Na+/K(+)-ATPase as an effector of synaptic transmission.
Evidence is presented in support of the hypothesis that transmitter monoamines can exert their post-synaptic effects by stimulation or inhibition of Na+/K(+)-ATPase in neuronal or glial cell plasma membranes. Stimulation of electrogenic sodium pumping, causing a hyperpolarization with an increase in membrane resistance, could account for the depression of neuronal spontaneous firing and the signal/noise enhancing actions of these amines. Conversely, inhibition of an electrogenic sodium pump in neuronal plasma membranes would lead to depolarization and enhanced excitability.
Department of Physiology, Wayne State University, School of Medicine, Detroit, MI 48201.
J W
JW
Phillis
D000818:Animals; D002462:Cell Membrane / Q000201:enzymology; D009457:Neuroglia / Q000502:physiology; D009474:Neurons / Q000502:physiology; D018377:Neurotransmitter Agents / Q000502:physiology*; D000254:Sodium-Potassium-Exchanging ATPase / Q000378:metabolism*; D013569:Synapses / Q000502:physiology*; D009435:Synaptic Transmission
D018377:Neurotransmitter Agents; D000254:Sodium-Potassium-Exchanging ATPase