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Biotech / Medical : Ligand (LGND) Breakout! -- Ignore unavailable to you. Want to Upgrade?

To: Flagrante Delictu who wrote (22667)	6/24/1998 10:51:00 PM
From: jayhawk969	Read Replies (1) \| Respond to of 32384

(HSBM) >>...glow in the dark mice << psychedelic to boot All over the walls after they have exploded Fugazi could create the next fad for artists I want your first canvass fuzzyguy, 100 shares of LGND if you can figure out how to sign it.

To: Flagrante Delictu who wrote (22667)	6/25/1998 8:07:00 AM
From: Henry Niman	Respond to of 32384

Speaking of sex and mice: S31-3 GALANIN REGULATION OF THE LUTEINIZING HORMONE-RELEASING HORMONE NEURONAL NETWORK F. J. Lopez1, 1, Ligand Pharmaceuticals Inc., San Diego, CA, Various studies have demonstrated multiple regulatory roles for galanin (GAL) since the isolation of the peptide in 1983. Galanin has been implicated in the control of several aspects of reproduction. Acting at several sites, GAL has been shown to play a major role in the regulation of the ovulatory surge of LH. The peptide is released into the hypophyseal portal blood allowing direct access to galanin receptors in the anterior pituitary. These receptors could mediate the effects of the neuropeptide on basal and LHRH-induced LH secretion. Moreover, GAL has also been shown to enhance the release of LHRH from nerve terminals of the median eminence suggesting modulatory activities for the peptide at the level of the LHRH neuronal network. Galanin has also been localized in hypothalamic LHRH neurons of the rat and this co-localization of the peptides is regulated by estrogens. Estradiol increases the incidence of co-localization in adult females and adult neonatally orchidectomized males indicating that expression of GAL in LHRH neurons is sexually dimorphic and neonatally determined. Recent studies have indicated that testradiol enhances GAL gene expression in GT1-7 cells via interaction with an endogenous estrogen receptor (ER). Reverse transcriptase-PCR and subsequent sequencing of the amplification product indicates the presence of ERa mRNA in GT1-7 cells. This implicates ERa on the estradiol-dependent increase of GAL gene expression; however, ERb, if present in GT1-7 neurons, could also contribute to the observed effects. To ascertain the relative contribution of ERa versus other mechanisms including ERb on estradiol induction of pituitary GAL gene expression, we have utilized the ERa knockout (ERKO) mouse. Estradiol induces a robust increase in pituitary GAL gene expression in wild type animals. In contrast, the treatment did not alter pituitry GAL gene expression in the ERKO mice. Therefore, these data support the notion that the effect of estrogen on GAL gene expression in the anterior pituitary is ERa-dependent. Overall, GAL plays a physiological role in the events leading to the surge of gonadotropins. Estrogens, in turn, modulate GAL gene expression in both LHRH neurons and the anterior pituitary. Current evidence points to ERa as the mediator of estrogen-dependent GAL gene induction in the anterior pituitary and immortalized LHRH neurons. However, the contribution of ERb to the actions of estrogen on GAL gene expression in the hypothalamus is not completely defined. Presentation Date, Time, Room: 26-Jun-98, 9:30A, CC-37 L=Special Session, N=Nurse Symposium, OR=Oral, P=Poster, S=Symposium