ENVIRONMENTALLY-INDUCED CHANGES IN PERIPHERAL BENZODIAZEPINE RECEPTORS ARE STRESSOR AND TISSUE-SPECIFIC

The stress-induced changes in peripheral benzodiazepine receptors (PBR ) can be observed in a number of different tissues, depending upon the nature and chronicity of the aversive experience. In addition, virtua lly all stress procedures that cause rapid changes in PBR simultaneous ly increase the physical activity or metabolic rate of the subjects. T he present study analyzed the contributions of rapid alterations in ac tivity or metabolic rate with and without aversive stimulation and the ir subsequent impact on PBR. Mechanically induced increases in activit y by forced running stress results in a significant reduction in [H-3] Ro 5-4864 binding to PBR in olfactory bulb, opposite to the PBR change s in this tissue following forced cold-water swim stress. Pharmacologi cal induction of increased locomotor activity as well as metabolic rat e by d-amphetamine causes a significant increase in cardiac PBR bindin g, again, opposite to the response typically observed following inesca pable shock stress. Finally, administration of the anxiogenic beta-car boline, FG-7142, causes increases in both hippocampus and adrenal glan d PBR binding reminiscent of acute noise stress exposure. These experi ments demonstrate that increased locomotor activity or metabolic rate alone is not a necessary and sufficient condition for previous stress- induced changes in PBR. Conversely, increased metabolic rate coupled w ith an aversive stimulus appears to be an important factor for inducin g stress-like changes in PBR. This data, coupled with previous reports , suggests that rapid alterations in these sites are stressor and tiss ue dependent. Finally, we propose that the PBR may be involved in many aspects of the stress response including: a) a biowarning system in a drenal gland, b) participation in stress-induced hypertension via rena l PBR, and c) a modulator of stress-induced immunosuppression and subs equent recovery of function or recuperation by actions on immune cells .