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首页> 外文期刊>Folia neuropathologica >Involvement of D1/D2 dopamine antagonists upon open-arms exploratory behaviours induced by intra-nucleus accumbens shell administration of N-methyl-D-aspartate
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Involvement of D1/D2 dopamine antagonists upon open-arms exploratory behaviours induced by intra-nucleus accumbens shell administration of N-methyl-D-aspartate

机译:D1 / D2多巴胺拮抗剂参与伏核内壳施用N-甲基-D-天冬氨酸诱导的张开双臂探索行为

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Glutamatergic system stimulation in some parts of the brain may affect anxiety-related behaviours, aversive learning and memory. This system retains many interactions with dopaminergic neurotransmission. We have studied the effect of nucleus accumbens (NAc) shell glutamatergic system activation on anxiety-related behaviours as well as aversive learning and memory in adult male Wistar rats using the N-methyl-D-aspartate (NMDA) receptor agonist, NMDA. Furthermore, the possible involvement of the NAc shell dopamine D1 and D2 receptors upon NMDA-induced effects was evaluated. The elevated plus-maze task was used to assess the drugs' concomitant effects on anxiety, learning and memory in rats. All drugs were delivered into the NAc shell via bilaterally implanted indwelling cannulae. The NMDA-induced anxiolytic-like behaviours upon retest could possibly be attributed to the further avoidance acquisition impairments. Moreover, the inhibition of dopaminergic system using SCH 23390 and sulpiride induced an anxiolytic-like response and impaired the aversive memory acquisition during retest. However, the concurrent intra-NAc shell microinjection of the subthreshold dose of SCH 23390 and sulpiride (0.125 μg/rat) reversed the anxiolytic- like effect and blocked the aversive memory impairment induced by intra-NAc shell NMDA. Our results suggest a modulatory role of the NAc shell dopaminergic system on NMDA-induced effects in the aversive memory.
机译:大脑某些部位的谷氨酸能系统刺激可能会影响与焦虑相关的行为,厌恶性学习和记忆。该系统保留了与多巴胺能神经传递的许多相互作用。我们使用N-甲基-D-天冬氨酸(NMDA)受体激动剂NMDA研究了伏伏核(NAc)壳谷氨酸能系统激活对成年雄性Wistar大鼠焦虑相关行为以及厌恶学习和记忆的影响。此外,评估了NAc壳多巴胺D1和D2受体可能参与了NMDA诱导的作用。高迷宫任务被用来评估药物对大鼠焦虑,学习和记忆的伴随作用。所有药物均通过双边植入的留置套管递送到NAc外壳中。重新测试后,NMDA诱导的抗焦虑样行为可能归因于进一步的避免获得障碍。此外,使用SCH 23390和舒必利抑制多巴胺能系统可引起抗焦虑样反应,并在重新测试期间损害厌恶性记忆的获得。然而,同时在阈值以下剂量的SCH 23390和舒必利(0.125μg/大鼠)的NAc外壳内显微注射逆转了抗焦虑样作用,并阻止了由NAc外壳内NMDA引起的厌恶性记忆障碍。我们的结果表明NAc壳多巴胺能系统对NMDA诱导的厌恶记忆效应的调节作用。

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