Immunohistochemical evidence of glutamatergic modulation of Nesfatin-1 neurons in the rat supraoptic nucleus during inflammatory stress.
TL;DR
Findings provide new immunohistochemical evidence linking glutamatergic transmission to stress-induced Nesfatin-1 activation, with potential implications for the neurobiological interaction between inflammation, energy homeostasis, and stress-related processes.
Abstract
Background
Stress triggers a complex network of neuroendocrine, immune, and behavioral responses aimed at maintaining homeostasis. Nesfatin-1, a hypothalamic peptide initially identified for its anorexigenic effects, has also been increasingly implicated in stress-related processes.
Methods
This study investigated whether acute inflammatory stress induced by lipopolysaccharide (LPS) activates Nesfatin-1 neurons in the supraoptic nucleus (SON) and examined the modulatory role of glutamatergic receptor antagonists. Female and male Sprague-Dawley rats were assigned to control, LPS, MK-801 + LPS, and CNQX + LPS groups. Neuronal activation was assessed using dual immunohistochemical staining for c-Fos and Nesfatin-1, followed by quantitative analysis of co-localized neurons in the SON.
Results
LPS administration significantly increased the proportion of c-Fos-positive Nesfatin-1 neurons in both female and male rats compared to controls (p = 0.001). Pretreatment with MK-801 and CNQX attenuated this activation (p < 0.01), indicating the involvement of both NMDA and non-NMDA glutamatergic pathways.
Conclusion
Acute inflammatory stress activates Nesfatin-1 neurons in the SON, and this response is modulated by glutamatergic signaling. These findings provide new immunohistochemical evidence linking glutamatergic transmission to stress-induced Nesfatin-1 activation, with potential implications for the neurobiological interaction between inflammation, energy homeostasis, and stress-related processes.