Background

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.

Methods

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.

Results

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.

Conclusions

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.

中文翻译：

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NE依赖的α2-ADR调节去卵巢大鼠POA中TRPV1表达的变化可能与潮热有关。

背景

绝经期雌激素水平低引起的潮热（HF）是由下丘脑前视区（POA）的温度调节过程变化引起的。在POA中，瞬态受体电位香草醛1（TRPV1）参与散热过程。研究表明，TRPV1的表达可能受到背根神经节中去甲肾上腺素（NE）激活的α2-肾上腺素能受体（α2-ADR）的调节。这项研究的目的是调查去卵巢大鼠POA中NE调节的TRPV1表达与HF发生之间的关系。

方法

将90只成年雌性Sprague-Dawley大鼠分为三组：SHAM，OVX和E2（每组n = 30）。雌激素治疗4周后，采用免疫组织化学染色法检测各组POA中TRPV1-和α2-ADR阳性细胞数以及TRPV1和α2-ADR表达。用蛋白质印迹法检测POA组织中TRPV1和α2-ADR的表达，并用高效液相色谱法检测POA组织中NE的含量。另外，使用免疫荧光染色研究了TRPV1和α2-ADR在POA神经元中的共表达。

结果

在去卵巢大鼠的POA中，TRPV1阳性细胞数量和TRPV1表达增加，而NE含量降低。同时，α2-ADR阳性细胞数量和α2-ADR表达下降。雌激素治疗逆转了去卵巢大鼠POA中的这些变化。此外，我们发现TRPV1和α2-ADR在POA神经元中共表达。

结论

在低雌激素条件下，NE激活的α2-ADR调节了POA中TRPV1的表达，而TRPV1的表达增加可能是触发HF的重要因素。