Where is an EPSP Formed?
The potential is generated at a chemical synapse, which consists of several structural elements:
- Presynaptic membrane — characterized by lattice-like thickenings and hexagonal spaces between them.
- Exocytosis zone — the site where a synaptic vesicle fuses with the presynaptic membrane, releasing the neurotransmitter into the synaptic cleft.
- Synaptic cleft — the intercellular space through which neurotransmitter molecules pass via passive diffusion.
- Postsynaptic membrane — the receiving part of the synapse containing specific receptors. It is here that ionic currents cause a change in membrane potential and the formation of an EPSP.
- Synaptic vesicles — store neurotransmitter molecules within the presynaptic terminal.
Stages and Mechanism of Generation
The process of synaptic transmission at an excitatory synapse includes a strict sequence of events:
- Arrival of excitation: An action potential (AP) reaches the presynaptic terminal.
- Calcium influx: Voltage-gated calcium channels open, and $Ca^{2+}$ ions enter the terminal.
- Exocytosis: Influenced by $Ca^{2+}$, synaptic vesicles fuse with the presynaptic membrane, releasing portions (quanta) of the excitatory neurotransmitter into the synaptic cleft.
- Reception: The neurotransmitter binds to protein-lipid receptors on the postsynaptic membrane.
- Depolarization: Pores for sodium ($Na^+$) ions open. The influx of $Na^+$ (and in some cases $Ca^{2+}$) into the cell causes local depolarization, generating an EPSP.
The mechanism of excitation largely depends on the specifics of postsynaptic chemical reactions, which can even extend to the genetic apparatus of the neuronal nucleus (gene expression).
Receptor Types and Transmission Speed
The speed of EPSP development depends on the mechanism of the receptors involved:
- Ligand-gated (neurotransmitter-gated) ion channels — provide rapid action. The channel opens immediately upon ligand binding. Example: fast EPSP mediated by acetylcholine acting on nicotinic (N) cholinergic receptors.
- G protein-coupled receptors — act much more slowly, triggering a cascade of intracellular signaling. Example: slow EPSP in sympathetic ganglia, which can last for minutes.
A special mechanism is observed in NMDA receptors within glutamatergic synapses: they are blocked by magnesium at resting membrane potential. The resulting membrane depolarization removes this magnesium block, rendering the receptors permeable.
Physiological Role and Effects
The primary outcome of excitatory synapse function is propagating the signal further along the neural network. Local currents from EPSPs summate, and upon reaching threshold, trigger an action potential in adjacent membrane segments.
Additionally, EPSP generation underlies vital CNS functions:
- Short-term memory: Based on the circulation (reverberation) of excitation through a closed neural circuit, sustained by EPSP generation in the circuit's neurons.
- After-discharge: The continuation of a reflex response after the stimulus ceases can be supported by high-amplitude polysynaptic EPSPs.
- Electrical processes in ganglia: In sympathetic ganglia of the autonomic nervous system, a characteristic sequence of potentials is recorded: a fast EPSP is followed by a slow IPSP, which is then followed by a prolonged slow EPSP.