Increased food intake following the manipulation of intracerebral dopamine levels with gamma-hydroxybutyrate.

The administration of gamma-hydroxybutyric acid (GHB) initially causes a temporary "sleep-like" state during which there is an increase in forebrain dopamine levels. The present series of experiments examined whether in the period following the GHB-induced behavioural depression, when accumulated dopamine is dispersed, there is any behavioural evidence of increased dopaminergic activity. The first experiment, in which GHB was injected directly into the cerebral ventricles, demonstrated that in the immediate post-recovery period rats exhibited various forms of stereotyped oral behaviour and stereotyped sniffing. Unexpectedly, it was also observed that if food were present animals preferred to eat. The nature of this feeding response was examined in two further experiments. Firstly, it was shown that in the period following the behavioural depression animals would perform, in a dose-dependent fashion, an operant response which was rewarded by food. Secondly, the GHB-induced increase in feeding was abolished by the pre-treatment of animals with either the dopamine synthesis inhibitor alpha-methyl-p-tyrosine, or the dopamine receptor blocker haloperidol. These data indicate that (i) in the period when it is known that the GHB-induced accumulation of dopamine is dispersing, there is behavioural evidence of increased dopaminergic activity; (ii) the feeding response is not a simple oral reflex; and (iii) in addition to being essential for food intake dopaminergic transmission may play a direct role in the production of feeding.