EXTRACELLULAR STRIATAL DOPAMINE AND GLUTAMATE AFTER DECORTICATION ANDKAINATE RECEPTOR STIMULATION, AS MEASURED BY MICRODIALYSIS

Disruption of corticostriatal glutamate input in the striatum decrease d significantly extracellular striatal glutamate and dopamine levels. Local administration of 300 mu M concentration of excitatory receptor agonist kainic acid increased significantly extracellular striatal dop amine in intact freely moving rats. These findings support the hypothe sis that glutamate exerts a tonic facilitatory effect on striatal dopa mine release. The effect of kainic acid on extracellular striatal glut amate concentration in intact rats was a biphasic increase. The first glutamate increase can be explained by stimulation of presynaptic kain ate receptors present on corticostriatal glutamatergic nerve terminals ; the second increase is probably the result of a continuous interacti on of the different striatal neurotransmitters after disturbance of th eir balance. Release of dopamine and glutamate was modulated different ly in the intact striatum and in the striatum deprived of corticostria tal input. Dopamine release in the denervated striatum after kainate r eceptor stimulation was significantly lower than in intact striatum, c onfirming the so-called cooperativity between glutamate and kainic aci d. Loss of presynaptic kainate receptors on the glutamatergic nerve te rminals after decortication resulted in a loss of effect of kainic aci d on glutamate release in denervated striatum. Aspartate showed no sig nificant changes in this study.