Effect of unilateral nucleus basalis lesion on cortical and striatal acetylcholine and dopamine release monitored in vivo with microdialysis.

Cortical and striatal extracellular acetylcholine (ACh), choline (Ch), dopamine (DA) and dihydroxyphenylacetic acid (DOPAC) levels were estimated in samples collected with microdialysis in halothane-anaesthetized rats which had received 0.6 microliter of ibotenic acid (5 micrograms/microliters) into the left nucleus basalis magnocellularis (microdialysis experiments were performed 3-4 weeks after the lesion). Samples were collected under basal (Ringer or Ringer including 10 microM neostigmine) and KCl (100 mM)-stimulated conditions. In the intact frontoparietal cortex and striatum, basal ACh (only detected under neostigmine perfusion) was in the 30 and 300 nM range, respectively. In the same conditions, Ch was in the 0.7 microM range in the cortex and in the 0.2 microM range in the striatum. The inclusion of KCl in the perfusion medium strongly enhanced cortical (greater than 7-fold) and striatal (greater than 10-fold) ACh. KCl only moderately increased striatal (65%) but not cortical Ch. In the lesion side, both basal and stimulated ACh were significantly reduced in the cortex (greater than 60%), but not in the striatum. Ch was not significantly changed in the cortex and striatum. The nucleus basalis lesion also produced a drop in extracellular levels of cortical and striatal DA (40% and 55%, respectively). Neither cortical nor striatal ACh levels were modified by a unilateral DA deafferentation (6-hydroxydopamine lesion into the medial forebrain bundle). However, the destruction of the intrinsic cortical ACh by injection of kainic acid into the frontoparietal cortex produced a 30% decrease in ACh.