C2.2 Neural signalling

A neuron is a specialized cell of the nervous system that conducts electrical impulses along elongated nerve fibres.

The cell body contains cytoplasm and the nucleus. Multiple shorter dendrites usually conduct impulses toward the cell body, while one long axon conducts impulses away toward other neurons or effector cells.

Identify the nucleus and cytoplasm in the cell body, then distinguish the long single axon from the multiple shorter dendrites. Fibre length and branching vary with neuron function.

A motor neuron's long axon can carry an impulse from the central nervous system to a distant muscle, while its dendrites receive inputs from other neurons.

An axon and dendrites are cellular projections, not separate cells. Neuron shape varies, so use fibre number, length and direction of impulse rather than assuming every drawing has the same layout.

The resting potential is the negative voltage across a resting neuron's polarized plasma membrane, maintained by sodium and potassium ion gradients.

ATP supplies energy to the sodium–potassium pump, which moves Na⁺ out and K⁺ in opposite directions against their gradients. The membrane is more permeable to K⁺ at rest, so more positive charge diffuses out than enters and the inside remains negative relative to outside.

ATP-driven pumping establishes and maintains high Na⁺ outside and high K⁺ inside; selective leak channels create unequal ion movement; separated charge produces membrane polarization and a measurable membrane potential.

If ATP production stops, the pump can no longer maintain the gradients. Existing gradients may persist briefly, but continued leakage gradually erodes the negative resting potential.

The pump maintains the gradients over time; it does not directly create each action potential. A concentration gradient and a voltage gradient both influence ion movement.

An action potential is a brief, threshold-triggered reversal of membrane potential that propagates along an axon.

Voltage-gated sodium channels open rapidly during depolarization, then inactivate while potassium channels open to repolarize the membrane. Refractory periods prevent immediate re-firing in the same segment. The threshold is a condition, not a fixed promise: if it is not reached, the full action potential does not start.

Trace the phases:

• threshold
• Na⁺ influx and depolarization
• K⁺ efflux and repolarization
• hyperpolarization and recovery

A stimulus below threshold produces no full impulse, while a threshold stimulus produces an impulse with a similar amplitude.

Stronger stimuli are coded mainly by impulse frequency, not by a larger action-potential amplitude.

Impulse conduction speed increases with axon diameter and myelination because both allow local currents to influence the next excitable membrane region more rapidly.

Describe a positive correlation when conduction speed rises as axon diameter rises, and a negative correlation when one variable falls as the other rises. The correlation coefficient r gives direction and strength; R² estimates the proportion of variation in conduction speed explained by the fitted relationship.

If r = 0.90 for diameter and speed, the association is strong and positive; R² = 0.81 means about 81% of the observed variation in speed is explained by the fitted relationship, not that diameter is proven to be the sole cause.

Correlation does not by itself prove causation. Faster impulses do not have larger action-potential amplitudes; speed and signal strength are different properties.

A synapse is a junction where a presynaptic cell communicates with a postsynaptic cell, usually through neurotransmitter release.

The synaptic cleft separates membranes, creating a one-way delay in chemical synapses. Receptors on the postsynaptic membrane convert transmitter binding into ion-flow or intracellular effects. The synapse is a junction, so the signal must be converted before it can cross to the next cell.

Describe a chemical synapse:

• presynaptic terminal
• vesicles and cleft
• postsynaptic receptors
• signal termination

An action potential at a motor neuron terminal releases transmitter that binds receptors on a muscle fibre.

A synapse is not simply a physical gap; receptor type and transmitter removal determine the response.

Arrival of an action potential at a presynaptic terminal opens voltage-gated calcium channels and triggers vesicle fusion.

Ca²⁺ entry binds release machinery, causing exocytosis of neurotransmitter into the synaptic cleft. Enzymatic breakdown, reuptake or diffusion then terminates the signal. This one-way sequence explains why changing calcium entry can alter how strongly a synapse communicates.

Trace release:

• action potential arrives
• Ca²⁺ channels open
• vesicles fuse
• transmitter binds and is cleared

Blocking presynaptic calcium entry reduces transmitter release even if the action potential still reaches the terminal.

The electrical impulse triggers release; it does not cross the cleft as the same electrical current.

An excitatory postsynaptic potential (EPSP) is a graded depolarization that makes the postsynaptic neuron more likely to reach action-potential threshold.

Neurotransmitter released from the presynaptic terminal diffuses across the synaptic cleft and binds a transmembrane receptor. Acetylcholine can open ligand-gated channels, allowing net positive charge to enter and depolarize the postsynaptic membrane.

Sequence: transmitter release → diffusion across cleft → receptor binding → channel opening → local depolarization. Acetylcholine acts at many synapses, including neuromuscular junctions.

One acetylcholine input may produce a small EPSP below threshold; overlapping excitatory inputs can sum at the axon hillock until an action potential is triggered.

An EPSP is local and graded, not an all-or-none action potential. The neurotransmitter does not carry the electrical impulse across the cleft; receptor-controlled ion movement changes voltage.