Nervous coordination

Question 1

Structure of a myelinated motor neurones

Answer 1

Dendrites

Nodes of Ranvier

Nucleus

Cell body

Myelin sheath made of Schwann cells

Axon

Question 2

The establishment of a resting potential

Answer 2

The sodium-potassium ion pump actively transports 3 sodium ions out of axon and 2 potassium ions into axon

An electrochemical (concentration) gradient is created e.g. higher concentration of potassium ions inside axon than outside or higher concentration of sodium ions outside axon than inside

Membrane more permeable to potassium ions (open K+ channels) than sodium ions (closed Na+ channels)

Potassium ions move out of axon by facilitated diffusion

The inside of axon negatively charged relative to outside; axon is polarised = resting potential

Question 3

Changes in membrane permeability lead to depolarisation and the generation of an action potential. The all-or-nothing principle.

(Stimulus)

Answer 3

Excites the neurone cell membrane

Membrane more permeable to sodium ions as sodium ion channels open

Sodium ions diffuse into neurone down the sodium ion electrochemical gradient

Makes the inside of the neurone less negative

Question 4

Changes in membrane permeability lead to depolarisation and the generation of an action potential. The all-or-nothing principle.

(Depolarisation)

Answer 4

If potential difference reaches threshold, action potential generated because more voltage-gated sodium ion channels open

More sodium ions diffuse rapidly into neurones

Question 5

Changes in membrane permeability lead to depolarisation and the generation of an action potential. The all-or-nothing principle.

(Repolarisation)

Answer 5

Sodium ion channels close (membrane less permeable to sodium ions) whilst (voltage-gated) potassium ion channels open so potassium ions diffuse out of neurone down the potassium-ion concentration gradient

This starts to get the membrane back to its resting potential

Question 6

Changes in membrane permeability lead to depolarisation and the generation of an action potential. The all-or-nothing principle.

(Hyperpolarisation)

Answer 6

Potassium ion channels are too slow to close so there’s a slight overshoot – too many potassium ions diffuse out of neurone

The potential difference becomes more negative than the resting potential

Question 7

Changes in membrane permeability lead to depolarisation and the generation of an action potential. The all-or-nothing principle.

(Resting potential restored)

Answer 7

Resting potential is restored by the sodium-potassium pump

Ion channels reset

Maintained until the membrane is excited by another stimulus

Question 8

The nature and importance of the refractory period

Answer 8

Refractory period is the time to restore axon to resting potential/no further action potential can be generated (time delay)

Produces discrete and discontinuous impulses (action potentials don’t overlap)

Limits frequency of impulse transmission at a certain intensity (limits strength of stimulus that can be detected); higher intensity stimulus causes higher frequency of action potentials but only up to certain intensity

Unidirectional action potential – can’t be propagated in a region that is refractory (only travel in one direction)

Question 9

All or nothing nature of action potentials

Answer 9

Once threshold is reached, an action potential will always fire with the same change in voltage, no matter how big the stimulus is

If the threshold isn’t reached, an action potential wont fire (all or nothing)

A bigger stimulus won’t cause a bigger action potential but will cause them to fire more frequently

Question 10

Factors affecting the speed of conductance

(Myelination)

Answer 10

The myelin sheath is an electrical insulator present on some neurones

Depolarisation only occurs at Nodes of Ranvier in myelinated neurone

Saltatory conduction (which is faster) can occur (impulse jumps from node to node)

Impulse doesn’t travel whole axon/no need to depolarise along whole length of axon unlike non-myelinated neurone, where depolarisation happens along the whole length of the membrane

Question 11

Factors affecting the speed of conductance

(Axon diameter)

Answer 11

Bigger diameter means less leakage of ions/less resistance to flow of ions

So depolarisation reaches other parts of the neurone cell membrane quicker

Question 12

Factors affecting the speed of conductance

(Temperature)

Answer 12

Increases rate of movement of ions Na+ and K+ as more kinetic energy (active transport/diffusion)

Higher rate of respiration (enzyme activity faster) so ATP produced faster and energy released faster, so active transport also occurs faster

But proteins could denature past a certain temperature and speed will decrease

Question 13

The passage of an action potential along a non-myelinated axon, resulting in nerve impulses

Answer 13

Action potential moves along the neurone as a wave of depolarisation

Influx of sodium ions in one region increases permeability of adjoining region to sodium ions by causing voltage-gated sodium ion channels to open so adjoining region depolarises

Question 14

The passage of an action potential along a myelinated axon, resulting in nerve impulses

Answer 14

Depolarisation of axon at nodes of Ranvier only

Resulting in saltatory conduction

So there is no need for depolarisation along whole length of axon

Question 15

What is synapse

Structure

Answer 15

Synapse is the junction between a neurone and another neurone or between a neurone and an effector cell e.g. a muscle or gland cell

The gap between the cells at a synapse is called the synaptic cleft

Presynaptic neurone has a swelling called a synaptic knob which contains synaptic vesicles filled with chemicals called neurotransmitters

When action potential reaches end of a neurone, neurotransmitters are released into the synaptic cleft and diffuse across to the postsynaptic membrane, binding to specific receptors (which might trigger an action potential, causing muscle contraction or hormone secretion)

Question 16

Transmission across a cholinergic synapse

Answer 16

1. Action potential arrives at the synaptic knob of a pre-synaptic neurone causing calcium ion channels to open and calcium ions diffuse into pre-synaptic neurone
2. This causes the synaptic vesicles containing neurotransmitter/ acetylcholine (which is made only in the presynaptic neurone) to fuse with pre-synaptic membrane, releasing acetylcholine into synaptic cleft (exocytosis)
3. Neurotransmitters diffuse across synaptic cleft and bind to specific cholinergic receptors found only on post-synaptic membrane
4. This causes sodium ion channels in the post-synaptic neurone to open and sodium ions diffuse into post-synaptic knob, causing depolarisation which initiates action potential (excitatory synapse)
5. Neurotransmitter removed from synaptic cleft so response doesn’t keep happening. It is broken down by an enzyme called acetylcholinesterase (AChE) and the products are reabsorbed by the presynaptic neurone and used to make more acetylcholine

Question 17

Neuromuscular junctions

Answer 17

A neuromuscular junction is a synapse between a motor neurone and a muscle cell

Neuromuscular junctions use the neurotransmitter acetylcholine (ACh), which binds to cholinergic receptors called nicotinic cholinergic receptors

Question 18

Comparison of transmission across cholinergic synapses and neuromuscular junctions

Answer 18

Cholinergic synapses go from neurone to neurone WHEREAS neuromuscular go from neurone to muscle

Neuromuscular junction: ACh is always excitatory and never inhibitory, so always triggers generator/action potential in a muscle cell

Neuromuscular junction: Post-synaptic membrane has more receptors than other synapses

Neuromuscular junction: Lots of folds on post-synaptic membrane which form clefts to store the enzyme (Acetylcholinerase/AChE) to break down neurotransmitter (Acetylcholine/Ach)

Question 19

Why synapses result in unidirectional nerve impulses

Answer 19

Neurotransmitter only made in/released from pre-synaptic neurone

Receptors only on post-synaptic membrane so impulses can only travel in one direction

Question 20

What is summation

Answer 20

Addition of a number of impulses converging on a single post-synaptic neurone

i.e. where the effect of neurotransmitter released from many neurones (or from one neurone that is stimulated a lot in a short period of time) is added together

Question 21

Spatial summation

Answer 21

Many pre-synaptic neurones share the same synaptic cleft/post-synaptic neurone i.e. many neurones connect to one neurone

Collectively release a sufficient amount of neurotransmitter to reach threshold in the postsynaptic neurone to trigger an action potential

If some neurones release an inhibitory neurotransmitter then the total effect of all the neurotransmitters might be no action potential

Question 22

Temporal summation

Answer 22

One pre-synaptic neurone releases neurotransmitter many times over a short period/in rapid succession

It is likely that there will be sufficient neurotransmitter released into the synaptic cleft to reach the threshold to trigger an action potential

Question 23

Excitatory neurotransmitters

Answer 23

Depolarise postsynaptic membrane, making it fire an action potential if threshold reached

e.g. acetylcholine is an excitatory neurotransmitter at cholinergic synapses in the CNS

It binds to cholinergic receptors to cause an action potential in the postsynaptic membrane and at neuromuscular junctions

Question 24

Inhibitory neurotransmitters

Answer 24

Hyperpolarise the postsynaptic membrane (make the potential difference more negative), preventing it from firing an action potential/inhibits transmission of nerve impulses by postsynaptic membranes

Can’t be depolarised and reduces the effect of sodium ions entering so much less likely to reach threshold

e.g. acetylcholine is an inhibitory neurotransmitter at cholinergic synapses in the heart, when it binds to receptors here, it can cause potassium ion channels to open on the postsynaptic membrane, hyperpolarising it

By having both excitatory and inhibitory neurones forming synapses with the same postsynaptic membrane, this gives control of whether post-synaptic membranes ‘fire’ or not, therefore ‘firing’ is not inevitable and stimulation can be overridden

Question 25

Effects of specific drugs on a synapse
(shape)

Answer 25

Some drugs are the same shape as neurotransmitters so they mimic their action at receptors (agonists)

This means more receptors are activated

e.g. nicotine mimics acetylcholine so binds to nicotinic cholinergic receptors in the brain

Question 26

Effects of specific drugs on a synapse
(block receptors)

Answer 26

Some drugs block receptors so they cant be activated by neurotransmitters (antagonists)

This means fewer receptors can be activated

e.g. curare blocks the effects of acetylcholine by blocking nicotinic cholinergic receptors at neuromuscular joints, so muscle cells cant be stimulated, leading to paralysis

Question 27

Effects of specific drugs on a synapse
(inhibit enzyme)

Answer 27

Some drugs inhibit the enzyme that breaks down neurotransmitters

More neurotransmitters in the synaptic cleft to bind to receptors and they are there for longer

e.g. nerve gases stop acetylcholine from being broken down in the synaptic cleft, leading to loss of muscle control

Question 28

Effects of specific drugs on a synapse
(stimulate)

Answer 28

Some drugs stimulate the release of neurotransmitter from the presynaptic neurone so more receptors are activated e.g. amphetamines

Question 29

Effects of specific drugs on a synapse
(inhibit neurotransmitter)

Answer 29

Some drugs inhibit the release of neurotransmitters from the presynaptic neurone so fewer receptors activated e.g. alcohol