Reconsolidation of appetitive memories for both natural and drug reinforcement is dependent on β-adrenergic receptors
Reconsolidation of appetitive memories for both natural and drug reinforcement is dependent on β-adrenergic receptors
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DOI：
10.1101/lm.825008
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发表时间：
2008-02-01
影响因子：
2
通讯作者：
Everitt, Barry J.
中科院分区：
文献类型：
--
作者：
Milton, Amy L.;Lee, Jonathan L. C.;Everitt, Barry J.
我们研究了记忆再巩固的神经化学机制，特别是β-肾上腺素能信号传导启动的细胞内机制的功能要求。我们发现，普萘洛尔，与记忆再激活会议，可以专门破坏条件强化性能的先前食欲加强条件刺激（CS），是否刺激已与自我管理的可卡因或蔗糖。这些数据表明，药物和非药物CS-US协会的记忆依赖于β-肾上腺素能受体介导的信号传导，其重新巩固，与药物成瘾和某些形式的肥胖症的新型治疗的潜在发展的影响。
We have investigated the neurochemical mechanisms of memory reconsolidation and, in particular, the functional requirement for intracellular mechanisms initiated by beta-adrenergic signaling. We show that propranolol, given in conjunction with a memory reactivation session, can specifically disrupt the conditioned reinforcing properties of a previously appetitively reinforced conditioned stimulus (CS), whether the stimulus had been associated with self-administered cocaine or with sucrose. These data show that memories for both drug and nondrug CS-US associations are dependent on beta-adrenergic receptor-mediated signaling for their reconsolidation, with implications for the potential development of a novel treatment for drug addiction and some forms of obesity.