electrochemical gradient through sodium channels into axon (If membrane reaches threshold potential (-50mV), voltage-gated Na+
    channels open)
  2. being positively charged, they trigger a reversal in p.d. across membrane [positive feedback]
  3. so as more Na+ ions diffuse into axon, more sodium channel open, causing even greater influx of Na+ ions by diffusion
  4. once A.P around +40mv established, sodium voltage gated channels close and voltage-gated potassium channels begin to open
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28
Q

what happens during repolarisation?

A 
1. Voltage-gated Na+ channels close and
voltage-gated K+ channels open.
2. Facilitated diffusion of K+ ions out of cell down their electrochemical gradient (starting repolarisation of axon)
3. p.d. across membrane becomes more
negative.
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29
Q

what happens during hyperpolarisation?

A
  1. temporary ‘Overshoot’ when K+ ions diffuse out = p.d. becomes more negative than usual resting potential (= hyperpolarisation)
  2. Refractory period: no stimulus is large enough to raise membrane potential to threshold (i.e. no A.P can be generated)
  3. Voltage-gated K+ channels close &
    sodium-potassium pump re-establishes resting potential.
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30
Q

why are the terms resting and action potential misleading?

A
  • action potential involves movement of Na+ inwards due to diffusion - which is passive
  • resting potential is maintained by active transport, which is an active process.
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31
Q

Explain the importance of the 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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32
Q

what are the two types of gradients acting on K+ ions during resting potential, and which is stronger?

A

electrical gradient → Pull K+ into cell
conc gradient → Pulls K+ out of cell

conc. gradient has stronger effect and so even more K+ ions leave the cell (so more +ve charge has left cell, resting potential of neurone decreases further)

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33
Q

What do diseases such as Multiple Sclerosis (MS) cause?

A
  • myelin acts as an insulator that prevents current from leaving the axon, increasing the speed of action potential conduction
  • diseases like MS cause degeneration of myelin, which slows action potential conduction because axon areas are no longer insulated so the current leaks.
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34
Q

what is saltatory conduction?

A
  • describes the way an electrical impulse skips from node to node down the full length of an axon (speeding the arrival of the impulse at nerve terminal in comparison with the slower continuous progression of depolarization spreading down an unmyelinated axon)
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35
Q

what’s a generator potential?

A
  • small depolarization that isn’t large enough to cause an action potential
  • A.P occurs when there are enough generator potentials and and so enough Na+ channels open, to cause significant depolarisation of the neurone.
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36
Q

when do voltage-gated sodium channels open?

A

at membrane potentials above -50mV

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37
Q

Draw and label the graph when an action potential is fired

A

Refer to nervous co-ordination notes or page 352 of textbook

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38
Q

describe the passage of an action potential along an umyelinated neurone

A
  1. when A.P happens, some of Na+ ions that enter neurone diffuse sideways
  2. causes Na+ ion channels in adjacent resting region of neurone to open and Na+ ions diffuse through that part
  3. causes wave of depolarisation to travel along neurone (bc Na+ ions trigger change in P.D stimulating another A.P)
  4. wave moves away from parts of membrane in refractory period b/c these parts can’t fire A.P
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39
Q

where are sodium ions channels concentrated on a myelinated neurone?

A
  • concentrated at the nodes (of ranvier)
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40
Q

where does depolarisation occur on myelinated neurones?

A
  • only at nodes of ranvier (where sodium ions can get through membrane)
41
Q

Explain why myelinated axons conduct impulses faster than unmyelinated axons

A
  • Saltatory conduction: Impulse ‘jumps’ from one node of Ranvier to another. (Cytoplasm can conduct an electrical impulse from one node of ranvier to the next.) Depolarisation cannot occur where myelin sheath acts as electrical insulator.
  • So impulse does not travel along whole axon length (i.e. minimises length of axon that needs to depolarise in order for an A.P. to propagate which reduces energy used)
42
Q

Describe Saltatory conduction

A
  • during an A.P when Na+ ions rush into the neuron, intracellular environment at node becomes more +ve charged relative to the next node along axon
  • so +ve ions within the already-depolarised section of the axon are ‘pushed’ along their electrical gradient towards the more negative environment at the next node
  • arrival of +ve ions at this node depolarises this section of the axon as well, initiating another A.P, process is repeated, allowing the A.P. to propagate rapidly along the axon, effectively ‘jumping’ between nodes.

This ‘jumping’ mechanism is known as saltatory conduction.

43
Q

what does myelin sheath prevent?

A

flow of current

44
Q

how does myelinated neurones promote energy efficiency?

A
  • b/c amount of Na+ and K+ ions that need to be pumped to bring the concentrations back to the resting state following each A.P is decreased
45
Q

describe how a local current is created

A
  • Na channels opening and allowing Na+ ions into cell (when A.P fired) creates localised disruption to balance created by Na+/K+ pump
  • creates local currents in cytoplasm of neurone
  • local currents stimulate Na+ channels further along membrane to open
46
Q

Describe the effect of myelination on the rate of conduction of an action potential and explain how this affect is achieved [5]

A

effect:
myelinated fibres conduct more quickly than unmyelinated

explanation: (allow max. 4 marks)
1. myelin sheath acts as (electrical) insulator
2. lack of Na and K gates in myelinated region;
3. depolarisation occurs at nodes of ranvier only;
4. (so) longer local circuits
5. (action potential) jumps from one node to another/ saltatory conduction

47
Q

describe which parts in passage of action potential along myelinated neurone is different to unmyelinated neruone

A
  • longer local circuits (in myelinated)
  • saltatory conduction (in myelinated)
  • fewer Na+ and K+ channels in myelinated
  • depolarisation can’t occur through myelin/impermeable to Na+ and K+ ions
  • ref. to insulating role of myelin/schwann cells
  • ref. to 1-3 micrometres distance between nodes of ranvier
48
Q

explain why ions can only be exchanged at nodes of ranvier

A
  • because remainder of axon covered by myelin sheath that prevents ions being exchanged
49
Q

describe what happens to size of an action potential as it moves along axon

A

remains the same

50
Q

“all or nothing” principle

A

If a stimulus is not big enough to reach threshold - an action potential will NOT occur.

Action potentials do not range is size; if a stimulus is very big, it will just mean action potentials occur more frequently down the neurone.

51
Q

state two ways an organism can perceive the size of a stimulus

A
  • number of impulses passing in given time (the larger the impulse, more generated in given time)
  • having different neurones w/ different threshold values (brain interprets no. and type of neuron that pass impulses as a result of stimulus and so determones size)
52
Q

factors affecting the speed at which an action potential travels

A
  • myelin sheath
  • diameter of axon
  • temperature
53
Q

how does myelin sheath affect speed at which action potential travels?

A
  • myelin is electrical insulator so prevents action potential forming there
  • so A.P jump from node of ranvier to another (saltatory conduction)
  • this increases speed of conductance (from 30m/s in umyelinated neurone to 90m/s in similar myelinated one)
54
Q

how does diameter of axon affect speed at which action potential travels?

A
  • greater diameter of axon = faster speed of conductance
  • due to less leakage of ions from larger membrane (leakage makes membrane potentials harder to maintain)
  • also less resistance to flow of ions than in cytoplam of smaller diameter (less resistance = depolarisation reaches parts of axon membrane quicker)
55
Q

how does temperature affect speed at which action potential travels?

A
  • higher temp = faster nerve impulse
  • higher temp increases rate of diffusion of ions
  • higher temp also increases rate of enzyme action (enzymes used in respiration to produce ATP, which are needed for Na+/K+ pump action)
  • speed only increases to around 40 degrees (C) bc proteins begin to denature (e.g. enzymes used in respiration which provides ATP for Na+/K+ pump, protein channels etc.) and speed decreases
56
Q

what occurs during the refractory period?

A
  • after A.P. created in any region of axon, there’s period afterwards where inward movement of Na+ ions is stopped bc Na voltage-gated channels are closed
  • during this time, it’s impossible for another action potential to be generated
    i. e. the refractory period
57
Q

how does refractory period ensure action potentials are propagated in one direction only?

A
  • A.P can only pass from active region to passive region
  • so they can only move in forward direction
  • prevents A.Ps spreading out in both directions
58
Q

how does refractory period ensure action potentials are produced discretely?

A
  • due to refractory period new A.P can’t be formed immediately behind first one
  • ensures A.Ps are separated from each other
59
Q

how does refractory period limit number of action potentials?

A
  • as A.Ps separated from each other this limit no. of A.P. that can pass along axon in given time (and so limits strength of stimulus that can be detected)
60
Q

Suggest an appropriate statistical test to
determine whether a factor has a
significant effect on the speed of
conductance.

A

Student’s t-test (comparing means of

continuous data)

61
Q

Suggest appropriate units for the
maximum frequency of impulse
conduction

A

Hz

62
Q

How can an organism detect the strength of a stimulus?

A

Larger stimulus raises membrane to
threshold potential more quickly after
hyperpolarisation = greater frequency of
impulses.

63
Q

what is a synapse?

A

a junction between a neurone and another neurone or between a neurone and an effector cell

64
Q

Describe the structure of a synapse

A

Presynaptic neuron ends in swollen knob called the synaptic knob: contains lots of mitochondria, endoplasmic reticulum and vesicles of neurotransmitter (synaptic vesicles).

synaptic cleft: 20-30 nm gap between neurons.

Postsynaptic neuron: has complementary receptors to neurotransmitter (ligand-gated Na+ channels).

65
Q

describe the presynaptic neurone (structure of a synapse)

A
  • neurone before the synapse
  • when A.P reaches end of neurone it’s transmitted across presynpatic membrane to postsynaptic membrane or effector cell e.g. muscle or gland cell
66
Q

describe the synaptic knob (structure of a synapse)

A
  • swelling at end of axon of presynaptic neurone
  • contains synpatic vesicles
  • contains lots of mitochondria (and ER) bc lots of energy needed to synthesise neurotransmitters
67
Q

describe the synaptic vesicles (structure of a synapse)

A
  • vesicles in synaptic knob
  • vesicles contain neurotransmitters
  • vesicles fuse w/ presynaptic membrane to release neurotransmitters into synaptic cleft
68
Q

describe neurotransmitters (structure of a synapse)

A
  • chemicals that allow action potential to be transferred across synapse
  • when neurotransmitters released from synaptic vesicles into synaptic cleft, they bind to specific receptors on postsynaptic membrane
69
Q

describe postsynaptic membrane (structure of a synapse)

A
  • membrane of postsynaptic neurone/effector cells
  • receptors on postsynaptic membrane have complementary shape to neurotransmitters released from synaptic knob
  • when neurotransmitters bind to their receptors, A.P. continues; this ensures nerve impulse is unidirectional
70
Q

how does a neuromuscular junction differ from a synapse?

A
  • NMJ is a type of synapse

- however it’s the synaptic connection between the terminal end of a motor nerve and a muscle

71
Q

state two differences between a synapse and neuromuscular junction

A
  • NMJ have more receptors on the postsynaptic membrane than other synapses.
  • When a motor neurone fires an A,P, it always triggers a response in the muscle cell.
72
Q

explain why synaptic transmission is unidirectional

A
  • only presynaptic neuron contains vesicles of neurotransmitter & only postsynaptic membrane has complementary receptors
  • so impulse always travels presynaptic →
    postsynaptic.
73
Q

how do neurotransmitters cross the synaptic cleft?

A

via simple diffusion

74
Q

Define summation and name the 2 types.

A

Neurotransmitter from several sub-threshold impulses accumulates to generate action potential:
● temporal summation
● spatial summation
NB no summation at neuromuscular junctions.

75
Q

What is the difference between temporal

and spatial summation?

A

Temporal: one presynaptic neuron releases neurotransmitter several times in quick succession.
Spatial: multiple presynaptic neurons release neurotransmitter

76
Q

what occurs during spatial summation?

A
  • takes place when multiple presynaptic neurones form junction with single neurone
  • each presynaptic neurone releases neurotransmitters so there are many neurotransmitters that bind to receptors on 1 postsynaptic membrane
  • together neurotransmitters can establish generator potential that reaches the threshold value and an A.P. is generated
77
Q

what occurs during temporal summation?

A
  • two or more nerve impulses arrive in quick succession from same presynaptic neurone
  • makes A.P more likely bc more neurotransmitter released into synaptic cleft
  • new A.P is more likely to be triggered
78
Q

low frequency action potential often leads to what?

A
  • release of insufficient concentrations of neurotransmitter to trigger new A.P

(so summation helps with this - temporal or spatial)

79
Q

what do excitatory neurotransmitters do?

A
  • depolarises postsynaptic membrane, making it fire an action potential if threshold is reached
80
Q

give example of excitatory neurotransmitter

A
  • acetylcholine is excitatory neurotransmitter at cholingeric synapses in CNS
  • it binds to cholingeric receptors to cause A.Ps in postsynaptic membrane (and at NMJ)
81
Q

what do inhibitory neurotransmitters do?

A
  • hyperpolarise postsynaptic membrane (more negative), preventing it from firing an a.p.
82
Q

give example of inhibitory neurotransmitters

A
  • acetylcholine is an inhibitory neurotransmitter at cholinergic synapses in heart
  • when it binds to receptors at heart, it can cause K+ channels to open on postsynaptic membrane, hyperpolarising
83
Q

what are cholinergic synapses?

A
  • synapses that use acetylcholine as primary neurotransmitter.
    Excitatory or inhibitory
84
Q

What happens in an inhibitory synapse?

A
  1. Neurotransmitter binds to and opens Cl- channels on postsynaptic membrane & triggers K+ channels to open.
  2. Cl- moves in & K+ moves out via facilitated diffusion.
  3. p.d. becomes more negative: hyperpolarisation (makes it less likely that a new A.P. will be created bc larger influx of Na+ ions needed to produce one)
85
Q

What happens to the neurotransmitter once they have attached to the receptors on the post synaptic membrane?

A

They are broken down by enzymes and their products are taken back into the neurone

86
Q

ATP is an energy source used in many cell processes. Give two ways in which ATP is a suitable energy source for cells to use.

A
  1. Releases relatively small amount of energy / little energy lost as heat;
  2. Releases energy instantaneously;
  3. Phosphorylates other compounds, making them more reactive;
  4. Can be rapidly re-synthesised;
  5. Is not lost from / does not leave cells.
87
Q

explain how a presynaptic neurone is adapted for the manafacture of neurotransmitter

A
  • possesses many mitochondria and large amounts of endoplasmic reticulum
88
Q

outline the events in transmission of information from one neurone to another across a synapse

A
  • action potential reaches synaptic knob
  • vesicles fuse to presynaptic membrane and are then released into synaptic cleft
  • neurotransmitters diffuses across synapse to receptor molecules on postsynaptic neurone where it binds
  • this sets up a new A.P
89
Q

explain why hyperpolarisation reduces likelihood of a new action potential being created

A
  • inside of membrane more negative than at resting potential
  • greater influx of Na+ needed to reach threshold potential
  • more difficult for depolarisation to occur and so action potential less likely to be fired
90
Q

Outline what happens in the presynaptic neuron when an action potential is transmitted from one neuron to another (cholinergic synapse)

A
  1. Wave of depolarisation (A.P.) travels down presynaptic neurone, causing voltage-gated Ca2+ channels to open, Ca2+ ions enter synaptic knob by facilitated diffusion
  2. Vesicles move towards & fuse with presynaptic membrane.
  3. Exocytosis of neurotransmitter into synaptic cleft (i.e. acetylcholine released into synaptic cleft)
91
Q

Outline what happens in the postsynaptic neuron when an action potential is transmitted from one neuron to another (cholinergic synapse)

A
  • depolarisation of presynaptic membrane
  • Ca2+ channels opened and Ca2+ ions enter synaptic knob
  • Ca2+ cause synaptic vesicles to fuse with presynaptic membrane and release acetylcholine
  • acetylcholine dffuses across synaptic cleft
  • acteylcholine attaches to receptors on post synaptic membrane
  • Na+ ions enter postsynaptic neruone leading to depolarisation

note: acetylcholine broken down by enzymes and reabsorbed by presynaptic neurone (Na+ protein channels close in absence of acetylcholine in receptor sites)

92
Q

Why is ACh (acetylcholine) removed from synaptic cleft?

A
  • removed so response doesn’t continue to happen (ensures discrete responses)
93
Q

What happens to acetylcholine from the synaptic cleft?

A
  1. Hydrolysis into acetyl and choline by
    acetylcholinesterase (AChE).
  2. Acetyl & choline diffuse back into presynaptic membrane.
  3. ATP is used to reform acetylcholine for storage in vesicles.
94
Q

Explain the importance of AChE (acetylcholinesterase)

A

● Prevents overstimulation of skeletal
muscle cells.
● Enables acetyl and choline to be
recycled.

95
Q

Describe the structure of a

neuromuscular junction.

A

Synaptic cleft between a presynaptic
neuron and a skeletal muscle cell.
- postsynaptic membrane also called motor end plate

96
Q

Contrast a cholinergic synapse and a

neuromuscular junction

A

DIfference:
1 postsynaptic cell: another neuron (cholinergic), skeletal muscle cell (neuromuscular)
2 AChE location: synaptic cleft (cholinergic), postsynaptic membrane (neuromuscular)
3 Action potential: new a.p. produced (cholinergic), end of neural pathway (neuromuscular)
4 Response: Excitatory or inhibitory (cholinergic), always excitatory (neuromuscular)
5 Neurons involved: motor, sensory or relay (cholinergic), only motor (neuromuscular)

(remember PAARN - people are always really negative)

97
Q

How might drugs increase synaptic transmission?

A

● Inhibit AChE (so more neurotransmitter in synaptic cleft to bind to receptors i.e. theyre there for longer)
● Mimic shape of neurotransmitter (so mimic their action and bind to receptors on postsynaptic membrane - drugs called agonists)

98
Q

How might drugs decrease synaptic transmission?

A

● Inhibit release of neurotransmitter (so fewer receptors activated)
● Decrease permeability of postsynaptic
membrane to ions.
● Hyperpolarise postsynaptic
membrane.
● block receptors so they can’t be activated by neurotransmitter (drugs called antagonists)

99
Q

list the similarities between a synapse and neuromuscular junction

A
  • have neurotransmitters transported by diffusion
  • have receptors, that on binding with neurotransmitter, cause influx of Na+ ions
  • use a Na-K pump to repolarise axon
  • use enzymes to breakdown neurotransmitter

A2 Biology (13 decks)

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