Regulation of cortical and striatal dopamine and acetylcholine release by glutamate mechanisms assayed in vivo with microdialysis: in situ stimulation with kainate-, quisqualate-and NMDA-receptor agonists

Abstract

Cortical and striatal dopamine and acetylcholine were measured in samples collected during microdialysis using Ringer or Ringer and kainic acid, quisqualic acid or N-methyl-D-aspartate as perfusion medium. In the striatum, kainic acid (10-5-10-3 M) increased dialysate dopamine (DA) in a dose dependent manner, while decreasing acetylcholine (ACh). In the cortex, kainic acid decreased DA, but increased ACh. Quisqualic acid and N-methyl-D-aspartate (10-310-4 M) moderately increased striatal DA, but increased ACh by more than 300%. The present results are in agreement with the idea of an excitatory regulation of striatal DA release by a glutamatergic pathway, with cell bodies located in the cortex and axons impinging on the ipsilateral DA terminals. It is probable that glutamate terminals have a stimulatory action on ACh neurons as well, since ACh was increased by NMDA and quisqualic acid, while DA release was only moderately increased.