最近,，科學家研究發(fā)現(xiàn)了一種基因變體，攜帶這種基因的人比一般人更容易對香煙和毒品上隱,。研究發(fā)現(xiàn)：可卡因上癮者中,，25％的人攜帶有這種基因。這一發(fā)現(xiàn)對治愈可卡因上癮提供了很大的幫助,，科學家希望它用來防止想嘗試毒品的行為以及研發(fā)相關的手段,。
組織這項研究的德國曼海姆的精神衛(wèi)生研究中心的精神藥理學教授Rainer Spanagel說：“如果你是這種基因變體的攜帶者，對可卡因上癮的可能性就高,，這是你的弱點,。”他還說,，現(xiàn)在主要是采取勸導或保護的手段抵制攜帶者對可卡因的誘惑?？茖W家正在研制一種疫苗,，攜帶者注射后可降低對毒品的興奮度。（生物谷Bioon.com）
生物谷推薦原始出處：
PNAS November 11, 2008 doi: 10.1073/pnas.0803959105
Loss of the Ca2+/calmodulin-dependent protein kinase type IV in dopaminoceptive neurons enhances behavioral effects of cocaine
Ainhoa Bilbao, Jan Rodriguez Parkitna, David Engblom, Stéphanie Perreau-Lenz, Carles Sanchis-Segura, Miriam Schneider, Witold Konopka, Magdalena Westphal, Gerome Breen, Sylvane Desrivieres, Matthias Klugmann, Camila Guindalini, Homero Vallada, Ronaldo Laranjeira, Fernando Rodriguez de Fonseca, Gunter Schumann, Günther Schütz, and Rainer Spanagel
The persistent nature of addiction has been associated with activity-induced plasticity of neurons within the striatum and nucleus accumbens (NAc). To identify the molecular processes leading to these adaptations, we performed Cre/loxP-mediated genetic ablations of two key regulators of gene expression in response to activity, the Ca2+/calmodulin-dependent protein kinase IV (CaMKIV) and its postulated main target, the cAMP-responsive element binding protein (CREB). We found that acute cocaine-induced gene expression in the striatum was largely unaffected by the loss of CaMKIV. On the behavioral level, mice lacking CaMKIV in dopaminoceptive neurons displayed increased sensitivity to cocaine as evidenced by augmented expression of locomotor sensitization and enhanced conditioned place preference and reinstatement after extinction. However, the loss of CREB in the forebrain had no effect on either of these behaviors, even though it robustly blunted acute cocaine-induced transcription. To test the relevance of these observations for addiction in humans, we performed an association study of CAMK4 and CREB promoter polymorphisms with cocaine addiction in a large sample of addicts. We found that a single nucleotide polymorphism in the CAMK4 promoter was significantly associated with cocaine addiction, whereas variations in the CREB promoter regions did not correlate with drug abuse. These findings reveal a critical role for CaMKIV in the development and persistence of cocaine-induced behaviors, through mechanisms dissociated from acute effects on gene expression and CREB-dependent transcription.
