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The **neuron resting membrane potential** refers to the stable voltage difference across a neuron's plasma membrane when it is not actively transmitting an electrical signal. In most neurons, this value is approximately **−70 mV**, with the inside of the cell being more negative relative to the outside[1][2][3][4]. This electrical gradient arises from differences in concentrations and permeabilities of key ions—primarily potassium (K⁺), sodium (Na⁺), chloride (Cl⁻), and organic anions—across the cell's lipid bilayer[1][2][3][4]. The **resting state** results mainly from high permeability to potassium ions via leak channels and active maintenance by transport proteins such as **the sodium-potassium pump**, which expends energy to move three Na⁺ ions out for every two K⁺ ions moved in[3]. The neuron’s ability to generate action potentials—and thus transmit signals—is critically dependent on maintaining this polarized state. Disruption in any component that establishes or maintains this gradient can lead to altered neuronal excitability and underlie various neurological diseases[5]. **Note:** "Neuron resting membrane potential" describes a physiological property—not an individual molecule, protein complex, receptor, enzyme, transporter or other canonical therapeutic target class. It cannot be directly targeted by drugs; instead pharmacological agents act on specific molecules such as ion channels or pumps that contribute to its establishment[1][2].
Drugs modulate the activity of ion channels—such as sodium, potassium, or chloride channels—or pumps like the Na⁺/K⁺ ATPase to indirectly alter the resting membrane potential.
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