Involvement of N- and non-N-type calcium channels in synaptic transmission at corticostriatal synapses

Abstract

Calcium channels participate in the events linking axon terminal depolarization to neurotransmitter secretion. We wished to evaluate the role of N-type and non-N-type calcium channels in glutamatergic transmission at corticostriatal synapses, since this is a well denned excitatory synapse. In addition, these synapses are subject to a variety of forms of presynaptic modulation, some of which may involve alterations in calcium channel function. Application of the selective N-type c hannel blocker ω-conotoxin GVIA produced an irreversible depression of excitatory synaptic transmission in rat neostriatal slices shown by a decrease of ~ 50% in the amplitude of the synaptically driven population spike during field potential recording and a similar decrease in the amplitude of excitatory postsynaptic potentials during whole-cell recording. The component of transmission which was resistant to ω-conotoxin GVIA was blocked by ω-conotoxin MVIIC. ω-Agatoxin IVA had little effect on transmission. Activation of a presynaptic metabotropic glutamate receptor depressed transmission to a similar extent before and after ω-conotoxin GVIA treatment. Likewise, protein kinase C-activating phorbol esters potentiated transmission to the same extent before and after ω-conotoxin GVIA treatment. N-type calcium channels appear to be crucial for a component of excitation-secretion coupling at corticostriatal synapses. A component of transmission 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-type channel function.