The excitatory postsynaptic potentials generated from a presynaptic neuron leads to the generation of the action potentials. The presynaptic neuron discharges the neurotransmitters in response to the excitatory postsynaptic potentials. The post-synaptic neurons have the receptors for the linkage of the neurotransmitters discharged into the synaptic cleft. The adjoining of the neurotransmitters causes the opening of numerous ion channels. The opening of such ion channels alters the permeability of the membrane and simultaneously alters the membrane potentials. The synapse is excitatory as the binding of the neurotransmitter elevates the voltage. The hyperpolarization of the membrane due to the binding of the neurotransmitter is inhibitory. The power of the voltage stimulus diminishes with time. The rise and drop of the voltage will causes the propagation of the signal to the adjacent regions of the membrane. The powerful stimuli cause the depolarization of the neural impulses at the axon hillock. Multiple excitatory potentials are needed for the generation of an action potential. The counteracting inhibitory postsynaptic potentials can cause the inhibit the synergistic effect of the multiple excitatory potentials.
Phases of the action potentials include the rising phase, the peak phase, the falling phase, the undershot phase, and the refractory phase. The depolarization of the membrane potential is identified during the rising phase and the interior region of the membrane tends to be more positive. The termination of the depolarization marks the peak phase which is followed by the falling phase and causes the drop of the membrane potential and the membrane tends to be more negative. The resting potential is attained by the drop of the membrane potential. The falling phase is followed by the afterhyperpolarization phase or the undershoot phase, which causes a negatively charged membrane potential. The final phase in the neural signaling is the refractory period and the membrane lacs the energy to stimulate an action potential. Two coupled effects influence the transmission of an action potential and include the effect of alteration of the membrane voltage in the opening and closing of the ion channels and the influence of the equilibrium potential in maintaining the permeability of the membrane between the ECF and ICF.
Phases in Transmission of Action Potential
The action potential is initiated at the axon hillock as a result of a depolarization. The depolarization takes place with the entry of the sodium ions from the external region into the membrane and the inputs causing the depolarization to include the pacemaker potentials, chemical synapses, and sensory impulses. The intracellular have high sodium concentration than the extracellular fluid during the resting phase and the ionic gradient causes the movement of ions from the high concentration to low concentration. The opening of t ionic channels pushes the sodium ions into the membrane during the depolarization and the membrane potential rises to a more positive state. A small depolarization is highly threatened by repolarization due to the concentration gradient.
The maximum opening of the sodium channels in the production of an action potential is the peak phase. The permeability of the sodium is at the highest during the peak phase and the membrane potential is more positive than the predecessor phases. The voltage has multiple effects and it also causes the closing of the sodium channels and causes the attainment of the resting membrane potential.
The calcium entering the membrane triggers the opening of the potassium channel and leads to the influx of numerous potassium ions leading to the further drop in the membrane potentials. The afterhyperpolarization state continues to exits until the reattainment of the normal membrane potassium permeability.
The refractory period is the state of the neuron during the lack of energy for the generation of an action potential. The refractory period is grouped as the absolute refractory period and the relative refractory period.
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