Chevassus-Au-Louis N, Jorquera I, Ben-Ari Y, Represa A
Inserm U29, Hôpital de Port-Royal, Paris, France.
Dev Neurosci. 1999 Nov;21(3-5):385-92. doi: 10.1159/000017388.
Prenatal treatment with methylazoxymethanol (MAM) in rats generates animals with a diffuse cortical malformation associated with hyperexcitability. These alterations are reminiscent of the cortical malformations associated with epilepsy in children. We hypothesised that one of the mechanisms supporting hyperexcitability in MAM rats could be the presence of abnormal cortical connections in the malformed cortex. Using a variety of anatomical techniques, we provide evidences for three types of such abnormal connections: (i) tangential bundles of corticocortical fibres in and below the neocortical molecular layer; (ii) partial deafferentation of neocortical heterotopias by afferent cortical fibres whatever their location; (iii) exuberant innervation of hippocampal CA3 pyramidal cells by mossy fibres that form ectopic mossy boutons on their basal dendrites. We conclude that these abnormal intrinsic cortical connections may support the propagation of paroxymal activity in the neocortex of MAM-treated rats.
在大鼠中，用甲基偶氮甲醇（MAM）进行产前治疗会产生患有与过度兴奋相关的弥漫性皮质畸形的动物。这些改变让人联想到与儿童癫痫相关的皮质畸形。我们推测，支持MAM大鼠过度兴奋的机制之一可能是畸形皮质中存在异常的皮质连接。使用多种解剖学技术，我们为三种此类异常连接提供了证据：（i）新皮质分子层及其下方的皮质皮质纤维切向束；（ii）无论传入皮质纤维位于何处，新皮质异位灶都会出现部分传入缺失；（iii）苔藓纤维对海马CA3锥体细胞的过度支配，这些苔藓纤维在其基底树突上形成异位苔藓终扣。我们得出结论，这些异常的皮质内连接可能支持MAM处理大鼠新皮质中阵发性活动的传播。
