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首页> 外文期刊>The European Journal of Neuroscience >Correlated species differences in the effects of cannabinoid ligands on anxiety and on GABAergic and glutamatergic synaptic transmission.
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Correlated species differences in the effects of cannabinoid ligands on anxiety and on GABAergic and glutamatergic synaptic transmission.

机译：大麻素配体对焦虑的影响以及对GABA能和谷氨酸能的突触传递的相关物种差异。

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摘要

Cannabinoid ligands show therapeutic potential in a variety of disorders including anxiety. However, the anxiety-related effects of cannabinoids remain controversial as agonists show opposite effects in mice and rats. Here we compared the effects of the cannabinoid agonist WIN-55,212 and the CB1 antagonist AM-251 in CD1 mice and Wistar rats. Special attention was paid to antagonist-agonist interactions, which had not yet been studied in rats. In mice, WIN-55,212 decreased whereas AM-251 increased anxiety. The antagonist abolished the effects of the agonist. In contrast, WIN-55,212 increased anxiety in rats. Surprisingly, the antagonist potentiated this effect. Cannabinoids affect both GABAergic and glutamatergic functions, which play opposite roles in anxiety. We hypothesized that discrepant findings resulted from species differences in the relative responsiveness of the two transmitter systems to cannabinoids. We investigated this hypothesis by studying the effects of WIN-55,212 on evoked hippocampal inhibitory and excitatory postsynaptic currents (IPSCs and EPSCs). IPSCs were one order of magnitude more sensitive to WIN-55,212 in mice than in rats. In mice, IPSCs were more sensitive than EPSCs to WIN-55,212. This is the first study showing that the relative cannabinoid sensitivity of GABA and glutamate neurotransmission is species-dependent. Based on behavioural and electrophysiological findings, we hypothesize that WIN-55,212 reduced anxiety in mice by affecting GABA neurotransmission whereas it increased anxiety in rats via glutamatergic mechanisms. In rats, AM-251 potentiated this anxiogenic effect by inhibiting the anxiolytic GABAergic mechanism. We suggest that the anxiety-related effects of cannabinoids depend on the relative cannabinoid responsiveness of GABAergic and glutamatergic neurotransmission.
机译：大麻素配体在包括焦虑症在内的多种疾病中均显示出治疗潜力。然而，由于激动剂在小鼠和大鼠中显示出相反的作用，因此大麻素与焦虑相关的作用仍存在争议。在这里，我们比较了大麻素激动剂WIN-55,212和CB1拮抗剂AM-251在CD1小鼠和Wistar大鼠中的作用。尚未对大鼠中尚未研究的拮抗剂-激动剂相互作用给予特别关注。在小鼠中，WIN-55,212减少，而AM-251增加焦虑。拮抗剂消除了激动剂的作用。相反，WIN-55,212增加了大鼠的焦虑感。令人惊讶地，拮抗剂增强了该作用。大麻素影响GABA能和谷氨酸能的功能，在焦虑中起相反的作用。我们假设，差异的发现是由于两种发射系统对大麻素的相对响应能力的物种差异所致。我们通过研究WIN-55,212对诱发的海马抑制性和兴奋性突触后电流（IPSC和EPSC）的影响，研究了这一假设。 IPSC对小鼠的WIN-55,212敏感性要比对大鼠高一个数量级。在小鼠中，IPSC对WIN-55,212比EPSC更敏感。这是第一项研究，表明GABA和谷氨酸神经传递的相对大麻素敏感性是物种依赖性的。基于行为和电生理结果，我们假设WIN-55,212通过影响GABA神经传递而减少了小鼠的焦虑，而通过谷氨酸能机制增加了大鼠的焦虑。在大鼠中，AM-251通过抑制抗焦虑的GABA能机制来增强这种抗焦虑作用。我们建议，大麻素的焦虑相关效应取决于GABA能和谷氨酸能神经传递的相对大麻素反应性。

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