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Altered Brain Serotonin Homeostasis and Locomotor Insensitivity to 3,4-Methylenedioxymethamphetamine
 

Summary: Altered Brain Serotonin Homeostasis and Locomotor
Insensitivity to 3,4-Methylenedioxymethamphetamine
("Ecstasy") in Serotonin Transporter-Deficient Mice
DIETMAR BENGEL, DENNIS L. MURPHY, ANNE M. ANDREWS, CHRISTINE H. WICHEMS, DOUGLAS FELTNER,
ARMIN HEILS, RAINALD M ¨OSSNER, HEINER WESTPHAL, and KLAUS-PETER LESCH
Laboratory of Clinical Science, National Institute of Mental Health, Bethesda, Maryland 20892-1264 (D.B., D.L.M., A.M.A., C.H.W.), Laboratory
of Mammalian Genes and Development, National Institute of Child Health and Human Development, Bethesda, Maryland 20982 (D.F., H.W.),
Department of Psychiatry, University of Wu¨ rzburg, 97080 Wu¨ rzburg, Germany (A.H., R.M., K.-P.L.)
Received August 1, 1997; Accepted December 8, 1997 This paper is available online at http://www.molpharm.org
ABSTRACT
The sodium-dependent, high affinity serotonin [5-hydroxytryp-
tamine (5-HT)] transporter (5-HTT) provides the primary mech-
anism for inactivation of 5-HT after its release into the synaptic
cleft. To further evaluate the function of the 5-HTT, the murine
gene was disrupted by homologous recombination. Despite
evidence that excess extracellular 5-HT during embryonic de-
velopment, including that produced by drugs that inhibit the
5-HTT, may lead to severe craniofacial and cardiac malforma-
tions, no obvious developmental phenotype was observed in
the 5-HTT /

  

Source: Andrews, Anne M. - Huck Institutes of the Life Sciences, Pennsylvania State University

 

Collections: Biology and Medicine