Synaptic excitation may activate a calcium-dependent potassium conductance in hippocampal pyramidal cells.
In hippocampal CAl pyramidal cells, orthodromic synaptic excitation is followed by an early hyperpolarization mediated by gamma-aminobutyric acid (GABA) and a late non-GABA-mediated hyperpolarization that has properties consistent with an increase in potassium conductance. Depolarizations produced by iontophoretically applied glutamate are followed by hyperpolarizations that have features in accordance with an increase in potassium conductance. The hyperpolarizations are independent of chloride and resistant to tetradotoxin but are blocked by a low-calcium, high-cobalt medium. Voltage clamping the glutamate depolarization does not reduce the subsequent hyperpolarization, indicating that the hyperpolarization results from a direct increase in calcium conductance produced by glutamate, rather than from activation of voltage-sensitive calcium channels. A single transmitter, possibly acting on one type of receptor and channel, may initiate both excitation and inhibition in the same postsynaptic cell.
D000818:Animals; D001640:Bicuculline / Q000494:pharmacology; D002118:Calcium / Q000494:pharmacology*; D004553:Electric Conductivity; D004558:Electric Stimulation; D005971:Glutamates / Q000494:pharmacology; D006624:Hippocampus / Q000502:physiology*; D066298:In Vitro Techniques; D008564:Membrane Potentials / Q000187:drug effects; D009433:Neural Inhibition / Q000187:drug effects; D011188:Potassium / Q000502:physiology*; D011712:Pyramidal Tracts / Q000502:physiology*; D051381:Rats; D009435:Synaptic Transmission
D005971:Glutamates; D011188:Potassium; D002118:Calcium; D001640:Bicuculline