Oxytocin-containing neurons in the hypothalamic parvicellular paraventricular nucleus of the jerboa: no plasticity related to acute immobilization.

OBJECTIVES AND METHODS: The presence of oxytocin (OT) and its putative participation to the phenotypic plasticity of CRH neurones in the stressed jerboa was investigated. We analysed by immunocytochemistry the OT expression within the hypothalamic parvicellular paraventricular nucleus (pPVN) of male jerboas submitted to an acute immobilization (30 min). RESULTS: OT presence was clearly demonstrated in the pPVN of the jerboa and no significant difference in the number of OT immunolabeled cells was observed whatever the experimental conditions. Interestingly, CRH-immunoreactive neurons coexpressed OT within cell bodies and terminals in a similar way both in control and stressed animals. The level of coexpression was regionally heterogeneous and was not sensitive to the stress immobilization. CONCLUSION: The present data reveal for the first time the occurrence of OT in hypothalamic pPVN neurons of the jerboa. Moreover, this OT expression level does not change upon an acute immobilization stress. These new data, coupled together with our previous work in the jerboa, incontestably establish a clear dichotomy between a stress-responsive CRH/CCK system and a stress non-responsive OT/VP system in the pPVN.

Specific localization of signal transducer and activator of transcription 1 immunoreactivity in oxytocin neurons of the rat hypothalamus.

The transcription factor STAT1 participates in signaling pathways and cellular responses triggered by several cytokines, growth factors and hormones. The present work demonstrates for the first time the immunohistochemical distribution of STAT1 in the rat hypothalamus. STAT1 immunoreactivity was observed in somas, dendrites and axons of neurons throughout the supraoptic and paraventricular nuclei and co-localized specifically with oxytocin. These findings indicate that STAT1 is positioned to participate in specific neuroendocrine regulation in the nonpathological rat brain.

Paraventricular nucleus neurons producing neurotensin after lipopolysaccharide treatment project to the median eminence.

Inflammation consists in secretion of cytokines that stimulate the hypothalamo-pituitary-adrenal (HPA) axis to release the anti-inflammatory corticosterone. Upstream in this axis are corticotropin-releasing hormone (CRH) neurons in the paraventricular nucleus (PVN) whose multipeptidergic phenotype changes: both corticotropin-releasing hormone mRNAs and neurotensin mRNAs are up-regulated. Combining in situ hybridization with a retrograde neuronal marker, we demonstrated that neurotensin-containing neurons in the paraventricular nucleus project to the median eminence.

Glucocorticoids down-regulate lipopolysaccharide-induced de novo production of neurotensin mRNA in the rat hypothalamic, paraventricular, corticotrophin-releasing hormone neurons.

OBJECTIVE: Intraperitoneal injection of the endotoxin lipopolysaccharide (LPS) produces inflammation accompanied by activation of the immune system and the secretion of cytokines. Cytokines stimulate the hypothalamo-pituitary-adrenal (HPA) axis to release the anti-inflammatory corticosterone which controls its own production by acting on the HPA axis. Upstream in the HPA axis are neuroendocrine corticotrophin-releasing hormone (CRH) neurons located in the paraventricular nucleus (PVN), whose multipeptidergic phenotype changes during inflammation: while CRH mRNA is up-regulated in these conditions, neurotensin (NT) mRNA expression is induced de novo. The negative feedback control of glucocorticoids on CRH production is well documented; however, their action on NT production in the PVN of the hypothalamus is poorly documented. The aim of this study was to determine if glucocorticoids modulate the de novo production of NT during inflammation. METHODS: Using quantitative in situ hybridization histochemistry, we examined whether the absence (adrenalectomy) or excess (corticosterone implants) of glucocorticoids modulate de novo production of NT mRNA in the PVN during inflammation induced by LPS treatment. RESULTS: A relatively low dose of LPS (50 microg/kg) that is not efficient to induce NT mRNA production in the PVN becomes efficient after adrenalectomy. Moreover, corticosterone excess reduces LPS-induced production of NT mRNA in the PVN. CONCLUSION: Glucocorticoids exert a negative control on NT mRNA production in the PVN of the hypothalamus, and this effect requires that NT mRNA production be triggered, such as during inflammation.