title: Evidence for suprachiasmatic vasopressin neurones innervating kisspeptin neurones in the rostral periventricular area of the mouse brain: regulation by oestrogen.
abstract: In rodents, a circadian signal from the suprachiasmatic nucleus (SCN) is essential for the pro-oestrous surge of gonadotrophin-releasing hormone (GnRH), which, in turn, induces luteinising hormone (LH) surge and ovulation. We hypothesised that kisspeptin (KP) neurones in the anteroventral periventricular and periventricular preoptic nuclei (AVPV/PeN) form part of the communication pathway between the SCN and GnRH neurones. In anterograde track tracing studies, we first identified vasopressin (VP)-containing axons of SCN origin in apposition to KP-immunoreactive (IR) neurones. Studies to quantify this input relied on the observation that VP-synthesising neurones in the SCN differ from other VP systems in their lack of galanin expression. In ovariectomised mice, 30.79 +/- 1.63% of KP-IR perikarya and proximal dendrites within the AVPV/PeN received galanin-negative VP-IR varicosities. Oestrogen-treatment significantly increased the number of KP-IR neurones, with their percentage apposed by galanin-negative VP-IR varicosities (46.95 +/- 1.88%) and the number of VP-IR appositions on individual KP-IR neurones. At the ultrastructural level, the VP-IR terminals formed symmetric synapses with KP-IR neurones, which was in accordance with the morphology of inhibitory synapses established by SCN neurones. By contrast to VP, vasoactive intestinal polypeptide (VIP), which is synthesised by a distinct subset of SCN neurones, occurred only rarely in axons apposed to KP-IR neurones. Altogether, our results are consistent with the hypothesis that KP neurones located in the mouse AVPV/PeN receive circadian information from the SCN via a vasopressinergic monosynaptic pathway, which is enhanced by oestrogen.
authors.affiliation: Laboratory of Endocrine Neurobiology, Institute of Experimental Medicine, Hungarian Academy of Sciences, Budapest, Hungary.
authors.forename: B
authors.initials: B
authors.lastname: Vida
authors.forename: L
authors.initials: L
authors.lastname: Deli
authors.forename: E
authors.initials: E
authors.lastname: Hrabovszky
authors.forename: T
authors.initials: T
authors.lastname: Kalamatianos
authors.forename: A
authors.initials: A
authors.lastname: Caraty
authors.forename: C W
authors.initials: CW
authors.lastname: Coen
authors.forename: Z
authors.initials: Z
authors.lastname: Liposits
authors.forename: I
authors.initials: I
authors.lastname: Kalló
mesh_terms: D000818:Animals; D001921:Brain / Q000187:drug effects* / Q000378:metabolism / Q000502:physiology; D004958:Estradiol / Q000494:pharmacology*; D005260:Female; D020646:Intralaminar Thalamic Nuclei / Q000378:metabolism / Q000502:physiology; D059648:Kisspeptins; D008297:Male; D051379:Mice; D009474:Neurons / Q000378:metabolism / Q000502:physiology*; D010835:Phytohemagglutinins / Q000493:pharmacokinetics; D013493:Suprachiasmatic Nucleus / Q000187:drug effects / Q000378:metabolism*; D013569:Synapses / Q000187:drug effects / Q000378:metabolism / Q000502:physiology; D025521:Tumor Suppressor Proteins / Q000378:metabolism*; D014667:Vasopressins / Q000378:metabolism*
chemical_list: C491407:Kiss1 protein, mouse; D059648:Kisspeptins; D010835:Phytohemagglutinins; D025521:Tumor Suppressor Proteins; C100156:leukoagglutinins, plants; D014667:Vasopressins; D004958:Estradiol