How is an IPSP Formed? (Transmission Steps)
The transmission of an inhibitory signal at a synapse involves the following sequential steps:
- Arrival of excitation: An action potential (AP) reaches the presynaptic terminal.
- $Ca^{2+}$ influx: The permeability of the presynaptic membrane to calcium ions increases, and they enter the terminal.
- Exocytosis: Influenced by $Ca^{2+}$, vesicles containing the inhibitory neurotransmitter move toward the presynaptic membrane, releasing the neurotransmitter into the synaptic cleft.
- Receptor binding: The neurotransmitter binds to receptors on the postsynaptic membrane of the target neuron.
- Ionic shift: Ion channels open, increasing membrane permeability to chloride ions ($Cl^-$) and potassium ($K^+$). Chloride enters the cell along its concentration gradient, while potassium leaves it.
- IPSP generation: The movement of ions results in membrane hyperpolarization, which constitutes the inhibitory postsynaptic potential.
Which Neurotransmitters Trigger IPSPs?
Depending on the region of the nervous system, IPSPs are generated by various chemical substances:
- In the central nervous system (CNS): The main inhibitory neurotransmitters are GABA and glycine.
- In the autonomic nervous system: Inhibitory synapses utilize acetylcholine and norepinephrine.
- In sympathetic ganglia (slow IPSP): Mediated by dopamine. Dopamine is secreted by small intensely fluorescent (SIF) interneurons of the ganglion, which are activated via muscarinic acetylcholine receptors (M-cholinoceptors). It is hypothesized that the slow IPSP itself is mediated by $\beta_2$-receptors, as it is independent of cAMP.
What is the Physiological Effect of an IPSP?
An IPSP causes inhibition of excitation. Postsynaptic inhibition strictly requires the participation of an inhibitory interneuron.
- Change in excitability: An IPSP prevents the attainment of the depolarization threshold. The stimulation threshold of the principal neuron increases, and its excitability drops.
- Signal blocking: Unlike an excitatory synapse, where the summation of EPSPs triggers an action potential and propagates the signal, the development of an IPSP makes action potential generation impossible. The conduction of excitation is blocked.
The Role of IPSPs in Physiological Processes
- Termination of short-term memory: The basis of short-term memory is the circulation (reverberation) of excitation through closed neural circuits, sustained by excitatory potentials (EPSPs). This process stops when an IPSP develops in one of the circuit's neurons under the influence of an inhibitory neuron.
- Generation of electrical potentials in ganglia: During stimulation of preganglionic sympathetic fibers, the IPSP is part of a sequential shift in potentials. A fast EPSP is recorded first, followed by a slow IPSP, which is then followed by a slow EPSP (capable of lasting minutes).