Anatomical and functional implications of CRH neurons in a septal nucleus of the avian brain: An emphasis on glial-neuronal interaction via V1a receptors in vitro

Abstract

Previously, we showed that corticotropin releasing hormone immunoreactive (CRH-ir) neurons in a septal structure are associated with stress and the hypothalamo-pituitary-adrenal axis in birds. In this study, we focused upon CRH-ir neurons 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 neurons in the NHpC were significantly larger than CRH-ir parvocellular neurons in the paraventricular nucleus of the hypothalamus (PVN) and lateral bed nucleus of the stria terminalis. Furthermore, these large neurons in the NHpC usually have more than two processes, showing characteristics of multipolar neurons. Utilizing an organotypic slice culture method enabled testing of how CRH-ir neurons 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 neurons reside in the NHpC along with the vasotocinergic system, comprising vasotocin (AVT) nerve terminals and immunoreactive vasotocin V1a receptors (V1aR) in glia. Hence, we hypothesized that AVT acts as a neuromodulator within the NHpC to modulate activity of CRH neurons via glial V1aR. Gene expression analysis of cultured slices revealed that AVT treatment increased CRH mRNA levels, whereas a combination of AVT and a V1a receptor 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 neurotropic factor (BDNF) and its receptor (TrkB) could be involved in the signaling 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, use of a selective TrkB antagonist decreased AVT induced increase in CRH gene expression levels. Results from this study collectively suggest that CRH neuronal activity is modulated by AVT via V1aR involving BDNF and TrkB glia in the NHpC.

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