TETRAETHYLAMMONIUM-INDUCED SYNAPTIC PLASTICITY IN RAT NEOCORTEX

Recordings were obtained from neurons in layer II/III of slices of rat frontal cortex maintained in vitro. We investigated whether brief app lication of the potassium channel blocker tetraethylammonium (TEA), wh ich induces a novel farm of synaptic plasticity in the CA1 region of t he hippocampus referred to as LTP(K), evokes similar responses in neoc ortex. Consistent with previous findings, TEA produced a persistent en hancement of excitatory transmission. which was independent of NMDA re ceptor activation but required the activation of nifedipine-sensitive voltage-dependent Ca2+ channels (VDCC), presumably the L-type. We also observed a persistent enhancement of presumptive Cl--dependent GABAA receptor-mediated transmission. Enhancement of excitatory and inhibito ry synaptic transmission did not require activation of synapses with e lectrical stimulation during TEA application. The enhancement of excit atory, but not inhibitory synaptic transmission, was blocked when the Ca2+ chelator 1.2-bis(2-aminophenoxy)-ethane N,N,N',N'-tetraacetic aci d (RAPTA) was included in the recording electrode. Under voltage clamp conditions that minimized the activation of L-type channels robust en hancement of both excitatory and inhibitory transmission was still obs erved. No enhancement of excitatory synaptic transmission was observed in the presence of NiCl2, a putative T-type channel blocker. The poss ible involvement of kinase activation was studied by including the non -specific and competitive kinase inhibitor +/-)-1-(5-isoquinolinesulfo nyl)-2-methylpiperazine dihydrochloride (H-7) in the patch pipette. H- 7 retarded the time course and reduced the magnitude of the enhancemen t of excitatory transmission. These results suggest that TEA-induced e nhancement of excitatory transmission in the neocortex requires entry of Ca2+ into the postsynaptic neuron via VDCCs and possibly the activa tion of a kinase.