Septal cholinergic neurons suppress seizure development in hippocampal kindling in rats: Comparison with noradrenergic neurons
Septal cholinergic neurons suppress seizure development in hippocampal kindling in rats: Comparison with noradrenergic neurons
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DOI：
10.1016/s0306-4522(00)00499-1
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发表时间：
2001-01-01
期刊：
影响因子：
3.3
通讯作者：
Lindvall, O
中科院分区：
文献类型：
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作者：
Ferencz, I;Leanza, G;Lindvall, O
脑室内注射192 IgG皂草素或6-羟多巴胺可分别引起前脑胆碱能或去甲肾上腺素能投射的广泛病变，加速点燃癫痫发生。在这里，我们证明了定量和定性的差异，这两种病变对大鼠海马点燃的影响。癫痫发生后去甲肾上腺素能相比，胆碱能去神经支配显着更快，当这两种病变相结合，点燃发展类似的h-羟基多巴胺病变单独的动物。此外，而192 IgG-皂草素病变促进发展的早期阶段的点燃，管理6-羟基多巴胺或两种神经毒素也加速了后期阶段。探讨基底前脑胆碱能系统不同亚区在海马点燃抑制癫痫发作中的作用。将192 IgG-皂草素注射到Broca斜角带内侧隔/垂直臂或基底大细胞核中，分别导致选择性海马或皮质胆碱能去传入。去神经支配的海马促进点燃类似于由脑室内192 IgG-皂草素引起的广泛病变，而皮质病变没有effect.These结果表明，虽然去甲肾上腺素能和胆碱能预测前脑海马点燃癫痫发生产生强大的抑制作用，胆碱能系统的行动是不太明显，具体发生在癫痫发作泛化之前。相反。去甲肾上腺素能神经元抑制局灶性和全身性癫痫发作的发展。隔-海马神经元负责海马点燃中胆碱能系统的抗癫痫作用，而皮质投射没有显著参与。相反，我们先前已经表明[Ferencz I.埃尔河（2000）Eur.神经科学杂志，12，2107-21 16]，杏仁核点燃中的癫痫抑制是通过皮质而不是海马胆碱能投射来施加的。这表明，根据原发性癫痫灶的位置，即刺激的部位，基底前脑胆碱能神经元通过不同的子系统来抵抗点燃中的癫痫发作发展。(C)2001年IBRO。由爱思唯尔科技有限公司出版。保留所有权利。
Widespread lesions of forebrain cholinergic or noradrenergic projections by intraventricular administration of 192 IgG-saporin or 6-hydroxpdopamine, respectively, accelerate kindling epileptogenesis. Here we demonstrate both quantitative and qualitative differences between the two lesions in their effects on hippocampal kindling in rats. Epileptogenesis was significantly faster after noradrenergic as compared to cholinergic denervation, and when both lesions were combined, kindling development resembled that in animals with h-hydroxydopamine lesion alone. Furthermore, whereas the 192 IgG-saporin lesion promoted the development only of the early stages of kindling, administration of 6-hydroxy-dopamine or both neurotoxins accelerated the late stages also. To investigate the contribution of different subparts of the basal forebrain cholinergic system to its seizure-suppressant action in hippocampal kindling. 192 IgG-saporin was injected into medial septum/vertical limb of the diagonal band of Broca or nucleus basalis magnocellularis, leading to selective hippocampal or cortical cholinergic deafferentation, respectively. The denervation of the hippocampus facilitated kindling similar to the extensive lesion caused by intraventricular 192 IgG-saporin, whereas the cortical lesion had no effect.These results indicate that although both noradrenergic and cholinergic projections to the forebrain exert powerful inhibitory effects on hippocampal kindling epileptogenesis, the action of the cholinergic system is less pronounced and occurs specifically prior to seizure generalization. In contrast. noradrenergic neurons inhibit the development of both focal and generalized seizures. The septo-hippocampal neurons are responsible for the antiepileptogenic effect of the cholinergic system in hippocampal kindling, whereas the cortical projection is not significantly involved, Conversely, we have previously shown [Ferencz I. er nl. (2000) Eur. J. Neurosci., 12, 2107-21 16] that seizure-suppression in amygdala kindling is exerted through the cortical and not the hippocampal cholinergic projection. This shows that, depending on the location of the primary epileptic focus, i.e. the site of stimulation, basal forebrain cholinergic neurons operate through different subsystems to counteract seizure development in kindling. (C) 2001 IBRO. Published by Elsevier Science Ltd. All rights reserved.