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首页> 外文期刊>The Journal of Neuroscience: The Official Journal of the Society for Neuroscience >Effects of digesting chondroitin sulfate proteoglycans on plasticity in cat primary visual cortex
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Effects of digesting chondroitin sulfate proteoglycans on plasticity in cat primary visual cortex

机译:消化硫酸软骨素蛋白聚糖对猫原发性视皮层可塑性的影响

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摘要

Monocular deprivation (MD) during a critical period of postnatal development produces significant changes in the anatomy and physiology of the visual cortex, and the deprived eye becomes amblyopic. Extracellular matrix molecules have a major role in restricting plasticity such that the ability to recover from MD decreases with age. Chondroitin sulfate proteoglycans (CSPGs) act as barriers to cell migration and axon growth. Previous studies showing that degradation of CSPGs by the bacterial enzyme chondroitinase can restore plasticity in the adult rat visual cortex suggest a potential treatment for amblyopia. HereMDwas imposed in cats from the start of the critical period until 3.5 months of age. The deprived eye was reopened, the functional architecture of the visual cortex was assessed by optical imaging of intrinsic signals, and chondroitinase was injected into one hemisphere. Imaging was repeated 1 and 2 weeks postinjection, and visually evoked potentials (VEPs) and single-cell activity were recorded. Immunohistochemistry showed that digestion of CSPGs had been successful. After 2 weeks of binocular exposure, some recovery of deprived-eye responses occurred when chondroitinase had been injected into the hemisphere contralateral to that eye; when injected into the ipsilateral hemisphere, no recovery was seen. Deprived-eye VEPs were no larger in the injected hemisphere than in the opposite hemisphere. The small number of neurons dominated by the deprived eye exhibited poor tuning characteristics. These results suggest that despite structural effects of chondroitinase in adult cat V1, plasticity was not sufficiently restored to enable significant functional recovery of the deprived eye.
机译:在产后发育的关键时期,单眼剥夺(MD)会导致视觉皮层的解剖结构和生理发生重大变化,并且剥夺的眼睛会变成弱视。细胞外基质分子在限制可塑性方面起着主要作用,因此随着年龄的增长,从MD中恢复的能力会降低。硫酸软骨素蛋白聚糖(CSPG)充当细胞迁移和轴突生长的障碍。先前的研究表明,细菌软骨素酶降解CSPGs可以恢复成年大鼠视觉皮层的可塑性,这提示了弱视的潜在治疗方法。从关键时期开始到3.5个月大,在猫身上施以MD。重新张开被剥夺的眼睛,通过固有信号的光学成像评估视觉皮层的功能结构,并将软骨素酶注入一个半球。注射后1和2周重复成像,并记录视觉诱发电位(VEP)和单细胞活性。免疫组织化学表明,CSPG的消化是成功的。双眼暴露2周后,当将软骨素酶注射到与该眼对侧的半球中时,弱视反应会有所恢复。当注入同侧半球时,未见恢复。注入的半球中的弱视VEP不大于相反的半球。被剥夺的眼睛支配的少数神经元表现出较差的调节特性。这些结果表明,尽管软骨素酶在成年猫V1中具有结构性作用,但可塑性并未得到充分恢复,无法使被剥夺的眼睛获得明显的功能恢复。

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