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Estrogen Receptor Immunoreactivity Is Present in the Majority of Central Histaminergic Neurons: Evidence for a New Neuroendocrine Pathway Associated with Luteinizing Hormone-Releasing Hormone-Synthesizing Neurons in Rats and Humans¹

Institute of Experimental Medicine (Cs.F., E.H., Zs.L.), Hungarian Academy of Sciences, Budapest, Hungary; Biomedical Sciences Division (P.H.S., F.R.A.C., C.W.C.), King’s College, London, United Kingdom; Department of Anatomy (I.K., E.D., E.M.), Albert Szent-Györgyi Medical University, Szeged, Hungary, The Women’s Health Research Institute (P.J.S., I.M.), Wyeth-Ayerst Research, Radnor, Pennsylvania; Department of Molecular Biology (H.O.), Nagoya City University School of Medicine, Nagoya, Japan; Department of Biology (P.P.), Abo Akademi University, Turku, Finland; Department of Membrane Biochemistry (L.B.), Walter Reed Army Institute for Research, Washington D.C.

Address all correspondence and requests for reprints to: Dr. Zsolt Liposits, Institute of Experimental Medicine, Hungarian Academy of Sciences, 1083 Budapest, Szigony u. 43, Hungary. E-mail: liposits{at}koki.hu

The central regulation of the preovulatory LH surge requires a complex sequence of interactions between neuronal systems that impinge on LH-releasing hormone (LHRH)-synthesizing neurons. The reported absence of estrogen receptors (ERs) in LHRH neurons indicates that estrogen-receptive neurons that are afferent to LHRH neurons are involved in mediating the effects of this steroid. We now present evidence indicating that central histaminergic neurons, exclusively located in the tuberomammillary complex of the caudal diencephalon, serve as an important relay in this system. Evaluation of this system revealed that 76% of histamine-synthesising neurons display ER-immunoreactivity in their nucleus; furthermore histaminergic axons exhibit axo-dendritic and axo-somatic appositions onto LHRH neurons in both the rodent and the human brain. Our in vivo studies show that the intracerebroventricular administration of the histamine-1 (H1) receptor antagonist, mepyramine, but not the H2 receptor antagonist, ranitidine, can block the LH surge in ovariectomized estrogen-treated rats. These data are consistent with the hypothesis that the positive feedback effect of estrogen in the induction of the LH surge involves estrogen-receptive histamine-containing neurons in the tuberomammillary nucleus that relay the steroid signal to LHRH neurons via H1 receptors.

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