Neurons and Synapses

Neuron structure.

• Dendrites receive signals from other neurons.
• Cell body contains nucleus and most organelles.
• Axon carries impulses away; can be very long (up to ~1 m in humans).
• Myelin sheath of Schwann cells (PNS) or oligodendrocytes (CNS) insulates the axon, with gaps called Nodes of Ranvier.
• Axon terminals form synapses with target cells.

Resting potential (~−70 mV inside relative to outside).

• The sodium-potassium pump actively transports 3 Na⁺ OUT and 2 K⁺ IN per ATP.
• Membrane is more permeable to K⁺ (via leakage channels) than Na⁺.
• Result: net positive charge outside; negative inside.

Action potential (depolarisation event triggered by stimulus reaching threshold):

1. Resting (~−70 mV) — Na⁺/K⁺ pump active; voltage-gated channels closed.
2. Depolarisation — stimulus opens voltage-gated Na⁺ channels → Na⁺ rushes in → membrane potential rises rapidly to ~+40 mV.
3. Repolarisation — Na⁺ channels close; K⁺ channels open; K⁺ flows out → membrane potential returns toward −70 mV.
4. Hyperpolarisation brief overshoot below resting before reset.
5. Refractory period — ~1 ms when no new action potential can fire (Na⁺ channels inactivated). Ensures the impulse travels one direction.

All-or-nothing. Stimulus must reach threshold (~−55 mV) to trigger the action potential; smaller stimuli die out.

Conduction. In unmyelinated axons, the impulse propagates as a continuous wave along the membrane.

In myelinated axons, the impulse JUMPS from one Node of Ranvier to the next — saltatory conduction — far faster (up to ~100 m/s vs ~1 m/s).

Synapse = junction between two neurons (or between a neuron and a target cell like muscle).

Pre-synaptic neuron ends in an axon terminal containing vesicles of neurotransmitter.

Synaptic cleft (~20 nm gap) separates pre- and post-synaptic membranes.

Post-synaptic neuron has receptors specific to the neurotransmitter.

Steps of synaptic transmission:

1. Action potential reaches axon terminal.
2. Voltage-gated Ca²⁺ channels open; Ca²⁺ enters terminal.
3. Vesicles move to and fuse with pre-synaptic membrane.
4. Neurotransmitter released by exocytosis into the cleft.
5. Neurotransmitter diffuses across cleft, binds receptors on post-synaptic membrane.
6. Receptor binding opens ion channels:
   • Excitatory (e.g. acetylcholine on muscle, glutamate in brain) — Na⁺ in → depolarisation.
   • Inhibitory (e.g. GABA) — Cl⁻ in → hyperpolarisation.
7. If sufficient depolarisation, a new action potential fires in the post-synaptic neuron.
8. Neurotransmitter is rapidly removed (enzymatically broken down, reuptake, or diffusion away) → synapse resets.

Why synapses matter.

• Direction — impulses pass one way (vesicles only on pre-synaptic side).
• Integration — many synapses converge; signals summed.
• Modulation — strength can change (basis of learning, memory, addiction).
• Drug targets — many neuroactive drugs work at synapses (e.g. SSRIs raise serotonin; opioids bind opioid receptors).

Neuromuscular junction. Special synapse where motor neurons trigger muscle contraction via acetylcholine.