Lesion-induced transneuronal plasticity of the cholinergic innervation in the adult rat entorhinal cortex.
Lesion-induced transneuronal plasticity of the cholinergic innervation in the adult rat entorhinal cortex.
复制标题
成年大鼠内嗅皮层胆碱能神经支配的损伤诱导的跨神经元可塑性。
DOI：
10.1046/j.1460-9568.1998.00116.x
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发表时间：
1998
期刊：
影响因子：
--
通讯作者：
Wiley,RG
中科院分区：
文献类型：
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作者：
deLacalle,S;Kulkarni,S;Wiley,RG
本实验旨在确定的影响，基底前脑胆碱能系统的损害施加在内嗅皮层（EC）内的胆碱能中间神经元在大鼠。将192 IgG‐皂草素单侧输注到Broca水平对角带（HDB）核中，使同侧胆碱乙酰转移酶免疫反应（ChAT‐ir）神经元的数量减少54%。损伤后2 - 4周，同侧EC表现出中度但显著的ChAT-ir纤维和中间神经元损失。相邻切片显示血管活性肠多肽（VIP）免疫反应性的平行损失。扣带皮层中的细胞计数不受影响，表明这种效应确实特异于HDB神经元的主要靶区域。鹅膏蕈氨酸损伤还诱导同侧HDB中胆碱能神经元数量显著减少36%，EC中ChAT终末消失，而EC中ChAT-ir神经元数量不变。由于鹅膏蕈氨酸影响所有细胞，而不仅仅是胆碱能细胞，因此我们的结果表明，192 IgG‐皂草素处理后HDB中胆碱能神经元的特异性变性可能会诱导对其靶点的跨突触效应。将192 IgG‐皂草素直接注射到EC中也损害了HDB的胆碱能投射，但对内在群体没有影响。免疫损伤后8周，EC中ChAT和VIP免疫反应性中间神经元的数量恢复到正常值，并持续长达6个月。我们的研究结果表明，内嗅皮层中间神经元胆碱能表型的短暂下调可能是活动依赖性可塑性的表现，而基底前脑胆碱能神经支配的丧失可能是通过输入失衡导致这些效应的原因。我们推测，内嗅中间神经元的表型表达的恢复可能是由于它们的神经支配的恢复，也许是来自同一领域中的发芽轴突，属于基底前脑中存活的胆碱能神经元。
The present experiments were designed to determine the effect that lesions of the basal forebrain cholinergic system exert on cholinergic interneurons within the entorhinal cortex (EC) in the rat. Unilateral infusion of 192 IgG‐saporin into the nucleus of the horizontal diagonal band of Broca (HDB) decreased the number of ipsilateral choline acetyltransferase immunoreactive (ChAT‐ir) neurons by 54%. Two–four weeks after the lesion, the ipsilateral EC exhibited a moderate but significant loss of ChAT‐ir fibres and interneurons. Adjacent sections revealed a parallel loss of vasoactive intestinal polypeptide (VIP) immunoreactivity. Cell counts in the cingulate cortex were unaffected, suggesting that this effect was indeed specific to the main target area for HDB neurons. Ibotenic acid lesions also induced a significant 36% decrease in the number of cholinergic neurons in the ipsilateral HDB, and disappearance of ChAT terminals in the EC, whereas the number of ChAT‐ir neurons in the EC was unchanged. Since ibotenic acid affects all cells and not only cholinergic ones, our results suggest that the specific degeneration of cholinergic neurons in the HDB after 192 IgG‐saporin treatment could be inducing transsynaptic effects on their targets. Injections of 192 IgG‐saporin directly into the EC also lesioned the cholinergic projection from the HDB, but had no effect on the intrinsic population.Eight weeks after immunolesion, the number of interneurons immunoreactive for ChAT and VIP in the EC had returned to normal values, and persisted for as long as 6 months after the lesion. By contrast, ChAT‐ir neurons in the HDB were permanently lost.Our results suggest that the transient down‐regulation of the cholinergic phenotype in entorhinal cortex interneurons could be a manifestation of activity‐dependent plasticity, and that the loss of cholinergic innervation from the basal forebrain could be responsible for these effects through an imbalance of inputs. We hypothesize that the recovery of the phenotypic expression of entorhinal interneurons could be due to a recovery in their innervation, perhaps from sprouting axons in the same fields, belonging to surviving cholinergic neurons in the basal forebrain.