Repeated asenapine treatment does not participate in the mild stress induced FosB/ΔFosB expression in the rat hypothalamic paraventricular nucleus neurons

Effect of repeated asenapine (ASE) treatment on FosB/Delta FosB expression was studied in the hypothalamic paraventricular nucleus (PVN) of male rats exposed to chronic mild stress (CMS) for 21 days. Our intention was to find out whether repeated ASE treatment for 14 days may: 1) induce FosB/Delta FosB expression in the PVN; 2) activate selected PVN neuronal phenotypes, synthesizing oxytocin (OXY), vasopressin (AVP), corticoliberin (CRH) or tyrosine hydroxylase (TH); and 3) interfere with the impact of CMS. Control, ASE, CMS, and CMS + ASE treated groups were used. CMS included restraint, social isolation, crowding, swimming, and cold. From the 7th day of CMS, rats received ASE (03 mg/kg) or saline (300 mu l/rat) subcutaneously, twice a day for 14 days. They were sacrificed on the day 22nd (16-18 h after last treatments). FosB/Delta FosB was visualized with avidin biotin peroxidase complex and OXY, AVP, CRH or TH antibodies by fluorescent dyes. Saline and ASE did not promote FosB/Delta FosB expression in the PVN. CMS and CMS + ASE elicited FosB/Delta FosB-expression in the PVN, whereas, ASE did not augment or attenuate FosB/Delta FosB induction elicited by CMS. FosB/Delta FosB-CRH occurred after CMS and CMS + ASE treatments in the PVN middle sector, while FosB/Delta FosB-AVP and FosB/Delta FosB-OXY after CMS and CMS + ASE treatments in the PVN posterior sector. FosB/Delta FosB-TH colocalization was rare. Larger FosB/Delta FosB profiles, running above the PVN, did not show any colocalizations. The study provides an anatomical/functional knowledge about an unaccented nature of prolonged ASE treatment at the level of PVN and excludes its positive or negative interplay with CMS effect. Data indicate that long-lasting ASE treatment might not act as a stressor acting at the PVN level. (C) 2016 Elsevier Ltd. All rights reserved.