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NMDA and quisqualate reduce a Ca-dependent K+ current by a protein kinase-mediated mechanism
A Baskys1, N K Bernstein, A W Barolet
1Playfair Neuroscience Unit, Toronto Western Hospital, Canada.
Abstract:
Stimulation of N-methyl-D-aspartate (NMDA) or quisqualate (Quis) receptors by submicromolar concentrations of NMDA or Quis but not alpha-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid (AMPA) reduced post-spike train after hyperpolarizations (AHPs) and blocked the underlying Iahp in dentate granule (DG) neurones in vitro. The NMDA but not Quis action was blocked by the NMDA receptor blocker 2-D,L-aminophosphonovaleric acid (APV). Actions of both NMDA and Quis were abolished by isoquinolinesulphonyl-2-methyl-piperazine dihydrochloride (H-7), an inhibitor of several protein kinases. These data suggest that there is a link between excitatory amino acid receptor activation, the protein kinase system, and neuronal excitability.