Hot flashes (HF) caused by low estrogen in menopause result from changes in thermoregulatory processes in the hypothalamic preoptic area (POA). In the POA, transient receptor potential vanilloid 1 (TRPV1) participates in heat dissipation processes. Studies suggest that TRPV1 expression may be regulated by norepinephrine (NE)-activated α2-adrenergic receptors (α2-ADR) in the dorsal root ganglia. The goal of this study was to investigate the relationship between NE-regulated TRPV1 expression in the POA of ovariectomized rats and the development of HF.
Ninety female adult Sprague-Dawley rats were divided into three groups: SHAM, OVX and E2 (n = 30 per group). The numbers of TRPV1- and α2-ADR-positive cells and the expression of TRPV1 and α2-ADR in the POA of each group were determined using immunohistochemical staining after 4 weeks of estrogen treatment. Western blotting was used to detect the expression of TRPV1 and α2-ADR in the POA tissue, and NE content in the POA tissue was detected using high-performance liquid chromatography. In addition, the coexpression of TRPV1 and α2-ADR in POA neurons was investigated using immunofluorescent staining.
In the POA of ovariectomized rats, the number of TRPV1-positive cells and TRPV1 expression increased while NE content decreased. Concomitantly, the number of α2-ADR-positive cells and α2-ADR expression decreased. Estrogen treatment reversed these changes in the POA of ovariectomized rats. In addition, we found that TRPV1 and α2-ADR were coexpressed in POA neurons.
Under low-estrogen conditions, NE-activated α2-ADR regulated TRPV1 expression in the POA, and increased expression of TRPV1 may be an important factor for triggering HF.

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