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首页> 外文期刊>Journal of Neurophysiology >Pitx3 deficiency in mice affects cholinergic modulation of GABAergic synapses in the nucleus accumbens.
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Pitx3 deficiency in mice affects cholinergic modulation of GABAergic synapses in the nucleus accumbens.

机译：小鼠中Pitx3缺乏会影响伏伏核中GABA能突触的胆碱能调节。

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We investigated to what extent Pitx3 deficiency, causing hyperdopaminergic transmission in the nucleus accumbens microcircuitry, may lead to developmental changes. First, spontaneous firing activity of cholinergic interneurons in the nucleus accumbens was recorded in vitro. Firing patterns in the Pitx3-deficient mice were more variable and intrinsically different from those observed in wild-type mice. Next, to test whether the irregular firing patterns observed in mutant mice affected the endogenous nicotinic modulation of the GABAergic input of medium spiny neurons, we recorded spontaneous GABAergic inputs to these cells before and after the application of the nicotinic receptor blocker mecamylamine. Effects of mecamylamine were found in slices of either genotype, but in a rather inconsistent manner. Possibly this was attributable to heterogeneity in firing of nearby cholinergic interneurons. Thus paired recordings of cholinergic interneurons and medium spiny neurons were performed to more precisely control the experimental conditions of the cholinergic modulation of GABAergic synaptic transmission. We found that controlling action potential firing in cholinergic neurons leads to a conditional increase in GABAergic input frequency in wild-type mice but not in Pitx3-deficient mice. We conclude that Pitx3-deficient mice have neural adaptations at the level of the nucleus accumbens microcircuitry that in turn may have behavioral consequences. It is discussed to what extent dopamine release in the nucleus accumbens may be a long-term gating mechanism leading to alterations in cholinergic transmission in the nucleus accumbens, in line with previously reported neural adaptations found as consequences of repeated drug treatment in rodents.
机译：我们调查了Pitx3缺乏在多大程度上导致伏伏核中的高多巴胺能传播，可能导致发育变化。首先，在体外记录了伏隔核中胆碱能中间神经元的自发放电活性。 Pitx3缺陷小鼠的放电模式与野生型小鼠相比，其可变性更大，本质上也有所不同。接下来，为了测试在突变小鼠中观察到的不规则放电模式是否影响中棘神经元的GABA能输入的内源性烟碱调节，我们记录了在应用烟碱受体阻滞剂美卡敏之前和之后向这些细胞的自发GABA能输入。在两种基因型的切片中均发现了美甲胺的作用，但方式不一致。这可能归因于附近胆碱能中间神经元的发射异质。因此，胆碱能中神经元和中棘神经元的配对记录被执行以更精确地控制GABA能突触传递的胆碱能调节的实验条件。我们发现，在胆碱能神经元中控制动作电位放电会导致野生型小鼠中GABA能输入频率有条件地增加，但在Pitx3缺陷型小鼠中则不会。我们得出的结论是，缺乏Pitx3的小鼠在伏伏核微电路水平上具有神经适应性，这反过来可能会产生行为后果。讨论了多巴胺在伏隔核中的释放在多大程度上可能是导致伏隔核中胆碱能传递发生变化的长期门控机制，这与先前报道的啮齿类动物反复药物治疗的神经适应性结果一致。

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