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首页> 外文期刊>The European Journal of Neuroscience >Selective cholinergic immunolesioning affects synaptic plasticity in developing visual cortex.
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Selective cholinergic immunolesioning affects synaptic plasticity in developing visual cortex.

机译：选择性胆碱能免疫损害影响发育中的视觉皮层的突触可塑性。

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Abstract Cholinergic neurotransmission is known to affect activity-dependent plasticity in various areas, including the visual cortex. However, relatively little is known about the exact role of subcortical cholinergic inputs in the regulation of plastic events in this region during early postnatal development. In the present study, synaptic transmission and plasticity in the developing visual cortex were studied following selective immunotoxic removal of the basal forebrain cholinergic afferents in 4-day-old rat pups. The lesion produced dramatic cholinergic neuronal and terminal fibre loss associated with decreased mRNA levels for the M(1) and M(2) muscarinic receptors, as well as clear-cut impairments of long-term potentiation (LTP) in visual cortex slices. Indeed, after theta burst stimulation of layer IV a long-term depression (LTD) instead of an LTP was induced in immunolesioned slices. This functional change appears to be due to the lack of cholinergic input as exogenous application of acetylcholine prevented the shift from LTP to LTD. In addition, lesioned rats showed an increased sensitivity to acetylcholine (ACh). While application of 20 microm ACh produced a depression of the field potential in immunolesioned rat slices, in order to observe the same effect in control slices we had to increase ACh concentration to up to 200 microm. Taken together, our results indicate that deprivation of cholinergic input affects synaptic transmission and plasticity in developing visual cortex, suggesting that the cholinergic system could play an active role in the refinement of the cortical circuitry during maturation.
机译：摘要已知胆碱能神经传递会影响视皮层等各个领域的活动依赖性可塑性。但是，关于皮层下胆碱能输入在产后早期发育过程中该区域可塑事件的调控中的确切作用了解甚少。在本研究中，在选择性免疫毒性去除4天大的幼仔的基础前脑胆碱能传入分子后，研究了发育中的视觉皮层的突触传递和可塑性。病变产生戏剧性的胆碱能神经元和终末纤维丧失，与M（1）和M（2）毒蕈碱受体的mRNA水平降低相关，以及视觉皮层切片中长期增强（LTP）的明显损伤。确实，在第IV层的θ爆裂刺激后，在免疫损伤切片中诱导了长期抑制（LTD）而不是LTP。这种功能变化似乎是由于缺乏胆碱能输入所致，因为外源应用乙酰胆碱阻止了LTP向LTD的转移。此外，患病大鼠对乙酰胆碱（ACh）的敏感性增加。尽管施加20微米ACh会使免疫损伤的大鼠切片中的场电位降低，但为了在对照切片中观察到相同的效果，我们必须将ACh浓度增加到200微米。两者合计，我们的研究结果表明胆碱能输入的剥夺会影响突触传递和可塑性发展中的视觉皮层，表明胆碱能系统可能在成熟过程中的皮层电路的完善中发挥积极作用。

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