Chapter 12: Physiology of Neurons

The foundation rests on understanding postsynaptic potentials, where ligand-gated ion channels opened by neurotransmitter binding produce localized changes in membrane potential. Excitatory postsynaptic potentials depolarize the membrane toward threshold through inward cation flow, while inhibitory postsynaptic potentials hyperpolarize the membrane by opening chloride or potassium channels, creating opposing electrical influences on the neuron. The chapter then explores how neurons combine multiple synaptic inputs through temporal summation, in which inputs arriving in close succession interact nonlinearly, and spatial summation, where inputs from different dendritic locations converge to influence the soma and axon initial segment. Dendritic architecture and passive membrane properties fundamentally shape this integration process, as resistance and capacitance filter signals and attenuate electrical changes with distance from their source. Beyond the immediate postsynaptic response, the chapter addresses synaptic plasticity mechanisms that allow synapses to strengthen or weaken with activity, including short-term facilitation and depression that modify transmission over seconds to minutes, and long-term potentiation that produces lasting enhancement through molecular cascades involving calcium influx and gene expression. Inhibitory neurotransmission mediated by gamma-aminobutyric acid and glycine provides critical stabilizing influence, preventing runaway excitation and enabling precise computational control. The clinical relevance becomes apparent through disorders such as epilepsy, where deficient inhibition or excessive excitation causes pathological synchronization, and neurodegenerative conditions that compromise synaptic function. This integrated perspective demonstrates how molecular-level mechanisms generate emergent network properties enabling sensory processing, motor control, and higher cognitive functions.