What is the mechanism of nerve impulse transmission at the synapse?

Together with its neurotransmitters, the synapse functions as a physiological valve, preventing random and chaotic nerve stimulation and guiding the conduction of nerve impulses in regular circuits.

Neurotransmitters are released when a nerve impulse fuses with membranes at the presynaptic terminal, causing a movement towards the synaptic vesicles. Different receptors may respond differently to the same neurotransmitter.

By diffusing across the synaptic cleft and binding to receptors on the post synaptic membranes, the neurotransmitter transfers the nerve impulse to the post synaptic fiber. This action sets off a sequence of events that open "channel shaped" protein molecules, allowing electrically charged ions to pass through the channels and enter or exit the neurons.

A new nerve of impulse known as an action potential is created if the net flow of positively charged ions is sufficiently large. Subsequently, the neurotransmitter molecules are deactivated by synaptic cleft enzymes.

The following steps are involved in the mechanism of nerve impulse transmission at the synapse: 1. Arrival of the action potential at the presynaptic terminal; 2. Activation of voltage-gated calcium channels, resulting in an influx of calcium ions; 3. Calcium ions trigger the fusion of neurotransmitter-containing vesicles with the presynaptic membrane; 4. Release of neurotransmitters into the synaptic cleft via exocytosis; 5. Diffusion of neurotransmitters across the synaptic cleft; 6. Binding of neurotransmitters to receptors on the postsynaptic membrane; 7. Opening of ion channels on the postsynaptic membrane, resulting in depolarization or hyperpolarization of the postsynaptic neuron; 8. Generation of a new action potential if the depolarization reaches the threshold; 9. Removal of neurotransmitt

At the synapse, the mechanism of nerve impulse transmission involves several steps:

1. Action potential reaches the presynaptic terminal: When an action potential, or electrical signal, reaches the presynaptic terminal of a neuron, it triggers the opening of voltage-gated calcium channels.

2. Calcium influx: The opening of calcium channels allows calcium ions to enter the presynaptic terminal from the extracellular space. The influx of calcium ions leads to an increase in calcium concentration within the presynaptic terminal.

3. Vesicle fusion and neurotransmitter release: The increased calcium concentration triggers the fusion of neurotransmitter-containing vesicles with the presynaptic membrane. This fusion causes the release of neurotransmitters, such as serotonin, dopamine, or acetylcholine, into the synaptic cleft.

4. Diffusion of neurotransmitters: Neurotransmitters released into the synaptic cleft diffuse across the short distance to reach the postsynaptic membrane, where they bind to specific receptor molecules.

5. Activation of postsynaptic receptors: When neurotransmitters bind to their respective receptors on the postsynaptic membrane, they induce a conformational change in the receptor molecules. This change may lead to the opening or closing of ion channels in the postsynaptic membrane.

6. Generation of postsynaptic potential: The opening or closing of ion channels in the postsynaptic membrane alters the membrane potential of the postsynaptic neuron, generating a postsynaptic potential. Depending on the type of ion channels involved and the direction of ion movement, the postsynaptic potential may be excitatory (depolarizing) or inhibitory (hyperpolarizing).

7. Integration of postsynaptic potentials: Postsynaptic potentials generated at multiple synapses on the postsynaptic neuron are integrated at the axon hillock. If the combined effect of excitatory and inhibitory inputs reaches the threshold for action potential initiation, a new action potential is generated in the postsynaptic neuron, propagating the nerve impulse further along the neuron.

8. Termination of neurotransmitter action: Neurotransmitter action is terminated through various mechanisms, including enzymatic degradation, reuptake into the presynaptic terminal or surrounding glial cells, and diffusion away from the synaptic cleft. This termination prevents continuous stimulation of the postsynaptic neuron and allows for precise control of synaptic transmission.