Ventral tegmental self-stimulation selectively induces opioid peptide release in rat CNS.
Ventral tegmental self-stimulation selectively induces opioid peptide release in rat CNS.
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腹侧被盖自我刺激选择性诱导大鼠中枢神经系统阿片肽释放。
DOI：
10.1002/syn.890130109
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发表时间：
1993
期刊：
影响因子：
--
通讯作者：
Stein,EA
中科院分区：
文献类型：
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作者：
Stein,EA
颅内自我刺激（ICS）被认为可以激活参与处理天然强化剂的神经元系统。代谢映射研究先前已经证明了在主动与被动接受刺激的动物中ICS特异性参与的CNS结构的子集。由于已知阿片类药物可增强JCS行为，并可能增强其强化特性，因此本研究探讨了阿片肽作为ICS介质的作用问题。大鼠在ICS维持的固定口粮（FR）20反应时间表上训练。在反应稳定后，将大鼠分配到2个强化时间表中的1个的主动刺激组或相应的轭刺激组（i.例如，FR 1-YFR 1、FR 20-YFR 20或久坐对照），并且从体内受体占有率推断阿片肽释放。放射自显影分析确定了3组结构。在丘脑内侧背核、基底外侧杏仁核、腹侧苍白球、内侧缰核、中缝背核、下丘脑后部、黑质腹侧部、无颗粒岛叶前皮质和齿状回中观察到给药诱导的占位性变化。根据结构，肽释放取决于刺激偶然性（主动与偶联）和/或时间表（FR 1与FR 20）。在缰核和前岛皮质中发现ICS诱导的肽释放抑制的证据。九个额外的结构，所有组件，或接收来自边缘系统的预测，揭示了ICS治疗和电极侧之间的复杂相互作用。最后，广泛的同侧增加的受体结合被认为是从扣带，嗅结节，和脑桥核，沿着外侧下丘脑和海马，并延伸到尾部的黑质和腹侧被盖。这些后期效应似乎与刺激诱导的血流变化和随后的配体呈递增加有关。总的来说，这些数据指向奖励脑刺激激活离散神经元阿片系统的能力，这取决于特定的行为以及刺激条件。© 1993 Wiley‐利斯公司
Intracranial self‐stimulation (ICS) is thought to activate neuronal systems involved in processing natural reinforcing agents. Metabolic mapping studies have previously demonstrated a subset of CNS structures specifically engaged by ICS in animals receiving stimulation actively vs. passively. Since opiates are known to enhance JCS behavior and presumably its reinforcing properties, the current study addressed the question of the role of opioid peptides as mediators of ICS. Rats were trained on a fixed ration (FR) 20 schedule of responding maintained by ICS. Following response stabilization, rats were assigned either to an active or a corresponding yoked stimulation group at 1 of 2 schedules of reinforcement (i. e., FR1‐YFR1, FR20‐YFR20, or sedentary control), and opioid peptide release was inferred from in vivo receptor occupancy. Autoradiographic analyses identified 3 groups of structures. Treatment‐induced alterations in occupancy were seen in the medial dorsal nucleus of the thalamus, basolateral amygdala, ventral pallidum, medial habenula, dorsal raphe, posterior hypothalamus, substantia nigra pars compacta, agranular preinsular cortex, and zona incerta. Depending upon the structure, peptide release was dependent upon stimulus contingency (active vs. yoked) and/or schedule (FR1 vs. FR20). Evidence for ICS‐induced inhibition of peptide release was found in the habenula and preinsular cortex. Nine additional structures, all components of, or receiving projections from, the limbic system, revealed complex interactions between ICS treatment and the electrode side. Finally, a widespread ipsilateral increase in receptor binding was seen rostrally from the cingulate, olfactory tubercle, and nucleus accumbens, along the lateral hypothalamus and hippocampus, and extending caudally to the substantia nigra and ventral tegmentum. These later effects appear to be related to stimulation‐induced changes in blood flow and subsequent ligant presentation increases. Collectively, these data point towards the ability of rewarding brain stimulation to activate discrete neuronal opioid systems contingent upon specific behavioral as well as stimulus conditions. © 1993 Wiley‐Liss, Inc.