Resting Potential, Depolarisation, Saltatory Conduction & Cholinergic Synapses

1

Resting Potential (-70 mV) Maintenance

When a neurone is not transmitting an impulse, the inside of the axon membrane is negatively charged (-70 mV) relative to the outside: 1. The sodium-potassium pump actively transports 3 Na⁺ ions out of the axon for every 2 K⁺ ions pumped in, using ATP hydrolysis. 2. Voltage-gated Na⁺ and K⁺ channels are closed, but the resting membrane contains more open potassium leak channels than sodium leak channels, so K⁺ diffuses back out down its concentration gradient faster than Na⁺ can diffuse in, establishing an electrochemical gradient.

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2

Depolarisation (+40 mV) & All-or-Nothing Principle

1. A stimulus causes a few Na⁺ channels to open; Na⁺ diffuses into the axon down its electrochemical gradient, making the inside less negative. 2. If the potential reaches the threshold potential (-55 mV), voltage-gated Na⁺ channels open rapidly (positive feedback), causing a massive influx of Na⁺ ions that reverses the membrane potential to +40 mV (depolarisation). 3. All-or-Nothing Law: below threshold, no action potential is generated; above threshold, action potentials always peak at the same amplitude (+40 mV), with stronger stimuli encoded by a higher frequency of action potentials.

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3

Repolarisation, Hyperpolarisation & The Refractory Period

At +40 mV, voltage-gated Na⁺ channels close and voltage-gated K⁺ channels open. K⁺ ions diffuse rapidly out of the axon down their electrochemical gradient, restoring the negative internal potential (repolarisation). Because voltage-gated K⁺ channels close slowly, excess K⁺ diffuses out, causing a brief overshoot past -70 mV to ~-80 mV (hyperpolarisation), before the Na⁺/K⁺ pump restores the resting potential. During the refractory period, Na⁺ channels cannot be reopened, which: 1. Ensures unidirectional impulse propagation, 2. Produces discrete (separate) impulses, and 3. Limits the maximum frequency of action potentials.

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4

Myelination, Saltatory Conduction & Factors Affecting Speed

Three factors increase conduction velocity: 1. Myelination: Schwann cells wrap around the axon to form an electrical insulator (lipid myelin sheath) impermeable to Na⁺/K⁺; voltage-gated ion channels are concentrated only at unmyelinated gaps (Nodes of Ranvier, 1-3 mm apart), so local currents jump from node to node (saltatory conduction), which is much faster and saves ATP. 2. Wider axon diameter: reduces internal cytoplasmic resistance to ion flow and decreases surface area-to-volume leakage. 3. Higher temperature (up to ~40°C): increases kinetic energy and rate of ion diffusion (and ATP generation), before membrane proteins denature.

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5

Cholinergic Synaptic Transmission

1. Action potential arrives at the presynaptic knob, depolarising the membrane and opening voltage-gated Ca²⁺ channels; Ca²⁺ ions diffuse into the presynaptic knob down their concentration gradient. 2. Influx of Ca²⁺ causes synaptic vesicles containing acetylcholine (ACh) to move to and fuse with the presynaptic membrane, releasing ACh into the synaptic cleft by exocytosis. 3. ACh diffuses across the cleft and binds to complementary receptor sites on ligand-gated Na⁺ channels on the postsynaptic membrane. 4. Na⁺ channels open and Na⁺ diffuses into the postsynaptic neurone, generating an excitatory postsynaptic potential (EPSP) that triggers an action potential if threshold is reached. 5. Acetylcholinesterase (AChE) hydrolyses ACh into choline and ethanoic acid (acetyl), which diffuse back into the presynaptic knob and are resynthesised into ACh using ATP from mitochondria.

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6

Unidirectionality, Summation & Inhibitory Synapses

Synapses are unidirectional because neurotransmitter vesicles only exist in the presynaptic knob and receptors only exist on the postsynaptic membrane. Spatial summation: multiple different presynaptic neurones release small amounts of neurotransmitter simultaneously onto one postsynaptic neurone to exceed threshold. Temporal summation: a single presynaptic neurone fires high-frequency action potentials in quick succession so neurotransmitter builds up to exceed threshold. Inhibitory synapses release neurotransmitters (e.g. GABA) that open Cl⁻ (influx) and K⁺ (efflux) channels on the postsynaptic membrane, hyperpolarising it (e.g. to -85 mV) so an action potential is less likely.

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1. Q1

   Describe how an action potential is generated at a point on an axon membrane and how the resting potential is subsequently restored at that point. (6 marks)

   Check Mark Scheme

   Click “Check Mark Scheme” to compare your answer, 1. When a stimulus depolarises the axon membrane to the threshold potential (-55 mV), voltage-gated sodium ion (Na⁺) channels open rapidly [1 mark]. 2. Na⁺ ions diffuse rapidly into the axon down their electrochemical gradient, reversing the membrane potential from -70 mV to +40 mV (depolarisation) [1 mark]. 3. At +40 mV, voltage-gated Na⁺ channels close and voltage-gated potassium ion (K⁺) channels open [1 mark]. 4. K⁺ ions diffuse out of the axon down their concentration and electrical gradient, returning the inside of the membrane to a negative potential (repolarisation) [1 mark]. 5. Because voltage-gated K⁺ channels are slow to close, too many K⁺ ions diffuse out, temporarily lowering the potential below -70 mV (hyperpolarisation) before K⁺ channels close [1 mark]. 6. The sodium-potassium pump actively transports 3 Na⁺ out and 2 K⁺ in (using ATP) to restore the ionic distribution of the resting potential (-70 mV) [1 mark].

2. Q2

   Multiple sclerosis (MS) is an autoimmune disease in which T-lymphocytes destroy the myelin sheath surrounding motor neurones. Explain how destruction of the myelin sheath slows down or blocks impulse transmission to skeletal muscles. (4 marks)

   Check Mark Scheme

   Click “Check Mark Scheme” to compare your answer, 1. In a healthy neurone, the lipid myelin sheath acts as an electrical insulator preventing Na⁺ and K⁺ ions from crossing the membrane except at the Nodes of Ranvier [1 mark]. 2. This forces local currents to jump from node to node in saltatory conduction, which is very rapid [1 mark]. 3. When the myelin sheath is destroyed, ions leak across the exposed axon membrane, dissipating the local electrical currents so they may fail to reach the threshold potential (-55 mV) at the next Node of Ranvier [1 mark]. 4. Also, the internodal membrane has very few voltage-gated Na⁺ channels, so continuous wave-like depolarisation along the unmyelinated region is slow or impossible [1 mark].

3. Q3

   Describe the sequence of events by which the arrival of an action potential at a presynaptic knob results in the generation of an action potential in a postsynaptic neurone at a cholinergic synapse. (5 marks)

   Check Mark Scheme

   Click “Check Mark Scheme” to compare your answer, 1. The arrival of an action potential depolarises the presynaptic membrane, causing voltage-gated calcium ion (Ca²⁺) channels to open so Ca²⁺ ions diffuse into the presynaptic knob down their concentration gradient [1 mark]. 2. The influx of Ca²⁺ causes synaptic vesicles containing acetylcholine (ACh) to move toward and fuse with the presynaptic membrane, releasing ACh into the synaptic cleft by exocytosis [1 mark]. 3. ACh diffuses across the narrow synaptic cleft and binds to complementary receptor sites on ligand-gated sodium ion (Na⁺) channels in the postsynaptic membrane [1 mark]. 4. This causes the Na⁺ channels to open and Na⁺ ions diffuse rapidly into the postsynaptic neurone down their concentration gradient [1 mark]. 5. The influx of Na⁺ depolarises the postsynaptic membrane (creating an EPSP); if this depolarisation reaches the threshold potential (-55 mV), voltage-gated Na⁺ channels open and an action potential is generated [1 mark].

4. Q4

   Explain how a drug with a molecular shape similar to acetylcholine can either stimulate or inhibit synaptic transmission, and explain how an inhibitory neurotransmitter such as GABA prevents an action potential in a postsynaptic neurone. (4 marks)

   Check Mark Scheme

   Click “Check Mark Scheme” to compare your answer, 1. An agonist drug with a complementary shape binds to ACh receptors on postsynaptic Na⁺ channels and causes them to open, mimicking ACh to trigger Na⁺ influx and depolarisation [1 mark]. 2. A competitive antagonist drug (like curare) binds to the ACh receptor site without opening the Na⁺ channel, blocking ACh from binding and preventing depolarisation [1 mark]. 3. An inhibitory neurotransmitter (GABA) binds to specific receptors on the postsynaptic membrane that open chloride ion (Cl⁻) channels and potassium ion (K⁺) channels [1 mark]. 4. Cl⁻ ions diffuse in and K⁺ ions diffuse out, making the inside of the postsynaptic membrane even more negative than resting potential (hyperpolarisation, e.g. -85 mV), so a much larger Na⁺ influx is required to reach the -55 mV threshold [1 mark].

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