Panagis G, Kastellakis A, Spyraki C
Department of Basic Sciences, School of Medicine, University of Crete, Greece.
Psychopharmacology (Berl). 1998 Oct;139(3):222-9. doi: 10.1007/s002130050708.
Enkephalinergic and dopaminergic mechanisms have been implicated in the electrical self-stimulation (SS) behavior. The present set of experiments investigated the role of opioid receptors within DA-innervated brain regions (nucleus accumbens and ventral tegmental area) in the ventral pallidum self-stimulation (VP-SS). Forty-one rats used in this study were implanted with a monopolar moveable stimulating electrode in the VP. A rate-frequency curve-shift method was applied to determine the reward (threshold) and motor functions (asymptotic rate) of self stimulation elicited from the VP. One group received systemic treatment of graded doses (vehicle; 1.25; 2.50 mg/kg) of morphine injected IP, 60 min before behavioural testing. The results showed a tendency for increased threshold of VP-SS and of the asymptotic rate of responding. Three additional groups were implanted with guide cannulae in the nucleus accumbens (NAC), the ventral tegmental area (VTA) or dorsally to the VTA and received microinjections of morphine (vehicle: 1.25; 2.50; 5.0; 10.0 microg/0.5 microl per side). Central injections of morphine higher than 1.25 microg/side into the VTA were associated with a significant reduction in VP-SS thresholds, indicating a potentiative effect on reward. Microinjections of morphine either into the NAC or into the dorsal tegmentum did not produce significant alterations on thresholds or responding of VP-SS. In order to investigate the extent to which the VTA-NAC dopamine projection was involved in the SS behavior elicited from the ventral pallidum, we tested SS in animals that suffered NAC 6-hydroxydopamine (6-OHDA) lesions. Rats suffering NAC dopamine depletion along with their corresponding controls showed similar levels of thresholds and responding to the ones exhibited prior to the lesion, revealing that NAC dopamine is not necessary to maintain VP-SS. The results suggest that stimulation of opioid receptor in the VTA increases the rewarding efficacy of VP-SS. This effect might be due to the modulation of VTA-DA neurons projecting to the VP rather than to the NAC.
脑啡肽能和多巴胺能机制与电刺激自身行为（SS）有关。本系列实验研究了多巴胺支配的脑区（伏隔核和腹侧被盖区）内的阿片受体在腹侧苍白球自我刺激（VP-SS）中的作用。本研究中使用的41只大鼠在腹侧苍白球植入了单极可移动刺激电极。采用频率曲线移位法来确定从腹侧苍白球引发的自我刺激的奖赏（阈值）和运动功能（渐近频率）。一组在行为测试前60分钟腹腔注射不同剂量（溶剂；1.25；2.50mg/kg）的吗啡进行全身治疗。结果显示腹侧苍白球自我刺激阈值和反应渐近频率有增加的趋势。另外三组在伏隔核（NAC）、腹侧被盖区（VTA）或腹侧被盖区背侧植入引导套管，并接受吗啡微量注射（溶剂：1.25；2.50；5.0；10.0μg/0.5μl/侧）。向腹侧被盖区内注射高于1.25μg/侧的吗啡会导致腹侧苍白球自我刺激阈值显著降低，表明对奖赏有增强作用。向伏隔核或背侧被盖区微量注射吗啡对腹侧苍白球自我刺激的阈值或反应没有产生显著改变。为了研究腹侧被盖区 - 伏隔核多巴胺投射在腹侧苍白球引发的自我刺激行为中所涉及的程度，我们对遭受伏隔核6 - 羟基多巴胺（6 - OHDA）损伤的动物进行了自我刺激测试。遭受伏隔核多巴胺耗竭的大鼠及其相应对照组显示出与损伤前相似的阈值水平和反应，表明伏隔核多巴胺对于维持腹侧苍白球自我刺激并非必需。结果表明，刺激腹侧被盖区内的阿片受体会增加腹侧苍白球自我刺激的奖赏效能。这种效应可能是由于投射到腹侧苍白球而非伏隔核的腹侧被盖区 - 多巴胺能神经元受到了调节。
