1. Dear Drugs-Forum readers: We are a small non-profit that runs one of the most read drug information & addiction help websites in the world. We serve over 4 million readers per month, and have costs like all popular websites: servers, hosting, licenses and software. To protect our independence we do not run ads. We take no government funds. We run on donations which average $25. If everyone reading this would donate $5 then this fund raiser would be done in an hour. If Drugs-Forum is useful to you, take one minute to keep it online another year by donating whatever you can today. Donations are currently not sufficient to pay our bills and keep the site up. Your help is most welcome. Thank you.
    PLEASE HELP

Receptor Mediation of Different In Vivo Effects of γ-Butyrolactone

Receptor Mediation of Different In Vivo Effects of γ-Butyrolactone

  1. Guigz
    From 1C.N.R. Institute of Neuroscience, Cagliari, Viale Armando Diaz 182, I-09126, Cagliari, Italy.

    2008 The Japanese Pharmacological Society.

    The endogenous brain constituent, γ-hydroxybutyric acid (GHB), as well as its prodrug, γ-butyrolactone (GBL), have recently gained interest in the drug addiction field due to
    their abuse potential and fatalities caused by overdose. It is known that GHB has two sites of
    actions: the γ-aminobutyric acidB (GABAB) receptor and a specific-GHB binding site. The
    present study was designed to extend to GBL the investigations on the contribution of the
    GABAB receptor and the specific-GHB binding site to its in vivo effects. To this aim, DBA mice
    were pretreated either with GABAB-receptor antagonists, (3-aminopropyl)(diethoxymethyl)phosphinic
    acid (CGP 35348) and (2S)(+)-5,5-dimethyl-2-morpholineacetic acid (SCH 50911), or a
    putative antagonist of the specific-GHB binding site, 6,7,8,9-tetrahydro-5-hydroxy-5H-benzocyclohept-
    6-ylideneacetic acid (NCS-382), prior to the administration of doses of GBL that
    induced hypothermia, motor-incoordination (measured as motor-impairment at the Rota-Rod
    task), and sedation/hypnosis. The capability of SCH 50911 and NCS-382 to protect against
    GBL-induced lethality was also investigated. Pretreatment with either GABAB-receptor antagonist
    completely prevented GBL-induced hypothermia, motor-incoordination, and sedation
    /hypnosis. SCH 50911 also provided complete protection against GBL-associated lethality. Vice
    versa, NCS-382 failed to exert any antagonistic or protective effect. These results suggest that
    the in vivo GBL effects tested in the present study are mediated by activation of the GABAB
    receptor.
Tags: