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首页> 外文期刊>Pharmacology, Biochemistry and Behavior >Benzodiazepine dependence: from neural circuits to gene expression.
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Benzodiazepine dependence: from neural circuits to gene expression.

机译：苯二氮卓依赖性：从神经回路到基因表达。

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The neural mechanisms underlying benzodiazepine dependence remain equivocal. The present studies tested the hypothesis that similar neural systems are recruited during diazepam tolerance and withdrawal, and that these are associated with changes in GABA(A) receptor properties. 2-Deoxyglucose quantitative autoradiography was employed to map the brain structures affected during chronic treatment and withdrawal from diazepam (5 mg/kg i.p. daily) in rats. Acute administration of diazepam evoked widespread reductions in local rates of cerebral glucose (LCGU) utilization throughout the brain. Brain structures associated with sensory processing developed tolerance to these depressant effects of diazepam after 3 days of treatment, whereas tolerance occurred in the Papez circuit of emotion after 28 days of treatment. These data suggest that adaptive changes in different neuroanatomical circuits may underlie tolerance to the various effects of diazepam. During flumazenil-precipitated withdrawal from diazepam there were marked increases in glucose use in structures of the Papez circuit, the nucleus accumbens, and the basolateral amygdala. These data suggest that the Papez circuit features strongly in diazepam tolerance and withdrawal and supports a common adaptive process being involved in these phenomena. While GABA enhancement of benzodiazepine binding was reduced in the nucleus accumbens after repeated diazepam treatment, there was little evidence to support adaptive changes in GABA(A) receptors or GABA(A) subunit gene expression (gamma2, alpha1, or alpha4) as underlying the functional changes in the identified circuits. Alternative neurochemical mechanisms, such as changes in glutamatergic function should be considered.
机译：苯并二氮杂dependence依赖性的神经机制仍然不清楚。本研究检验了以下假设：在地西epa耐受和戒断期间募集了类似的神经系统，并且这些系统与GABA（A）受体特性的变化有关。使用2-脱氧葡萄糖定量放射自显影技术绘制大鼠慢性治疗和从地西epa停药（每天5 mg / kg腹膜内注射）过程中受影响的大脑结构的图。地西epa的急性给药引起整个大脑局部局部葡萄糖（LCGU）利用率的广泛降低。在治疗3天后，与感觉处理相关的大脑结构对地西epa的这些抑郁作用产生了耐受性，而在治疗28天后，帕皮兹情绪循环中出现了耐受性。这些数据表明，不同神经解剖回路的适应性变化可能是对地西epa各种作用的耐受性的基础。在氟马西尼沉淀的地西epa停药期间，Papez回路，伏隔核和基底外侧杏仁核的结构中葡萄糖的使用显着增加。这些数据表明，帕皮兹回路在地西epa耐受性和退缩方面具有很强的特征，并支持涉及这些现象的常见适应性过程。虽然重复地西epa治疗后伏隔核中GABA增强了苯二氮卓结合的增强作用，但几乎没有证据支持GABA（A）受体或GABA（A）亚基基因表达（gamma2，alpha1或alpha4）的适应性改变作为基础。识别电路的功能变化。应考虑其他神经化学机制，例如谷氨酸能功能的改变。

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