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  • Book
    edited by William J. Brock, Kenneth L. Hastings, and Kathy McGown.
    Contents:
    Introduction to the development of drugs / Kathy McGown
    ICH / Ken Hastings
    USFDA / Bill Brock
    Latin America : MERCOSUR countries / Cristiana Leslie Corra
    Canada / Mark T. Goldberg
    EMEA / Adam Woolley
    Africa / Fariza Feraoun
    China / Lijie Fu
    Japan / Kazuichi Nakamura
    India / K.S. Rao
    Australia / Doug Francis
    Chronic repeat dose testing / Shana Azri-Meehan
    Carcinogenicity / James Popp
    Genotoxicity / Mark Powley
    Developmental and reproductive toxicology / Robert Parker
    Juvenile testing and pediatric claim / Melissa Tassinari
    Immunotoxicology / Leigh Ann Burns Naas
    Biologics / Chris Ellis
    Vaccines / Robert House
    Phototoxicity and photocarcinogenicity / Chris Sambuco
    Degradants, impurities excipients, and metabolites / Bob Osterberg.
    Digital Access Wiley 2013
  • Article
    Kehr W, Speckenbach W, Zimmermann R.
    J Neural Transm. 1977;40(2):129-47.
    The interaction of (+)-amphetamine with haloperidol and gamma-butyrolactone on synthesis of monoamines in rat brain regions was investigated using an in vivo method, in which the accumulation of dopa and 5-hydroxytryptophan (5-HTP) was measured after inhibition of the aromatic amino acid decarboxylase by means of 3-hydroxybenzylhydrazine. The accumulation of 3-methoxytyramine (3-MT) after inhibition of the monoamine oxidase with pargyline was taken as an indicator of the in vivo release of dopamine (DA) into the extraneuronal space. (+)-Amphetamine at doses of 1--3 mg/kg caused an increase of dopa formation in the DA-rich areas c. striatum and mesolimbic forebrain but had no effect on dopa formation in neocortex and 5-HTP formation in all brain regions investigated. At a dose of 10 mg/kg (+)-amphetamine decreased dopa as well as 5-HTP formation in all brain regions studied. 3-MT accumulation in whole rat brain was stimulated by (+)-amphetamine as well as haloperidol and inhibited by gamma-butyrolactone. Combined treatment with haloperidol and (+)-amphetamine not only potentiated the stimulation of dopa formation but also the increase of 3-MT accumulation. Pretreatment with gamma-butyrolactone antagonized the stimulation of 3-MT formation induced by (+)-amphetamine at a dose of 10 mg/kg. This dose of (+)-amphetamine markedly counteracted the gamma-butyrolactone-induced increase in dopa formation especially in the DA-rich areas. The data support the view that impulse flow in DA neurons facilitates the effect of (+)-amphetamine on DA release and DA synthesis. Inhibition of catecholamine synthesis after high doses of (+)-amphetamine may be due to an increase in cytoplasmatic DA concentration causing end-product inhibition of tyrosine hydroxylase.
    Digital Access Access Options