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首页> 外文期刊>The European Journal of Neuroscience >Direct pyrogenic input from prostaglandin EP3 receptor-expressing preoptic neurons to the dorsomedial hypothalamus.
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Direct pyrogenic input from prostaglandin EP3 receptor-expressing preoptic neurons to the dorsomedial hypothalamus.

机译：从表达前列腺素EP3受体的视神经前神经元直接热源输入到背部丘脑下丘脑。

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摘要

Fever is induced by a neuronal mechanism in the brain. Prostaglandin (PG) E2 acts as a pyrogenic mediator in the preoptic area (POA) probably through the EP3 subtype of PGE receptor expressed on GABAergic neurons, and this PGE2 action triggers neuronal pathways for sympathetic thermogenesis in peripheral effector organs including brown adipose tissue (BAT). To explore pyrogenic efferent pathways from the POA, we determined projection targets of EP3 receptor-expressing POA neurons with a special focus on rat hypothalamic regions including the dorsomedial hypothalamic nucleus (DMH), which is known as a center for autonomic responses to stress. Among injections of cholera toxin b-subunit (CTb), a retrograde tracer, into hypothalamic regions at the rostrocaudal level of the DMH, injections into the DMH, lateral hypothalamic area (LH) and dorsal hypothalamic area (DH) resulted in EP3 receptor immunolabelling in substantial populations of CTb-labeled neurons in the POA. Bilateral microinjections of muscimol,a GABA(A) receptor agonist, into the DMH and a ventral region of the DH, but not those into the LH, inhibited thermogenic (BAT sympathetic nerve activity, BAT temperature, core body temperature and expired CO2) and cardiovascular (arterial pressure and heart rate) responses to an intra-POA PGE2 microinjection. Further immunohistochemical observations revealed a close association of POA-derived GABAergic axon swellings with DMH neurons projecting to the medullary raphe regions where sympathetic premotor neurons for febrile and thermoregulatory responses are localized. These results suggest that a direct projection of EP3 receptor-expressing POA neurons to the DMH/DH region mediates febrile responses via a GABAergic mechanism.
机译：发烧是由大脑的神经元机制引起的。前列腺素（PG）E2可能通过GABA能神经元上表达的PGE受体的EP3亚型在视前区（POA）中作为热介质，并且该PGE2作用触发了包括棕色脂肪组织（BAT）在内的周围效应器官中交感生热的神经元途径。 ）。为了探索POA的热源传出途径，我们确定了表达EP3受体的POA神经元的投射靶标，特别关注大鼠下丘脑区域，包括背侧丘脑下丘脑核（DMH），该区域被称为对压力的自主反应中心。在DMH的后丘脑水平向下丘脑区域注射逆行示踪剂霍乱毒素b亚基（CTb），向DMH，下丘脑外侧区域（LH）和后丘脑背面区域（DH）注射导致EP3受体免疫标记在POA中有大量CTb标记的神经元。向DMH和DH的腹侧区域双向注射muscimol，一种GABA（A）受体激动剂，但不向LH进行双侧显微注射，可抑制致热性（BAT交感神经活性，BAT温度，核心体温和CO2释放） POA内PGE2显微注射对心血管（动脉压和心率）的反应。进一步的免疫组织化学观察显示，POA衍生的GABA能轴突肿胀与DMH神经元投射到髓质网状区密切相关，髓质网状区是交感性前运动神经元对发热和体温调节反应的定位。这些结果表明，表达EP3受体的POA神经元直接投射到DMH / DH区将通过GABA能机制介导发热反应。

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