AMYGDALOID CENTRAL NUCLEUS LESIONS AND CHOLINERGIC BLOCKADE ATTENUATETHE RESPONSE OF THE RENAL PERIPHERAL BENZODIAZEPINE RECEPTOR TO STRESS

Previous research has demonstrated that the density of peripheral benz odiazepine receptors (PBR) in rat kidney rapidly drops following expos ure to 80 min of stress. The present experiments examined the contribu tion of the central and autonomic nervous systems in mediating this ef fect. Ibotenic acid lesions of the amygdaloid central nucleus (ACe), b ut not the lateral and basolateral amygdala, diminished the magnitude of the reduction in renal PBR binding caused by stress. Pretreating ra ts with methyl-scopolamine also inhibited the response of the PBR to s tress. Adrenergic blockade with nadolol was ineffective. In order to t est whether the PBR was under direct or indirect neural control during stress, unilateral renal denervation was performed. The stress-induce d reduction in PBR binding persisted in denervated kidneys revealing t hat any neural control over the PBR that might exist must be indirect. Together the results suggest that the CNS may be involved in regulati ng the PBR during stress through the activation of intermediate, possi bly hormonal, factors. The involvement of the central nervous system i n the modulation of the PBR indicates the relevance of the PBR to phys iological adaptations to stress.