Starter Questions 1.Following a stimulus, explain how the opening of sodium ion channels affects the potential difference across a neurone cell membrane. 2.Describe and explain the movement of sodium ions if the potential difference across a neurone cell membrane reaches the threshold level. 3.Describe the structure of a militated neurone.

Answers 1.Sodium ions diffuse into the neurone down the sodium ion electrochemical gradient. This makes the inside of the neurone less negative and so decreases the potential difference across the membrane. 2.More sodium ions diffuse into the neurone because more sodium ion channels open. 3.A myelinated neurone has a myelin sheath. The myelin sheath is made of a type of cell called a schwann cell. Between the schwann cells are tiny patches of bare membrane called the nodes of ranvier. Sodium ion channels are concentrated at the nodes of ranvier.

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Synapses are gaps between neurones Information is sent between neurones by chemical transmission Neurotransmitters pass across the synaptic cleft A new action potential will be triggered in the post synaptic neurone

The synapse Where two neurones meet, there is a gap, usually about 20nm wide. This is the synaptic cleft The end of the neurone immediately before the synaptic cleft, ends in a presynaptic bulb. After the synaptic cleft is the postsynaptic bulb, i.e. the start of the next neurone Together they make up the synapse

Structure of the synapse

Neurotransmitters There are more than 40 different neurotransmitter substances. Noradrenalin and acetylecholine (ACh) are found throughout the nervous system Dopamine and glutamate are found only in the brain. Synapses releasing achetylcholine and known as cholinergic synapses

Postsynaptic Neurone Presynaptic Neurone Synaptic Cleft Synaptic Knob Calcium ion channel Sodium ion channels Membrane of postsynaptic neurone Synaptic vesicle containing neurotransmitter Smooth Endoplasmic Reticulum Mitochondrion Incoming Action Potential

Incoming Action Potential New action Potential Neurotransmitter

The incoming action potential causes depolarisation in the synaptic knob This causes calcium channels to open Calcium ions (Ca 2+ ) flood into the synaptic knob

Incoming Action Potential Ca 2+

The influx of calcium ions causes synaptic vesicles to fuse with the presynaptic membrane This releases neurotransmitter in to the cleft  So calcium ions cause the release of neurotransmitter

Incoming Action Potential Ca 2+

Neurotransmitter (acetylcholine) is released into the synaptic cleft. Acetylcholine binds to the receptor site on the sodium ion channels. Sodium ion channels open

Ca 2+ Neurotransmitter (acetlycholine) is released into the synaptic cleft. Acetlycholine binds to the receptor site on the sodium ion channels.

The sodium channels on the postsynaptic membrane are normally closed. When the neurotransmitter binds there is a conformational change opening the channel. This allows sodium ions to flood in and causes depolarisation. Neurotransmitter binds and opens the channel. Na +

Sodium ions diffuse into the postsynaptic neurone Depolarised Empty Synaptic Vesicles

Neurotransmitter (acetylcholine) is released into the synaptic cleft. Acetylcholine binds to the receptor site on the sodium ion channels. Sodium ion channels open Sodium ions diffuse in (down steep concentration gradient) Postsynaptic neurone depolarises

Depolarisation inside the postsynaptic neurone must be above a threshold value If the threshold is reached a new action potential is sent along the axon of the post synaptic neurone

Incoming Action Potential New action Potential Neurotransmitter

When do the calcium channels open and close? Why are the calcium ions important? What is the name of the neurotransmitter? Explain how the neurotransmitter causes a new action potential to be generated.

Step 1 Calcium channels open Step 2 Neurotransmitter release Step 3 Sodium Channels Step 4 New action potential Step 5 Acetylcholinesterase Step 6 Remaking acetylcholine

A hydrolytic enzyme Breaks up acetylcholine (the neurotransmitter) into acetyl (ethanoic acid) and choline.

Acetylcholinesterase is an enzyme that hydrolyses acetylcholine in to separate acetyl (ethanoic acid) and choline. Sodium ion channels close. The two bits diffuse back across the cleft into the presynaptic neurone. This allows the neurotransmitter to be recycled.

Acetylcholine binds and opens Sodium channels Acetylcholinesterase breaks up acetylcholine. Sodium channels close Depolarised

If the neurotransmitter is not broken down this could allow it to continuously generate new action potentials Breaking down acetylcholine prevents this

Name the hydrolytic enzyme and the products of the reaction. Why must the neurotransmitter be broken down? What happens to the remnants of the neurotransmitter?

ATP released by mitochondria is used to recombine acetyl (ethanoic acid) and choline thus recycling the acetylcholine. This is stored in synaptic vesicles for future use. More acetylcholine can be made at the SER. Sodium ion channels close in the absence of acetylcholine at their receptor sites. The synapse is now ready to be used again.

The Whole Process

Incoming Action Potential Ca 2+

A neuromuscular junction is a specialised cholinergic between a motor neurone and a muscle cell. Neuromuscular junctions use the neurotransmitter acetylcholine (Ach), which binds to cholinergic receptors called nicotinic cholinergic receptors.

Very similar to Cholinergic synapses with a few differences Postsynaptic membrane has lots of folds that form clefts. These clefts store the enzyme that breaks down Ach (acetylcholinesterase) Postsynaptic membrane has more receptors than other synapses Motor neurone fires an action potential, it always triggers a response in a muscle cell. This isn't always the case for a synapse between two neurones.

Excitable neurotransmitters depolarise the postsynaptic membrane. E.g.Acetylcholine. Inhibitory neurotransmitters e.g. GABA is an inhibitory neurotransmitter, when it binds to its receptors it causes potassium ion channels to open on the postsynaptic membrane, hyperpolarising the neurone.

Low frequency action potentials often release insufficient amounts of neurotransmitter to exceed the threshold in the postsynaptic neurone Summation allows action potentials to be generated This enables a build up of neurotransmitter in the synapse

A number of different presynaptic neurones share the same synaptic cleft Together they can release enough neurotransmitter to create an action potential Multiple neurones

Threshold reached action potential can be sent

A single presynaptic neurone releases neurotransmitter many times over a short period If the total amount of neurotransmitter exceeds the threshold value an action potential is sent 1 neurone

Low frequency action potentials

High frequency action potentials

What is summation? What is the main difference between temporal summation and spatial summation? Explain how temporal summation allows the postsynaptic membrane to reach the threshold value. Suggest an advantage of responding to high-level stimuli but not low-level ones.

There are chloride ion channels on the postsynaptic membrane If these are made to open chloride ions (Cl - ) flood into the postsynaptic neurone This hyperpolarises the neurone This make it harder to achieve a action potential

Chloride ion (Cl - )channel on the postsynaptic membrane Neurotransmitter that opens calcium channels

Chloride ions diffuse into the postsynaptic neurone Hyperpolarised

Inhibitory and excitatory neurones will work antagonistically at the same synapse Summation will occur

1.(a)(i)AThree marks for three of: Negatively charged proteins / large anions inside axon; Membrane more permeable to potassium ions than to sodium ions; Potassium ions diffuse* out faster than sodium ions diffuse in; Sodium / potassium pump; Sodium ions pumped* out faster than potassium ions pumped in / 3 for 2; [3 max] * mechanism is necessary for mark

BSodium ion gates open / membrane more permeable to sodium ions / sodium ions rush in;[1] (ii)Two marks for two of: Membrane impermeable to sodium ions / sodium ion channels closed; Sodium ions cannot enter axon; Membrane becomes more negative than resting potential;[2 max] (b)(i)Two marks for two of: Unique shape of receptor protein / binding site; reject ‘active site’ Due to (tertiary) structure of protein molecule; Concept of complementary shape / ref. to neurotransmitter ‘fitting’;[2 max] (ii)Cause vesicles to move to presynaptic membrane / fuse with membrane;[1]

(c)(i)Two marks for two of: Impulses / action potentials from neurones A and B together /spatial summation; Cause sufficient depolarisation / open sufficient sodium ion channels; For threshold to be reached;[2 max] (ii)Two marks for two of: Impulses from A and B independent / no summation; Threshold not reached; Insufficient sodium ion channels opened;[2 max] (iii)Inhibitory; More IPSPs than EPSPs / reduces membrane potential / makes more negative (allow hyperpolarisation) / cancels effect of action potential from A;[2 max]

2.(a)Initially membrane impermeable to Na+; Sodium channels open; allowing Na+ into axon; reverses potential difference across membrane/ charge on either side/depolarised; membrane becomes more permeable to K+ ions/K+ leave the axon;[max. 4]

(b)(i)All action potentials are the same size; threshold value for action potential to occur [2] (ii)frequency of action potentials[1] (c)several (sub-threshold) impulses add to produce an action potential[1]

Drugs at Synapses Drugs can affect the synaptic transmission. They can do this by various ways. E.g. Some drugs are the same shape of neurotransmitters so they mimic their action at receptors (Agonists) Example: Nicotine mimics acetylcholine so binds to nicotinic cholinergic receptors in the brain.