PMID- 28614607 OWN - NLM STAT- MEDLINE DCOM- 20180423 LR - 20181128 IS - 1365-2826 (Electronic) IS - 0953-8194 (Linking) VI - 29 IP - 7 DP - 2017 Jul TI - Anatomical and functional implications of corticotrophin-releasing hormone neurones in a septal nucleus of the avian brain: an emphasis on glial-neuronal interaction via V1a receptors in vitro. LID - 10.1111/jne.12494 [doi] AB - Previously, we showed that corticotrophin-releasing hormone immunoreactive (CRH-IR) neurones in a septal structure are associated with stress and the hypothalamic-pituitary-adrenal axis in birds. In the present study, we focused upon CRH-IR neurones located within the septal structure called the nucleus of the hippocampal commissure (NHpC). Immunocytochemical and gene expression analyses were used to identify the anatomical and functional characteristics of cells within the NHpC. A comparative morphometry analysis showed that CRH-IR neurones in the NHpC were significantly larger than CRH-IR parvocellular neurones in the paraventricular nucleus of the hypothalamus (PVN) and lateral bed nucleus of the stria terminalis. Furthermore, these large neurones in the NHpC usually have more than two processes, showing characteristics of multipolar neurones. Utilisation of an organotypic slice culture method enabled testing of how CRH-IR neurones could be regulated within the NHpC. Similar to the PVN, CRH mRNA levels in the NHpC were increased following forskolin treatment. However, dexamethasone decreased forskolin-induced CRH gene expression only in the PVN and not in the NHpC, indicating differential inhibitory mechanisms in the PVN and the NHpC of the avian brain. Moreover, immunocytochemical evidence also showed that CRH-IR neurones reside in the NHpC along with the vasotocinergic system, comprising arginine vasotocin (AVT) nerve terminals and immunoreactive vasotocin V1a receptors (V1aR) in glia. Hence, we hypothesised that AVT acts as a neuromodulator within the NHpC to modulate activity of CRH neurones via glial V1aR. Gene expression analysis of cultured slices revealed that AVT treatment increased CRH mRNA levels, whereas a combination of AVT and a V1aR antagonist treatment decreased CRH mRNA expression. Furthermore, an attempt to identify an intercellular mechanism in glial-neuronal communication in the NHpC revealed that brain-derived neurotrophic factor (BDNF) and its receptor (TrkB) could be involved in the signalling mechanism. Immunocytochemical results further showed that both BDNF and TrkB receptors were found in glia of the NHpC. Interestingly, in cultured brain slices containing the NHpC, the use of a selective TrkB antagonist decreased the AVT-induced increase in CRH gene expression levels. The results from the present study collectively suggest that CRH neuronal activity is modulated by AVT via V1aR involving BDNF and TrkB glia in the NHpC. CI - (c) 2017 British Society for Neuroendocrinology. FAU - Nagarajan, G AU - Nagarajan G AD - The Center of Excellence for Poultry Science, University of Arkansas, Fayetteville, AR, USA. FAU - Jurkevich, A AU - Jurkevich A AD - Molecular Cytology Research Core Facility, University of Missouri, Columbia, MO, USA. FAU - Kang, S W AU - Kang SW AD - The Center of Excellence for Poultry Science, University of Arkansas, Fayetteville, AR, USA. FAU - Kuenzel, W J AU - Kuenzel WJ AUID- ORCID: 0000-0001-8312-4153 AD - The Center of Excellence for Poultry Science, University of Arkansas, Fayetteville, AR, USA. LA - eng PT - Journal Article PT - Research Support, Non-U.S. Gov't PL - United States TA - J Neuroendocrinol JT - Journal of neuroendocrinology JID - 8913461 RN - 0 (Brain-Derived Neurotrophic Factor) RN - 0 (Receptors, Vasopressin) RN - 1F7A44V6OU (Colforsin) RN - 7S5I7G3JQL (Dexamethasone) RN - 9015-71-8 (Corticotropin-Releasing Hormone) RN - EC 2.7.10.1 (Receptor, trkB) SB - IM MH - Animals MH - Brain-Derived Neurotrophic Factor/metabolism MH - Chickens MH - Colforsin/pharmacology MH - Corticotropin-Releasing Hormone/*metabolism MH - Dexamethasone/pharmacology MH - Gene Expression/drug effects MH - Hypothalamo-Hypophyseal System/metabolism MH - Male MH - Neuroglia/*metabolism MH - Neurons/*metabolism MH - Pituitary-Adrenal System/metabolism MH - Receptor, trkB/metabolism MH - Receptors, Vasopressin/*metabolism MH - Septal Nuclei/*metabolism OTO - NOTNLM OT - BDNF OT - CRH OT - TrkB OT - neurone-glia OT - receptor OT - vasotocin EDAT- 2017/06/15 06:00 MHDA- 2018/04/24 06:00 CRDT- 2017/06/15 06:00 PHST- 2017/03/30 00:00 [received] PHST- 2017/05/31 00:00 [revised] PHST- 2017/06/09 00:00 [accepted] PHST- 2017/06/15 06:00 [pubmed] PHST- 2018/04/24 06:00 [medline] PHST- 2017/06/15 06:00 [entrez] AID - 10.1111/jne.12494 [doi] PST - ppublish SO - J Neuroendocrinol. 2017 Jul;29(7). doi: 10.1111/jne.12494.