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The **neuron membrane potential**, also known as resting or transmembrane electrical potential difference (\(V_m\)), refers to the difference in electric charge across the plasma membrane of a neuron at rest—typically between −60 mV and −75 mV inside relative to outside[1][3]. This negative internal environment results from selective permeability to ions like K⁺ and Na⁺ via various ion channels and active transport by pumps such as Na⁺/K⁺ ATPase[2]. Changes in this electrical gradient underlie all neural signaling processes—including depolarization during action potentials when voltage-gated sodium channels open—and are fundamental for synaptic communication throughout nervous tissue[5][7]. The value fluctuates dynamically during neural activity due to opening/closing of ligand-gated or voltage-gated ion channels responding either to neurotransmitters or changes in local electric fields respectively[6]. While essential for brain function and targeted indirectly by many neuroactive drugs acting on specific proteins involved in its regulation, “neuron membrane potential” itself is *not* considered a direct molecular drug target.
Drugs do not act on the neuron’s resting or action potentials directly; rather they alter the probability that neurons will fire action potentials by changing their underlying ionic currents. This is achieved by mechanisms such as blocking voltage-gated sodium channels to inhibit depolarization, opening potassium channels to promote hyperpolarization, modulating chloride conductance via GABA_A receptors for inhibitory effects, or inhibiting calcium influx through voltage-gated calcium channels.
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