Structure, Cell Types & Glia

The single most useful idea for exams is that a neuron is polarised and compartmentalised: its structure maps directly onto the job each region does, and information flows through it in one direction — dendrites → soma → axon hillock → axon → terminals. This is not just anatomy; it is functional logic.

You can think of three functional zones. The receptive (input) zone — dendrites and soma — collects signals from many other neurons. The trigger (decision) zone — the axon hillock and initial segment — sums those signals and decides whether to fire. The conductive zone — the axon — carries the resulting impulse over distance, and the transmissive (output) zone — the terminals — passes the message to the next cell.

Why does this compartmental, one-way design matter? Because it separates integration (weighing up many inputs) from conduction (reliable long-distance signalling) from transmission (chemical hand-off at the synapse). Keeping these jobs in different compartments — each with its own mix of ion channels and receptors — lets a single cell both compute and communicate without the two interfering. The one-way rule also keeps signalling orderly: information does not slosh back and forth, so circuits behave predictably.

Dendrites are the neuron's antennae. Their branching shape (the "dendritic tree") massively increases surface area, so one neuron can receive contacts from hundreds or thousands of others. Most of these inputs arrive at tiny protrusions called dendritic spines.

Spines matter because they are the physical sites of most excitatory synapses, and they are plastic — they can grow, shrink, change shape, or appear and disappear with experience. A spine's density and shape are a rough readout of a neuron's connectivity and its history of activity: more and stronger spines generally mean more, stronger inputs. This spine plasticity is a structural basis for learning and memory (Topic 6), and abnormal spine density is seen in conditions such as intellectual disability and some psychiatric disorders. The take-home point: the receptive surface is not fixed — it is continually sculpted.

The soma (cell body) contains the nucleus and the protein-making machinery, so it keeps the whole cell alive and supplied. Electrically, the soma and dendrites together integrate incoming signals — excitatory inputs push the membrane one way, inhibitory inputs the other — and these summed potentials spread toward the base of the axon.

That base — the axon hillock and the initial segment just beyond it — is the true decision point. It carries the highest density of voltage-gated sodium (Na⁺) channels in the neuron, which makes it the most excitable spot and therefore where the all-or-none decision is made: if the summed input crosses threshold here, an impulse fires; if not, nothing travels down the axon. (The full biophysics of how that impulse is generated is a separate topic.) The nuance worth stating is why the trigger sits here rather than out on the dendrites — placing the decision at a single, highly excitable gateway means the cell makes one clean go/no-go judgement on all its inputs combined.

The axon is a single fibre that carries the impulse away from the soma, sometimes over long distances. Many axons are wrapped in myelin, a fatty insulating sheath produced by glial cells. Myelin is not continuous: it comes in segments separated by small bare gaps called nodes of Ranvier, where voltage-gated channels are concentrated.

Insulation plus nodes speeds conduction dramatically. Instead of the impulse crawling smoothly along the whole membrane, it effectively jumps from node to node (saltatory conduction), so myelinated axons conduct far faster than bare ones of the same diameter. Myelination is also energy-efficient: because the membrane is only "worked" at the nodes rather than along its entire length, the cell spends less energy restoring ion gradients. Unmyelinated fibres are slower and are typical of small local or slow-signalling pathways, whereas heavily myelinated fibres suit fast, long-range signalling. This is exactly why losing myelin is so disabling — see the clinical note below.

Neurons are grouped by how many processes leave the soma, and the shape follows the function.

Multipolar neurons have one axon and many dendrites. They are by far the commonest type in the CNS — motor neurons of the spinal cord and pyramidal cells of the cortex are classic examples. Many dendrites means a large receptive surface for integrating many inputs, which suits complex processing.

Bipolar neurons have two processes — one dendrite and one axon — extending from opposite ends of the soma. They occur in specialised sensory pathways, such as the retina and the olfactory epithelium, where a signal is passed straight through with little integration.

Unipolar / pseudounipolar neurons have a single process that splits into two branches. These are the sensory neurons of the dorsal root ganglia, carrying signals like touch and pain from the body toward the CNS. The single-process design lets sensory information travel from the periphery to the spinal cord almost directly, bypassing the soma.

By job, neurons are sensory (afferent), carrying information toward the CNS from receptors; motor (efferent), carrying commands away from the CNS to muscles and glands; and interneurons, which connect neurons to one another within the CNS.

Interneurons dominate the central nervous system — the vast majority of CNS neurons are interneurons. The reason is computational: sensing and acting are relatively simple end-points, but everything interesting — integrating, comparing, remembering, deciding — happens in the layers of interneurons in between. The more sophisticated the processing, the more interneurons a nervous system needs.

Glia roughly match neurons in number and are indispensable partners, not inert packing. Each type has a defined role.

Astrocytes are the multitaskers of the CNS. They help form and maintain the blood–brain barrier, buffer extracellular potassium (K⁺) to keep the environment stable for signalling, take up and recycle the transmitter glutamate (preventing toxic build-up), and provide metabolic support to neurons. At synapses they wrap the junction so closely that the neuron–neuron contact plus its astrocyte is called the tripartite synapse — the astrocyte actively influences transmission.

Oligodendrocytes and Schwann cells both make myelin but differ by location and pattern. Oligodendrocytes work in the CNS and each one myelinates many axon segments at once. Schwann cells work in the PNS and each one wraps a single segment of a single axon. This difference also affects repair — PNS axons regenerate far better than CNS ones.

Microglia are the resident immune cells. They carry out immune surveillance, clearing pathogens and debris, and they also perform synaptic pruning — trimming weak or unused synapses to refine circuits during development and learning. Ependymal cells line the brain's ventricles and help produce and circulate cerebrospinal fluid (CSF). The overarching message for an exam answer: glia regulate the chemical environment, insulate and speed signalling, defend and remodel circuits — they are woven into how neurons actually work.

"Glia are just glue." The name means "glue," but as above, glia buffer ions, recycle transmitter, build the blood–brain barrier, myelinate axons, prune synapses and mount immune defence. They are active participants in signalling.

"Signals can travel backwards." Under normal conditions the neuron is functionally one-way: dendrites and soma receive, the axon conducts away, and the synapse is a one-directional chemical relay from terminal to next cell.

"Myelin is a continuous coat." It is segmented, with bare nodes of Ranvier between segments — and those gaps are precisely what make fast saltatory conduction possible.

Linking structure to disease makes the material stick and shows genuine understanding. In multiple sclerosis (MS), the immune system attacks CNS myelin (oligodendrocyte myelin); demyelinated axons conduct slowly or fail, producing symptoms such as weakness, numbness and visual problems — a direct demonstration of why myelin matters. In Guillain–Barré syndrome, the same principle applies in the PNS, where Schwann-cell myelin is damaged, causing rapid-onset weakness.

Glia are increasingly implicated in disease too: astrocyte and microglial dysfunction and abnormal microglial pruning are studied in neurodegenerative and psychiatric conditions, and altered dendritic spine density appears in intellectual disability. The recurring lesson is that when a specific compartment or cell type fails, you can predict the deficit from what that structure normally does.