Chapter 6: Synaptic & Junctional Transmission

Synaptic & Junctional Transmission details the functional anatomy of chemical synapses, describing how presynaptic terminals utilize synaptic vesicles and active zones to release neurotransmitters across the synaptic cleft to bind with receptors on the postsynaptic density. The text elaborates on the molecular machinery of exocytosis, specifically the interaction of SNARE proteins like synaptobrevin and syntaxin, and the absolute requirement for calcium influx through voltage-gated channels to trigger vesicle fusion. Electrical events in the postsynaptic neuron are categorized into fast Excitatory Postsynaptic Potentials (EPSPs), driven by sodium or calcium entry, and fast Inhibitory Postsynaptic Potentials (IPSPs), typically caused by chloride influx, with the integration of these signals occurring through temporal and spatial summation to determine action potential generation. The chapter distinguishes between various forms of inhibition, including postsynaptic inhibition via glycine or GABA, and presynaptic inhibition or facilitation, which modulate calcium entry at the axon terminal. Special attention is given to the neuromuscular junction, explaining the release of acetylcholine, the generation of endplate potentials via nicotinic receptors, and the termination of signaling by acetylcholinesterase. Clinical pathologies are extensively reviewed, including the mechanisms of neurotoxins like botulinum and tetanus which cleave fusion proteins, and autoimmune diseases such as Myasthenia Gravis and Lambert-Eaton Syndrome which attack postsynaptic receptors and presynaptic calcium channels, respectively. Additionally, the chapter covers the autonomic neuroeffector junctions characterized by varicosities and "synapses en passant," as well as the physiological consequences of nerve injury, such as Wallerian degeneration and the development of denervation hypersensitivity due to receptor upregulation.