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.
Phillis
J W
JW
Department of Physiology, Wayne State University, School of Medicine, Detroit, MI 48201.
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