Arckens L, Schweigart G, Qu Y, Wouters G, Pow D V, Vandesande F, Eysel U T, Orban G A
Laboratory of Neuroendocrinology and Immunological Biotechnology, Katholieke Universiteit Leuven, Naamsestraat 59, B-3000 Leuven, Belgium.
Eur J Neurosci. 2000 Dec;12(12):4222-32. doi: 10.1046/j.0953-816x.2000.01328.x.
Different intracortical mechanisms have been reported to contribute to the substantial topographic reorganization of the mammalian primary visual cortex in response to matching lesions in the two retinas: an immediate expansion of receptive fields followed by a gradual shift of excitability into the deprived area and finally axonal sprouting of laterally projecting neurons months after the lesion. To gain insight into the molecular mechanisms of this adult plasticity, we used immunocytochemical and bioanalytical methods to measure the glutamate and GABA neurotransmitter levels in the visual cortex of adult cats with binocular central retinal lesions. Two to four weeks after the lesions, glutamate immunoreactivity was decreased in sensory-deprived cortex as confirmed by HPLC analysis of the glutamate concentration. Within three months normal glutamate immunoreactivity was restored. In addition, the edge of the unresponsive cortex was characterized by markedly increased glutamate immunoreactivity 2-12 weeks postlesion. This glutamate immunoreactivity peak moved into the deprived area over time. These glutamate changes corresponded to decreased spontaneous and visually driven activity in unresponsive cortex and to strikingly increased neuronal activity at the border of this cortical zone. Furthermore, the previously reported decrease in glutamic acid decarboxylase immunoreactivity was found to reflect decreased GABA levels in sensory-deprived cortex. Increased glutamate concentrations and neuronal activity, and decreased GABA concentrations, may be related to changes in synaptic efficiency and could represent a mechanism underlying the retinotopic reorganization that occurs well after the immediate receptive field expansion but long before the late axonal sprouting.
据报道,不同的皮质内机制促成了哺乳动物初级视觉皮层在响应双眼视网膜匹配损伤时的显著拓扑重组:损伤后,感受野立即扩大,随后兴奋性逐渐转移至剥夺区域,最终在损伤数月后,侧向投射神经元出现轴突发芽。为深入了解这种成年可塑性的分子机制,我们采用免疫细胞化学和生物分析方法,测量了患有双眼中央视网膜损伤的成年猫视觉皮层中的谷氨酸和γ-氨基丁酸(GABA)神经递质水平。损伤后两到四周,通过对谷氨酸浓度的高效液相色谱分析证实,感觉剥夺皮层中的谷氨酸免疫反应性降低。在三个月内,谷氨酸免疫反应性恢复正常。此外,在损伤后2 - 12周,无反应皮层边缘的谷氨酸免疫反应性显著增加。随着时间的推移,这个谷氨酸免疫反应性峰值向剥夺区域移动。这些谷氨酸变化与无反应皮层中自发和视觉驱动活动的减少相对应,也与该皮质区域边界处神经元活动的显著增加相对应。此外,先前报道的谷氨酸脱羧酶免疫反应性降低被发现反映了感觉剥夺皮层中GABA水平的降低。谷氨酸浓度和神经元活动的增加以及GABA浓度的降低,可能与突触效率的变化有关,并且可能代表了一种机制,该机制发生在感受野立即扩大之后很久,但在晚期轴突发芽之前很久就发生的视网膜拓扑重组的基础。