Article ID | Journal | Published Year | Pages | File Type |
---|---|---|---|---|
8633794 | Neuropeptides | 2017 | 9 Pages |
Abstract
Effect of repeated asenapine (ASE) treatment on FosB/ÎFosB 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/ÎFosB 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 (0.3 mg/kg) or saline (300 μl/rat) subcutaneously, twice a day for 14 days. They were sacrificed on the day 22nd (16-18 h after last treatments). FosB/ÎFosB was visualized with avidin biotin peroxidase complex and OXY, AVP, CRH or TH antibodies by fluorescent dyes. Saline and ASE did not promote FosB/ÎFosB expression in the PVN. CMS and CMS + ASE elicited FosB/ÎFosB-expression in the PVN, whereas, ASE did not augment or attenuate FosB/ÎFosB induction elicited by CMS. FosB/ÎFosB-CRH occurred after CMS and CMS + ASE treatments in the PVN middle sector, while FosB/ÎFosB-AVP and FosB/ÎFosB-OXY after CMS and CMS + ASE treatments in the PVN posterior sector. FosB/ÎFosB-TH colocalization was rare. Larger FosB/ÎFosB 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.
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Authors
Alexander Kiss, Zuzana Majercikova,