Our study explores the role of the CB1 receptor in age-related changes in the ventromedial hypothalamic nucleus (VMH), a key brain region for neuroendocrine regulation.
We used stereotaxic injections in mice to delete or restore the CB1 receptor in the VMH.
We found that site-specific deletion of the CB1 receptor led to increased local pro-inflammatory glial activity and higher expression of insulin-like growth factor-1 receptor (Igf1r) mRNA in the hypothalamus, though gonadotropin-releasing hormone (GnRH) levels were unaffected. Conversely, restoring CB1 in CB1-deficient mice reduced inflammation and decreased Igf1r expression, also without affecting GnRH production.
Our findings suggest that the CB1 receptor in the VMH plays a crucial role in mitigating age-related inflammation and modulating IGF-1R signaling