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.

Depolarization is the rising phase of an action potential as sodium conductance increases; repolarization returns the membrane toward negative values as potassium conductance rises.

Voltage-gated channels have distinct activation and inactivation timing. The overlap creates a refractory period and ensures the impulse moves forward rather than immediately backward. The changing voltage is evidence of ion movement across the membrane, not a flow of the whole neuron along its axon.

Read the voltage trace with channel states:

• Na⁺ activation: rising phase
• Na⁺ inactivation: peak
• K⁺ activation: falling phase
• delayed K⁺ closing: undershoot

A sodium-channel blocker removes the rapid rising phase, while a potassium-channel blocker prolongs repolarization.

The membrane does not become permanently positive; ion gradients and channel timing restore the resting state.

An action potential propagates along an axon when local currents from one depolarized region bring the adjacent membrane to threshold.

Na⁺ entering through open voltage-gated channels diffuses sideways inside the axon toward the next resting region. Compensating positive charge moves in the extracellular fluid, completing a local current circuit and depolarizing the next membrane segment to threshold.

The next segment opens its sodium channels and regenerates the action potential. The refractory region behind cannot immediately reopen sodium channels, so propagation normally proceeds forward.

Each newly depolarized segment supplies local current to the next segment, so a full-amplitude action potential is regenerated rather than gradually fading along the axon.

The action potential is not a single group of ions travelling the full axon length. Ions move short distances locally while sequential channel opening propagates the voltage change.

An oscilloscope trace displays voltage against time, allowing action-potential threshold, amplitude, duration and frequency to be compared.

The vertical scale reports membrane potential and the horizontal scale reports time. Repeated spikes indicate frequency; baseline shifts or noise must be distinguished from true action potentials. Reading the trace means linking each voltage change to a stage of channel opening or closing.

Read a trace in order:

• calibrate axes
• locate threshold and peak
• measure duration or interval
• calculate frequency from repetition

If five spikes occur in 0.1 seconds, the firing frequency is 50 Hz, not an amplitude of five units.

A taller trace is not automatically a stronger stimulus; check what the axis represents.

Saltatory conduction is rapid propagation in a myelinated fibre in which action potentials are regenerated from one node of Ranvier to the next.

Myelin insulates internodes and reduces current loss. Ion channels and pumps are clustered at the exposed nodes, so local current spreads quickly beneath myelin and brings the next node to threshold.

Internode: insulated rapid current spread. Node: concentrated voltage-gated channels generate the next action potential and pumps maintain the ion gradients. Fewer membrane regions need direct ion exchange.

Demyelination increases current leakage, so the next node may reach threshold later or not at all, slowing or blocking the impulse.

The impulse appears to jump, but electrical current still spreads through the axon between nodes. Action potentials are regenerated only at nodes rather than travelling through empty space.

Exogenous chemicals can alter synaptic transmission by acting on receptors or by changing how long neurotransmitter remains in the synaptic cleft.

If reuptake is blocked, a released neurotransmitter is cleared more slowly, so receptor stimulation continues after it would normally have ended.

The two examples act differently: neonicotinoids act at receptor sites, whereas cocaine blocks neurotransmitter reuptake. Do not infer a single behavioural outcome without considering dose, receptor distribution and organism.

Inhibitory neurotransmitters make a postsynaptic neuron less likely to reach action-potential threshold.

They may open chloride channels, increase potassium efflux or reduce excitatory channel activity. The resulting hyperpolarization or shunting inhibition opposes excitatory inputs. Inhibition is relational: the same transmitter can have different effects if receptor types differ, and the receiving circuit determines the outcome.

Identify inhibition by checking:

• receptor and ion channel
• current direction or conductance
• membrane-potential effect
• threshold probability

Opening chloride channels can stabilize the membrane near its resting potential and reduce the effect of a simultaneous EPSP.

Inhibition is not always a large negative voltage; increased conductance can also shunt excitatory current.

Summation combines graded postsynaptic potentials across space and time at the axon hillock.

Spatial summation adds inputs from different synapses; temporal summation adds repeated inputs from one synapse. The net potential reaches threshold only if excitation outweighs inhibition. The result depends on timing as well as size, because inputs that overlap can combine before the threshold decision.

Separate the two forms:

• spatial: different locations
• temporal: different times
• EPSPs add
• IPSPs subtract or shunt

Two small EPSPs arriving together at the axon hillock can reach threshold even though neither would trigger an action potential alone.

The neuron integrates potentials, not neurotransmitter names; receptor effects determine the sign and size.

Pain perception can begin at free sensory nerve endings in the skin that act as nociceptors for potentially damaging stimuli.

High temperature, acid or chemicals such as capsaicin open stimulus-sensitive channels for positively charged ions. Ion entry depolarizes the ending; if threshold is reached, action potentials travel along the sensory neuron to the brain, where pain is perceived.

Sequence: damaging stimulus → positive-ion channels open in free nerve ending → depolarization reaches threshold → impulses propagate to brain → conscious pain perception.

Capsaicin in chilli peppers activates ion channels in free nerve endings, producing depolarization and impulses that the brain interprets as burning pain even without high temperature.

Nociceptor activation is the neural input to pain, not pain perception itself. Conscious pain emerges after processing in the brain.

Consciousness is associated with coordinated activity across interacting brain networks rather than one isolated neuron or single region.

Arousal systems regulate wakefulness while cortical and subcortical networks integrate sensory information, memory and self-related processing. Evidence from sleep, anaesthesia and brain injury links changes in network connectivity to conscious state. Conscious awareness is therefore an emergent interpretation of coordinated neural activity, not a single switch in one neuron.

Separate the components:

• arousal and wakefulness
• information integration
• communication among brain regions
• reportable experience

During deep anaesthesia, widespread connectivity and coordinated responses fall, while local sensory circuits may still respond to stimulation.

A neural response alone does not prove a conscious experience; integration and reportability require additional evidence.