title: Peripheral benzodiazepine receptors in cerebral cortex, but not in internal organs, are increased following inescapable stress and subsequent avoidance/escape shuttle-box testing.
abstract: Stress-induced alterations in peripheral benzodiazepine receptor (PBR) density have been reported in humans and in rats. However, the PBR response is highly specific, and its function remains largely unexplained. The aim of the present study was to investigate the relationship between behavior in the two-way active avoidance paradigm (2WAA) and post-test PBR densities in adrenal, testis, kidney, and cerebral cortex. Adult male Wistar rats were tested in the 2WAA either in the naive state (AA) or 24 h following shock preexposure (PE), known to interfere with avoidance/escape response acquisition, and decapitated immediately after testing. Control subjects were decapitated without experimental experience. The stressful characteristic of the experiment was validated by significantly increased post-test corticosterone levels in AA and PE subjects compared with controls, with a trend towards higher corticosterone levels in PE relative to AA rats. Similarly, PE compared with AA subjects tended to show retarded acquisition of the escape/avoidance response. PBR densities in adrenal, kidney, and testis and central benzodiazepine receptors (CBR) in the cerebral cortex remained unaffected by avoidance testing. Cerebral cortex PBR density was significantly increased in PE subjects. These findings suggest that avoidance testing, although stressful to the animals, led to changes confined to cerebral cortex PBR, indicating that the hypothalamic-pituitary-adrenal (HPA) response occurs independently of the PBR response in peripheral organs, and also suggest that the opportunity for coping alters the impact of the stressor on the subject and prevents the expression of PBR response in peripheral organs.
authors.affiliation: Laboratory of Behavioural Biology, Swiss Federal Institute of Technology, Schwerzenbach, Switzerland.
authors.forename: J
authors.initials: J
authors.lastname: Lehmann
authors.forename: R
authors.initials: R
authors.lastname: Weizman
authors.forename: C R
authors.initials: CR
authors.lastname: Pryce
authors.forename: S
authors.initials: S
authors.lastname: Leschiner
authors.forename: I
authors.initials: I
authors.lastname: Allmann
authors.forename: J
authors.initials: J
authors.lastname: Feldon
authors.forename: M
authors.initials: M
authors.lastname: Gavish
mesh_terms: D000311:Adrenal Glands / Q000378:metabolism; D000818:Animals; D000970:Antineoplastic Agents / Q000378:metabolism; D001362:Avoidance Learning / Q000502:physiology*; D001921:Brain / Q000378:metabolism; D002540:Cerebral Cortex / Q000378:metabolism*; D003345:Corticosterone / Q000097:blood*; D005442:Flumazenil / Q000378:metabolism; D018757:GABA Modulators / Q000378:metabolism; D007546:Isoquinolines / Q000378:metabolism; D007668:Kidney / Q000378:metabolism; D008297:Male; D051381:Rats; D017208:Rats, Wistar; D011963:Receptors, GABA-A / Q000378:metabolism*; D013312:Stress, Physiological / Q000378:metabolism*; D013737:Testis / Q000378:metabolism
chemical_list: D000970:Antineoplastic Agents; D018757:GABA Modulators; D007546:Isoquinolines; D011963:Receptors, GABA-A; D005442:Flumazenil; D003345:Corticosterone; C037850:PK 11195