Effect of Brain Lesions and Chlorpromazine on Accumulation and Disappearance of Catecholamines Formed in vivo from14C‐Tyrosine

Abstract Rats were subjected to a unilateral stereotaxic lesion at the level of the mesencephalic‐hypothalamic junction where the nigro‐striatal dopamine (DA) pathway is known to pass. Between 6 and 18 h after the lesion the level of DA in the striatum on the same side was increased by about 50 per cent. Between 18 and 48 h after the lesion the content of DA declined to 15 per cent of that of the contralateral striatum and stayed at this low level during the following 6 days. The content of noradrenaline (NA) tended to be increased 24 h after the lesion but no change was found on the following days. The accumulation and disappearance of14C‐DA formed from14C‐tyrosine in the striatum 12–24 h after the nigral lesion were decreased on the lesion side in comparison with the contralateral side. The accumulation and disappearance of14C‐NA did not differ between the 2 sides. Chlorpromazine accelerated both accumulation and disappearance of14C‐DA in the striatum on the side contralateral to the lesion but not in the striatum of the lesion side. In animals with a unilateral lesion above the DA pathway, in the posterior thalamus, chlorpromazine accelerated the accumulation of14C‐DA on both sides. The accumulation of14C‐XA in the striatum was increased by chlorpromazine on the intact side following both types of lesions. The disappearance of14C‐NA, however, was not influenced by the drug. The results are taken as evidence that chlorpromazine accelerates DA turnover in the striatum by activating the nerve impulse flow in the nigro‐striatal DA pathway.