Nerves and Neurones: Action Potentials, Myelination and Synapses

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Homework type: Essay

Added: 17.01.2026 at 10:42

Biology F214 — Nerves

The nervous system forms the central communication network of all animals, enabling organisms to perceive their environment, form memories, and perform complex, coordinated actions. The functional unit of this system is the neurone—a highly specialised cell evolved for the rapid transmission and processing of electrical signals. This essay will explore the electrical properties of neurones, the way impulses propagate along axons, and how information passes between cells at synapses. By referencing landmark experiments and considering disorders such as multiple sclerosis or myasthenia gravis, the physiological principles will be linked to both the history of neuroscience and to clinical relevance. The discussion begins with neurone structure, proceeds to the mechanisms of resting and action potentials, follows on to myelination and conduction, and concludes with an analysis of synaptic transmission, grounding each section in evidence and cultural context familiar to UK analytical biology.

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Structure of Neurones and Supporting Cells

Extending from the soma is the axon, generally a single, elongated fibre. It begins at the axon hillock, an area densely packed with voltage-gated ion channels and therefore primed for initiating action potentials. The axon’s terminal branches, each ending in a presynaptic knob, facilitate communication with targets—either with other neurones, muscle fibres, or glands—by releasing neurotransmitters.

Variations in neurone form reflect function. Sensory neurones, which carry afferent signals from the periphery to the spinal cord, are typically pseudo-unipolar with a cell body offset in the dorsal root ganglion; their structure allows rapid relay from receptor to CNS. In contrast, motor neurones are multipolar, sprouting numerous dendritic branches but maintaining a single, long axon, ideal for conveying signals from spinal cord to distant muscles. Interneurones, prevalent within the central nervous system (CNS), display shorter axons and are tailored for integrative processing.

Supporting these neurones are glial cells. In the peripheral nervous system (PNS), Schwann cells wrap axons in layers of myelin, while in the CNS, this role is fulfilled by oligodendrocytes—one oligodendrocyte myelinating multiple axons, in comparison to the one-to-one association of Schwann cells. Myelin dramatically alters the electrical properties of the axon, as explained later. Unmyelinated gaps known as nodes of Ranvier are crucial for the rapid progression of electrical impulses. Other glia include astrocytes, which buffer extracellular ions and contribute to the blood–brain barrier, and microglia, the CNS’s resident immune cells.

*Tip*: When drawing and annotating diagrams of neurone structure for exams, always clearly indicate the sites of synaptic contact and the distinction between myelinated and unmyelinated regions, as this can clarify questions of function as well as structure.

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Resting Membrane Potential: Origin and Maintenance

The source of the RMP lies in both the specific ionic gradients across the membrane and the membrane’s selective permeability. The neurone’s membrane is far more permeable to potassium ions (K⁺) than to sodium ions (Na⁺) at rest. Potassium, concentrated highly inside the cell, tends to leak out through potassium leak channels, making the inside more negative. Sodium, meanwhile, is concentrated outside but is largely prevented from entering except for a tiny persistent leak.

A further key player is the sodium-potassium pump (Na⁺/K⁺ ATPase), an enzyme which hydrolyses ATP to pump three sodium ions out for every two potassium ions it brings in. This action maintains the gradients over the long term, and because more positive charges are moved out than in, it contributes a small direct hyperpolarising effect.

The concept of equilibrium potential emerges here: each ion has a specific value at which its electrical and concentration forces balance (known as the Nernst potential). The membrane potential sits closest to the potassium equilibrium because of high potassium permeability at rest. Where ionic imbalances exist, as in diseased tissue, this can have marked effects on resting potential and therefore neural function.

RMP is typically recorded by inserting a fine glass microelectrode inside the axon and comparing the potential with an extracellular reference, a method developed and popularised by British physiologists such as Hodgkin and Huxley using the squid giant axon—a model still referenced in UK curricula.

*Exam note*: While the sodium-potassium pump is essential, it maintains the gradients rather than creating the immediate RMP. Precise language and a realistic appreciation of membrane properties are vital for top marks.

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Generation and Propagation of the Action Potential

Trigger and Threshold: A neurone fires an AP if depolarising inputs—via synapses or sensory stimulation—raise the membrane potential to a critical threshold (usually about –55 mV). The response is all-or-nothing: an action potential follows, or it does not.

Phases of the Action Potential:

1. Depolarisation: Upon reaching threshold, voltage-gated sodium channels open, permitting a massive but brief influx of sodium ions. This inward current rapidly inverts the membrane voltage, often peaking around +30 mV. 2. Peak and Inactivation: Sodium channels swiftly inactivate (a different conformation to being simply closed), halting further sodium entry. 3. Repolarisation: Almost simultaneously, voltage-gated potassium channels open. Potassium exits the cell, removing positive charge and returning the membrane potential towards the negative resting state. 4. Hyperpolarisation: Potassium channels close slowly, allowing the potential to undershoot RMP, creating an “afterpotential”. 5. Restoration: Eventually, all voltage-gated channels reset, and the sodium-potassium ATPase re-establishes steady gradients.

Refractory Periods: The absolute refractory period is a brief interval in which no new AP can be initiated, as sodium channels are inactivated. The subsequent relative refractory period allows APs only if a markedly larger stimulus is provided, because some channels have recovered. This system ensures that APs travel in one direction and encode the intensity of stimuli as frequency, not amplitude.

Propagation in Unmyelinated Axons: Here, local circuit currents cause depolarisation of adjacent segments of membrane, prompting them, in turn, to reach threshold and fire. This wave-like progression is inevitably slower than in myelinated fibres. Larger axon diameters conduct faster due to reduced internal resistance—a principle exploited by the squid but rare in mammals owing to spatial constraints.

*Figure*: [Insert labelled diagram showing AP waveform, with sodium and potassium currents annotated by channel state, and a schematic of local circuit propagation.]

*Tip*: Use the correct terminology—“depolarisation” for rising phase, “repolarisation” for return towards rest, and “inactivation” for temporary non-conducting state of sodium channels.

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Myelination, Saltatory Conduction, and Factors Influencing Speed

Myelination: Encircling the axon with concentric layers of glial cell membrane, myelin acts as an electrical insulator. Schwann cells provide this in the PNS, whereas oligodendrocytes fulfil the role in the CNS, wrapping multiple axons each.

Nodes of Ranvier: These tiny uncovered sections of axon are rich in voltage-gated sodium and potassium channels. Only here are APs actively regenerated.

Saltatory Conduction: The AP effectively leaps from node to node, with local currents "jumping" beneath the myelin sheath. This dramatically speeds up conduction—up to 120 m/s in the largest myelinated human nerves—while also reducing the metabolic load, as fewer ions cross the membrane and need to be pumped back.

Other Factors: Larger diameter axons conduct more rapidly; colder temperatures slow channel kinetics (hence why our fingers may feel numb and clumsy in winter). Disease states such as multiple sclerosis, characterised by myelin loss, slow or block conduction, resulting in muscle weakness, impaired sensation, and characteristic UK disability patterns.

Comparative studies highlight the difference: unmyelinated C fibres, carrying dull pain, conduct slowly (~1 m/s), while large myelinated A fibres, responsible for precise proprioceptive feedback or motor reflexes, are much faster.

*Figure*: [Insert diagram illustrating a myelinated axon with saltatory conduction between nodes.]

*Tip*: When answering exam questions, always quantify (e.g. “several times faster with myelin”) and link structural changes to functional outcomes.

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Synaptic Transmission: Chemical and Electrical

Chemical Synapses: These predominate in vertebrate nervous systems. When an AP reaches the presynaptic terminal, voltage-gated calcium channels open. Calcium enters, triggering vesicles containing neurotransmitter (e.g., acetylcholine) to fuse with the membrane and release their contents into the synaptic cleft. Transmitter molecules then diffuse across to bind to specific receptors on the postsynaptic membrane. Depending on receptor type, this binding either depolarises the postsynaptic cell (excitatory postsynaptic potential, EPSP) or hyperpolarises it (inhibitory postsynaptic potential, IPSP), primarily by altering sodium, potassium, or chloride conductances.

Termination mechanisms prevent overstimulation: neurotransmitter is broken down by enzymes, reabsorbed by the presynaptic terminal, or simply diffuses away.

Electrical Synapses: Unlike chemical synapses, these involve direct ionic flow through gap junctions. They are fast and can be bidirectional, found in some escape reflexes (such as the startle circuit in the fish Mauthner system, a classic reference in British comparative neurobiology) and in heart tissue.

Neuromuscular Junction: This synapse, connecting motor neurone to skeletal muscle, exemplifies precision and reliability. Acetylcholine release triggers robust muscle APs. Disruption here produces striking clinical symptoms—weakness as in myasthenia gravis (due to lost acetylcholine receptors) or paralysis with curare.

Synaptic Modulation and Plasticity: Repeated activity can enhance (facilitate) or diminish (depress) synaptic transmission—a key process in learning and memory, both active research areas in British neuroscience.

*Figure*: [Insert labelled diagram of a chemical synapse, showing calcium entry, vesicle fusion, transmitter release, and postsynaptic receptor binding.]

*Tip*: When explaining EPSPs and IPSPs, always state which ions are responsible and the resulting membrane effect.

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Experimental and Clinical Relevance

Experimental Evidence: British physiologists Alan Hodgkin and Andrew Huxley, using the squid giant axon and voltage clamp techniques, separated sodium and potassium currents and thereby founded the ionic theory of the AP—a triumph of the British tradition of empirical science. Microelectrode recordings and pharmacological tools (e.g. tetrodotoxin to block sodium channels) remain standard in both research and diagnostic practice.

Clinical Conditions: Many neurological diseases can be understood as disturbances of these underlying processes. Multiple sclerosis, extremely prevalent in the UK, features immune attack on CNS myelin, resulting in slowed or absent AP conduction—causing weakness, visual loss, and, eventually, disability. Local anaesthetics such as lidocaine act by reversibly blocking voltage-gated sodium channels—providing safe, temporary loss of sensation during dentistry or minor surgery. Myasthenia gravis, classically described in UK clinics, involves antibodies targeting acetylcholine receptors at the neuromuscular junction, explaining the characteristic fatigable muscle weakness.

Broader Implications: Understanding energetic efficiency explains why myelinated nerves dominate in vertebrates, where both speed and sustainability are priorities. Contemporary therapies under investigation in the UK range from drugs targeting synaptic function (as with epilepsy or depression) to regenerative approaches for remyelination.

*Tip*: Clinical examples not only illuminate the physiology but also demonstrate a rounded, applied understanding.

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Conclusion

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Glossary

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Suggested Diagrams:

1. Typical multipolar neurone with labelled dendrites, soma, axon hillock, myelinated axon, node of Ranvier, and presynaptic terminal. 2. Action potential trace annotated with phases and main ionic flows. 3. Myelinated axon showing saltatory conduction (jumping between nodes). 4. Chemical synapse, highlighting vesicle fusion and postsynaptic response.

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References (Examples)

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Final Preparation Checklist:

- Have all key terms been defined and appropriately used? - Are explanations logically linked—stimulus to channel opening to ion movement to voltage change? - Are diagrams clear, labelled, and referenced in the text? - Have clinical or experimental examples been used to demonstrate applied understanding? - Is every section precise, concise, and relevant to the UK curriculum context?

By meeting these standards, you display both knowledge of nerve physiology and an ability to relate theory to practice—a core competence in Biology F214.