BRAIN-STEM MEDIATES DIAZEPAM ENHANCEMENT OF PALATABILITY AND FEEDING - MICROINJECTIONS INTO 4TH VENTRICLE VERSUS LATERAL VENTRICLE

The hypothesis that benzodiazepine-induced hyperphagia is due to a spe cific enhancement of the palatability of foods has been supported by p revious 'taste reactivity' studies of affective (hedonic and aversive) reactions to taste palatability. Diazepam and chlordiazepoxide enhanc e hedonic reactions of rats (rhythmic tongue protrusions, etc.) to swe et tastes in a receptor-specific fashion. A role for brainstem circuit s has been indicated by a previous demonstration of the persistence of the taste reactivity enhancement by diazepam after midbrain decerebra tion. The present study examined whether benzodiazepine brainstem rece ptors are the chief substrates for palatability enhancement even in in tact brains. We compared the effectiveness of benzodiazepine microinje ctions to elicit feeding and enhance hedonic reactions when delivered into either the lateral ventricle (forebrain) or the fourth ventricle (brainstem) of rats. The results show diazepam is reliably more effect ive at eliciting feeding and enhancing positive hedonic reactions to o ral sucrose when microinjections are made in the fourth ventricle than in the lateral ventricle. We conclude that brainstem neural systems c ontaining benzodiazepine-GABA receptors are likely to be the chief sub strates for benzodiazepine-induced palatability enhancement.