ArticleScientific reports2024
Raphe glucose-sensing serotonergic neurons stimulate KNDy neurons to enhance LH pulses via 5HT2CR: rat and goat studies.
Article in Scientific reports, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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Who cites it
7 citing papers in PubMed.
- Establishment and Characterization of a Brain-Derived Cell Line from Japanese Eel (Animals : an open access journal from MDPI · 2026Article
- Neurokinin receptor antagonists for vasomotor symptoms: from KNDy neurons to clinical translation.Nature reviews. Endocrinology · 2026Review
- Robust serotonin activation of the kisspeptin GnRH pulse generator in male and female mice.Endocrinology · 2026Article
- Neuroendocrine mechanisms leading to novel control techniques of reproduction in livestock: Regulation of the GnRH pulse generator activity.The Journal of reproduction and development · 2026Review
- Citalopram-induced decrease of CLOCK-ir and BMAL1-ir kisspeptin neurons in the anteroventral periventricular nucleus of adult male mice.IBRO neuroscience reports · 2025Article
- Sexually dimorphic distribution of Kiss1 neurons in the bed nucleus of the stria terminalis.Journal of neuroendocrinology · 2025Article
- Malnutrition alters protein expression of KNDy neuropeptides in the arcuate nucleus of mature ewes.Frontiers in physiology · 2024Article
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12 authors.
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Abstract
Dysfunction of central serotonergic neurons is known to cause depressive disorders in humans, who often show reproductive and/or glucose metabolism disorders. This study examined whether dorsal raphe (DR) serotonergic neurons sense high glucose availability to upregulate reproductive function via activating hypothalamic arcuate (ARC) kisspeptin neurons (= KNDy neurons), a dominant stimulator of gonadotropin-releasing hormone (GnRH)/gonadotropin pulses, using female rats and goats. RNA-seq and histological analysis revealed that stimulatory serotonin-2C receptor (5HT2CR) was mainly expressed in the KNDy neurons in female rats. The serotonergic reuptake inhibitor administration into the mediobasal hypothalamus (MBH), including the ARC, significantly blocked glucoprivic suppression of luteinizing hormone (LH) pulses and hyperglycemia induced by intravenous 2-deoxy-D-glucose (2DG) administration in female rats. A local infusion of glucose into the DR significantly increased in vivo serotonin release in the MBH and partly restored LH pulses and hyperglycemia in the 2DG-treated female rats. Furthermore, central administration of serotonin or a 5HT2CR agonist immediately evoked GnRH pulse generator activity, and central 5HT2CR antagonism blocked the serotonin-induced facilitation of GnRH pulse generator activity in ovariectomized goats. These results suggest that DR serotonergic neurons sense high glucose availability to reduce gluconeogenesis and upregulate reproductive function by activating GnRH/LH pulse generator activity in mammals.
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