These exchangers are responsible for pumping sodium out of the cells into the extracellular space, potassium into the intracellular compartment. This resting (steady-state) potential is critical for the neuron’s physiological state, maintained by an unequal distribution of ions across the cellular membrane and established by ATP-dependent pumps-most notably, sodium-potassium antiporters. The lipid bilayer of the neuronal cell membrane acts as a capacitor, the transmembrane channels as resistors. The neuron’s membrane potential gets generated via a difference in the concentration of charged ions. Disruption of this mechanism can have drastic effects resulting in lack of impulse generation and conduction, illustrated by various neurotoxins and demyelinating disorders. They also are crucial for communication among neurons through synapses. Neuronal action potentials are vital for propagation of impulses along any nerve fiber even at a distance. This change in membrane potential will open voltage-gated cationic channel (sodium channel) resulting in the process of depolarization and generation of the neuronal action potential. A neuronal action potential gets generated when the negative inside potential reaches the threshold (less negative). This state is the resting membrane potential of about -60mV. Normally, the cell’s interior is negative, compared to its outside. This action is the way these cells can interact with each other, i.e., at synapses via synaptic transmission. These action potentials are generated and propagated by changes to the cationic gradient (mainly sodium and potassium) across their plasma membranes. These action potentials finally reach the axonal terminal and cause depolarization of neighboring cells through synapses. Neurons are electrically excitable, reacting to input via the production of electrical impulses, propagated as action potentials throughout the cell and its axon.
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