新一期英國(guó)《自然》(Nature)雜志一篇研究報(bào)告說,，動(dòng)物實(shí)驗(yàn)顯示,，可卡因成癮與腦部特定區(qū)域神經(jīng)元活動(dòng)偏弱有關(guān)，刺激這一區(qū)域有助于減少對(duì)可卡因的依賴,。這一成果為開發(fā)戒毒新方法提供了思路,。
美國(guó)國(guó)家吸毒研究所研究人員報(bào)告說，他們對(duì)可卡因成癮的實(shí)驗(yàn)鼠大腦進(jìn)行研究后發(fā)現(xiàn),，這些實(shí)驗(yàn)鼠大腦前額葉皮質(zhì)的某一區(qū)域神經(jīng)元活動(dòng)明顯偏弱,。此前研究發(fā)現(xiàn)，人腦中的相應(yīng)區(qū)域與行為控制能力有關(guān),，該區(qū)域受損或有缺陷者更容易對(duì)可卡因上癮,，戒除毒癮也更困難。
實(shí)驗(yàn)中,，研究人員用光遺傳學(xué)技術(shù)對(duì)實(shí)驗(yàn)鼠中“癮君子”腦部的這一區(qū)域進(jìn)行刺激,，發(fā)現(xiàn)這些實(shí)驗(yàn)鼠尋求可卡因的行為有所減少。相反，如果抑制該區(qū)域神經(jīng)元的活動(dòng),，實(shí)驗(yàn)鼠則表現(xiàn)出毒癮增強(qiáng)的跡象,。光遺傳學(xué)技術(shù)是將光與遺傳工程相結(jié)合，可改變神經(jīng)細(xì)胞的活性,。
研究人員說,，這一結(jié)果表明，大腦前額葉皮質(zhì)特定區(qū)域的神經(jīng)元活性與可卡因成癮有密切關(guān)系,，通過刺激該區(qū)域的神經(jīng)元可有效提高對(duì)毒癮的控制能力,，這將有助于開發(fā)新療法，幫助人們戒除毒癮,。(生物谷Bioon.com)
doi:10.1038/nature12024
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Rescuing cocaine-induced prefrontal cortex hypoactivity prevents compulsive cocaine seeking
Billy T-Chen, Hau-Jie Yau, Christina Hatch,Ikue Kusumoto-Yoshida,Saemi L-Cho, F-Woodward Hopf, Antonello Bonci.
Loss of control over harmful drug seeking is one of the most intractable aspects of addiction, as human substance abusers continue to pursue drugs despite incurring significant negative consequences1. Human studies have suggested that deficits in prefrontal cortical function and consequential loss of inhibitory control2, 3, 4 could be crucial in promoting compulsive drug use. However, it remains unknown whether chronic drug use compromises cortical activity and, equally important, whether this deficit promotes compulsive cocaine seeking. Here we use a rat model of compulsive drug seeking5, 6, 7, 8 in which cocaine seeking persists in a subgroup of rats despite delivery of noxious foot shocks. We show that prolonged cocaine self-administration decreases ex vivo intrinsic excitability of deep-layer pyramidal neurons in the prelimbic cortex, which was significantly more pronounced in compulsive drug-seeking animals. Furthermore, compensating for hypoactive prelimbic cortex neurons with in vivo optogenetic prelimbic cortex stimulation significantly prevented compulsive cocaine seeking, whereas optogenetic prelimbic cortex inhibition significantly increased compulsive cocaine seeking. Our results show a marked reduction in prelimbic cortex excitability in compulsive cocaine-seeking rats, and that in vivo optogenetic prelimbic cortex stimulation decreased compulsive drug-seeking behaviours. Thus, targeted stimulation of the prefrontal cortex could serve as a promising therapy for treating compulsive drug use.
