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首页> 外文期刊>The European Journal of Neuroscience >Galanin-induced decreases in nucleus accumbens/striatum excitatory postsynaptic potentials and morphine conditioned place preference require both galanin receptor 1 and galanin receptor 2
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Galanin-induced decreases in nucleus accumbens/striatum excitatory postsynaptic potentials and morphine conditioned place preference require both galanin receptor 1 and galanin receptor 2

机译:甘丙肽诱导的伏隔核/纹状体兴奋性突触后电位的降低和吗啡条件性位置偏爱都需要甘丙肽受体1和甘丙肽受体2

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The neuropeptide galanin has been shown to alter the rewarding properties of morphine. To identify potential cellular mechanisms that might be involved in the ability of galanin to modulate opiate reward, we measured excitatory postsynaptic potentials (EPSPs), using both field and whole-cell recordings from striatal brain slices extracted from wild-type mice and mice lacking specific galanin receptor (GalR) subtypes. We found that galanin decreased the amplitude of EPSPs in both the dorsal striatum and nucleus accumbens. We then performed recordings in slices from knockout mice lacking either the GalR1 or GalR2 gene, and found that the ability of galanin to decrease EPSP amplitude was absent from both mouse lines, suggesting that both receptor subtypes are required for this effect. In order to determine whether behavioral responses to opiates were dependent on the same receptor subtypes, we tested GalR1 and GalR2 knockout mice for morphine conditioned place preference (CPP). Morphine CPP was significantly attenuated in both GalR1 and GalR2 knockout mice. These data suggest that mesolimbic excitatory signaling is significantly modulated by galanin in a GalR1-dependent and GalR2-dependent manner, and that morphine CPP is dependent on the same receptor subtypes. Galanin modulates morphine's behavioral effects in mice. This study identifies direct actions on excitation of striatal neurons and identifies the galanin receptor (GalR) subtypes involved. Galanin decreases the amplitude of excitatory postsynaptic potentials in medium spiny neurons of wild type mice, but not mice lacking the GalR1 or GalR2 subtype. Neither GalR1 nor GalR2 knockout mice exhibit conditioned place preference for morphine. Thus both phenotypes depend on GalR1 and GalR2.
机译:已经证明神经肽甘丙肽会改变吗啡的有益特性。为了确定可能与甘丙肽调节阿片奖励有关的潜在细胞机制,我们使用从野生型小鼠和缺乏特异性小鼠中提取的纹状体脑切片的野​​外和全细胞记录,测量了兴奋性突触后电位(EPSP)。甘丙肽受体(GalR)亚型。我们发现甘丙肽降低了背侧纹状体和伏隔核中EPSP的幅度。然后,我们在缺少GalR1或GalR2基因的基因敲除小鼠的切片中进行了记录,发现这两种小鼠品系均缺乏甘丙肽降低EPSP幅度的能力,这表明该效应需要两种受体亚型。为了确定对鸦片的行为反应是否依赖于相同的受体亚型,我们测试了吗啡条件位置偏爱(CPP)的GalR1和GalR2敲除小鼠。在GalR1和GalR2基因敲除小鼠中,吗啡CPP均显着减弱。这些数据表明中脑边缘兴奋性信号转导由甘丙肽以GalR1依赖性和GalR2依赖性方式显着调节,并且吗啡CPP依赖于相同的受体亚型。甘丙肽调节吗啡在小鼠中的行为作用。这项研究确定了纹状体神经元兴奋的直接作用,并确定了涉及的甘丙肽受体(GalR)亚型。甘丙肽降低了野生型小鼠的中棘神经元中兴奋性突触后电位的幅度,但没有缺乏GalR1或GalR2亚型的小鼠。 GalR1和GalR2基因敲除小鼠均未表现出对吗啡的条件位置偏爱。因此,两种表型均依赖于GalR1和GalR2。

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