神经传递
能量稳态
终纹
雌激素受体
探地雷达
长时程增强
抑制性突触后电位
生物
内分泌学
内科学
γ-氨基丁酸受体
内大麻素系统
突触可塑性
受体
神经科学
化学
下丘脑
生物化学
医学
癌症
肥胖
乳腺癌
作者
James Gardner Gregory,Emily R. Hawken,Staci Angelis,Jean‐François Bouchard,Éric C. Dumont
标识
DOI:10.1016/j.psyneuen.2019.03.030
摘要
17ß-Estradiol (E2) is a potent neuromodulator capable of producing changes in inhibitory synaptic transmission by either changing pre-synaptic GABA release or post-synaptic GABAA receptor function. Physiologically, E2 is important for energy homeostasis, influencing food consumption, body weight, adipose tissue metabolism and energy expenditure. E2 may influence energy homeostasis through estrogen receptor-rich regions such as the oval bed nucleus of the stria-terminalis (ovBNST). However, the neurophysiological effects of estradiol within the ovBNST remain largely unknown. Understanding how E2 affects inhibitory transmission may elucidate the ovBNST's contribution to energy homeostasis. Here, using brain slice electrophysiology, we saw that E2 produced a long-term potentiation (LTP) of GABAA synaptic transmission (LTPGABA) in the ovBNST in male rats. E2 acted on estrogen receptors α and G-protein coupled estrogen receptors (GPER), involved protein kinase activation and required an intact endocannabinoid system. The effects of E2 in males were sensitive to 24 h of food deprivation. In females, E2 was 100-fold more potent at producing LTPGABA ovBNST compared to male rats and involved all three known subtypes of estrogen receptors (ERα, ERß, and GPER). These results demonstrate that E2 is a potent neuromodulator of inhibitory synaptic transmission within the ovBNST of both sexes to potentially regulate energy homeostasis.
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