Contribution of NMDA receptors to tetanus-induced increase in postsynaptic Ca2+ in visual cortex of young rats.

Mechanisms underlying the Ca2+ increase during tetanic synaptic inputs in layer II/III of visual cortical slices of young rats were investigated with microfluorometry using a Ca2+ indicator, rhod-2, and simultaneous recordings of field potentials evoked by white matter stimulation. Application of an antagonist for N-methyl-D-aspartate (NMDA) receptors, 2-amino-5-phosphonovalerate, did not significantly affect field potentials but reduced the tetanus-induced fluorescence rise to 56%, on average, of the control values. Application of a broad-spectrum antagonist for both NMDA and non-NMDA receptors, kynurenate, completely abolished the synaptically evoked component of field potentials and decreased the tetanus-induced fluorescence rise to 42%. Application of a non-NMDA receptor antagonist, 6-cyano-7-nitroquinoxaline-2,3-dione, in the Mg(2+)-free medium diminished the field potentials but did not decrease the tetanus-induced fluorescence increase. Nifedipine and diltiazem, L-type Ca2+ channel blockers, and Ni2+, a relatively selective blocker for T-type Ca2+ channels, did not affect the tetanus-induced fluorescence rise. These results indicate that NMDA receptors play a significant role in the increase of intracellular Ca2+ during tetanic synaptic inputs in the visual cortex of young rats.