Effect of Brain Lesions and Chlorpromazine on Accumulation and Disappearance of Catecholamines Formed in vivo from 14C-Tyrosine

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 of ¹⁴C-DA formed from ¹⁴C-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 of ¹⁴C-NA did not differ between the 2 sides. Chlorpromazine accelerated both accumulation and disappearance of ¹⁴C-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 of ¹⁴C-DA on both sides. The accumulation of ¹⁴C-XA in the striatum was increased by chlorpromazine on the intact side following both types of lesions. The disappearance of ¹⁴C-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.