Neurotransmission II: Action Potentials and Synapses (Concise Notes)

Sequence of events: threshold potential reached → depolarisation via Na+ channel opening → repolarisation as Na+ channels inactivate and voltage-gated K+ channels open → hyperpolarisation while K+ channels remain open → Na+ channels recover from inactivation (can fire again).
Threshold voltage: the point at which voltage-gated Na+ channels begin to open; triggers positive feedback leading to a full action potential.
All-or-nothing: once threshold is reached, the action potential is complete; if not reached, it does not occur.

High K+ inside the cell; high Na+ outside; inside is negatively charged relative to outside.
Resting potential around $V_{rest} \approx -70\,\text{mV}$ ; membrane is more permeable to K+ than Na+ at rest.
Equilibrium potential for K+ about $E_K \approx -82\,\text{mV}$ ; resting potential is near this value due to permeability.
Ions move down electrochemical gradients when membranes are permeable; pumps restore gradients to maintain resting state.

Absolute refractory period: all Na+ channels are inactivated → no new AP possible.
Relative refractory period: some Na+ channels remain inactivated → a stronger than normal stimulus is needed to trigger another AP.
Refractoriness enforces one-way transmission and limits firing frequency.

APs propagate along axons without decreasing in size; each segment depolarises the next.
Generation in a local region depolarises adjacent membrane to threshold, opening Na+ channels there.
The area that just fired cannot fire again until Na+ channels recover from inactivation.

Speed ranges from about $0.1\,\text{m/s}$ to $100\,\text{m/s}$ ; variability due to:
- Membrane leakiness (resistance): more leakage slows depolarisation spread.
- Membrane capacitance: larger membranes require more charge to change voltage.
- Axon diameter: larger diameter lowers internal resistance and speeds conduction.
Myelination increases speed and efficiency by reducing charge loss between nodes.

Myelin insulates the membrane, reducing charge loss.
Saltatory conduction: action potentials jump from node to node (nodes of Ranvier).
Benefits: faster conduction; lower ATP cost due to less ion resetting.

An action potential arriving at the axon terminal opens voltage-gated Ca^{2+} channels.
Ca^{2+} influx triggers fusion of synaptic vesicles with the presynaptic membrane and release of neurotransmitter into the synaptic cleft.
Neurotransmitter diffuses across the cleft to bind receptors on the postsynaptic membrane.

Neurotransmitter binds to ligand-gated ion channels on the postsynaptic membrane.
Ion flow through these channels leads to depolarisation (excitatory) or hyperpolarisation (inhibitory) of the postsynaptic cell.

Glutamate is the main excitatory neurotransmitter; opens cation channels → EPSP (depolarising).
GABA is the main inhibitory neurotransmitter; opens Cl^{-} channels → IPSP (hyperpolarising) or stabilises membrane potential.

The soma integrates excitatory and inhibitory inputs to decide whether to fire an action potential at the axon hillock.
Input weight is affected by: distance from the axon hillock, neuron shape, and proximity to inhibitory inputs (gating).
Information is coded by when and how many action potentials fire; synaptic inputs are integrated to produce an output.

Different neurons perform different computations based on how they integrate inputs.
Wiring of excitatory and inhibitory connections yields diverse circuit functions (e.g., various reflexes and processing).

Afferent fibers excite extensor motor neurons (feedforward excitation).
Interneurons and inhibitory pathways ensure coordinated contraction of antagonistic muscles via feedforward inhibition.

Action potentials are fast, all-or-nothing events whose speed is enhanced by larger diameter axons and myelination.
Synapses mediate information transfer between neurons via presynaptic Ca^{2+}-dependent neurotransmitter release and postsynaptic ligand-gated channels.
Glutamate and GABA balance excitation and inhibition to regulate membrane potential at the axon hillock.
Neurons integrate multiple excitatory and inhibitory inputs to decide whether to fire, with information coded by spike timing and frequency.
Neural circuits and their wiring determine computational outcomes, such as reflexes and higher-order processing.