Biochemical Effects of Baclofen (β‐Parachlorophenyl‐GABA) on the Dopamine and the Noradrenaline in the Rat Brain

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Abstract
Baclofen (fi-parachlorophenyl-GABA) caused an increase in the concentration of dopamine in the rat brain with a maximum of about 170 % of the control value after 1 hr and after doses of 50 mg/kg or more intraperitoneally. The α-methyltyrosine-induced disappearance of dopamine was inhibited to about the same extent in the corpus striatum and in the limbic system by baclofen. The accumulation of DOPA following decarboxylase inhibition was stimulated more in the corpus striatum than in the limbic system by baclofen, thus accounting for the fact that the concentration of dopamine was elevated about three times as much in the corpus striatum as in the limbic system. Amphetamine almost completely inhibited the rise in dopamine produced by baclofen. Baclofen did not cause any consistent changes in the concentration, the synthesis and the utilization of noradrenaline. These effects of baclofen are similar to those described following gammahydroxybutyric acid or axotomy. Hence, baclofen might also interrupt the nerve impulse flow in central dopamine neurones, perhaps by stimulating a central GABA mechanism.