Sodium and potassium are critically important ions in excitable cells for the transmission of impulse. Discuss the statement in an unmyelinated post synaptic neuron beginning with the events at the neuronal junction
In an unmyelinated post-synaptic neuron, the transmission of impulses relies on the movement of sodium and potassium ions. To better understand the significance of these ions in excitable cells, let's delve into the events that occur at the neuronal junction.
At the neuronal junction, which is the point of contact between the presynaptic neuron (the one sending the signal) and the post-synaptic neuron (receiving the signal), an action potential is generated. This action potential is an electrical signal that travels down the axon of the presynaptic neuron towards the neuronal junction.
When the action potential reaches the neuronal junction, it triggers the opening of voltage-gated calcium channels in the presynaptic neuron. Calcium ions then rush into the presynaptic neuron from the extracellular fluid. The influx of calcium ions causes the synaptic vesicles, which store neurotransmitters, to fuse with the presynaptic membrane. As a result, the neurotransmitters are released into the synaptic cleft (the small gap between the presynaptic and post-synaptic neurons).
The neurotransmitters, which can be excitatory or inhibitory depending on the context, diffuse across the synaptic cleft and bind to specific receptors on the post-synaptic neuron's membrane. In the case of an excitatory neurotransmitter, such as glutamate, the binding to its receptor opens ligand-gated sodium channels on the post-synaptic neuron.
The opening of the sodium channels allows sodium ions to rapidly flow into the post-synaptic neuron, leading to depolarization of the neuron's membrane. This depolarization creates an excitatory post-synaptic potential (EPSP) that brings the membrane potential closer to the threshold required for an action potential to be generated.
If the depolarization is strong enough and reaches the threshold, voltage-gated sodium channels in the post-synaptic neuron open, and sodium ions rush into the neuron. This influx of sodium ions generates a new action potential that propagates down the axon of the post-synaptic neuron.
Following the generation of an action potential, the excitatory neurotransmitter is quickly removed from the synaptic cleft through processes like reuptake or enzymatic breakdown. This removal ensures that the signal is terminated, allowing the post-synaptic neuron to return to its resting state.
Meanwhile, to repolarize and restore the post-synaptic neuron's resting membrane potential, voltage-gated potassium channels open. This allows potassium ions to flow out of the neuron, counteracting the effect of sodium influx. The movement of potassium ions hyperpolarizes the neuron, temporarily making it more negative than its resting potential. This hyperpolarization phase, also known as the refractory period, ensures that the neuron cannot be re-excited immediately.
In summary, in an unmyelinated post-synaptic neuron, sodium and potassium ions play crucial roles in the transmission of impulses. Sodium ions are responsible for depolarization, bringing the membrane potential closer to the threshold and triggering action potentials. Potassium ions are involved in repolarizing the neuron, enabling it to return to its resting state. These intricate mechanisms ensure the efficient and accurate transmission of signals between neurons.