ELEVATED STRIATAL FOS IMMUNOREACTIVITY FOLLOWING 6-HYDROXYDOPAMINE LESIONING OF THE RAT IS MEDIATED BY EXCITATORY AMINO-ACID TRANSMISSION

Pharmacological depletion of dopaminergic neurotransmission can result in an elevation in striatal Fos levels. This elevation may occur as a direct result of decreased dopaminergic neurotransmission or indirect ly via elevated corticostriatal glutamatergic neurotransmission which occurs secondary to dopamine depletion. To test the hypothesis that el evated N-methyl-D-aspartic acid (NMDA)-mediated corticostriatal transm ission may underlie the increase in striatal Fos levels upon dopamine depletion, rats were unilaterally 6-hydroxydopamine lesioned under ana esthesia induced by either barbiturate or the NMDA antagonist, ketamin e. Following surgery the animals remained under light anaesthesia for 6 h prior to sacrifice acid quantification of striatal Fos immunoreact ivity. The results demonstrate that dopamine depletion following 6-hyd roxydopamine lesioning can result in elevated striatal Fos levels whic h can be attenuated by contiguous treatment with an NMDA antagonist. T his suggests that the increase in striatal Fos levels observed followi ng dopamine depletion may occur as a result of elevated cytoplasmic ca lcium levels in the striatal cells.