INVOLVEMENT OF N-TYPE AND NON-N-TYPE CALCIUM CHANNELS IN SYNAPTIC TRANSMISSION AT CORTICOSTRIATAL SYNAPSES

Calcium channels participate in the events linking axon terminal depol arization to neurotransmitter secretion. We wished to evaluate the rol e of N-type and non-N-type calcium channels in glutamatergic transmiss ion at corticostriatal synapses, since this is a well defined excitato ry synapse. In addition, these synapses are subject to a variety of fo rms of presynaptic modulation; some of which may involve alterations i n calcium channel function. Application of the selective N-type channe l blocker omega-conotoxin GVIA produced an irreversible depression of excitatory synaptic transmission in rat neostriatal slices shown by a decrease of similar to 50% in the amplitude of the synaptically driven population spike during field potential recording and a similar decre ase in the amplitude of excitatory postsynaptic potentials during whol e-cell recording. The component of transmission which was resistant to omega-conotoxin GVIA was blocked by omega-conotoxin MVIIC. omega-Agat oxin IVA had little effect on transmission. Activation of a presynapti c metabotropic glutamate receptor depressed transmission to a similar extent before and after omega-conotoxin GVIA treatment. Likewise, prot ein kinase C-activating phorbol esters potentiated transmission to the same extent before and after omega-conotoxin GVIA treatment. N-type c alcium channels appear to be crucial for a component of excitation-sec retion coupling at corticostriatal synapses. A component of transmissi on involves non-N-, non-L-type high-voltage-activated calcium channels . The effects of presynaptic metabotropic receptors and protein kinase C activation cannot be accounted for solely by alterations in the N-t ype channel function.