摘要
目的探索听觉系统发育和损伤后修复的神经可塑性的分子机制,探索GAP-43与幼鼠听皮层发育和可塑性的关系;方法应用免疫组织化学方法,检测正常幼鼠(3周龄、4周龄及8周龄大鼠)及耳毒性药物致聋鼠发育的不同阶段(2周2天龄大鼠氨基糖苷类抗生素致聋后5天、12天及40天,即致聋的3周龄、4周龄及8周龄大鼠)GAP-43在听皮层的阳性神经元表达变化;结果发现GAP-43在刚出生大鼠听皮层阳性神经元高表达,随发育表达逐渐降低,出生后3周(NC P3W)的大鼠听皮层平均每高倍视野阳性神经元数为111.50±4.90,出生后4周(NC P4W)为84.17±3.24,出生后8周(NC P8W)为66.67±4.17;耳蜗损伤后早期GAP-43在幼鼠听皮层的表达反应性升高;结论 GAP-43与幼鼠听皮层发育和可塑性密切相关,GAP-43可作为听皮层乃至听觉系统发育和可塑性的重要标志。
Objective To study the molecular mechanisms of neural plasticity in the development and post-injury re?pair of the auditory system, particularly the changes and plasticity of GAP-43 expression in the developing auditory cortex (AC) in young rats. Methods We measured levels of growth associated protein-43 (GAP-43) expression in the auditory cortex of developing rats(3, 4 or 8 weeks of age)and in ototoxicity deafened rats(3, 4 or 8 weeks of age)by immunohistochemistry. Results In the immediate postnatal stage, AC was found to contain high levels of GAP-43. Over the first few postnatal weeks, a continuous reduction of GAP-43 occurred. Positively stained neurons count was 111.50±4.90 per high power field in the au?ditory cortex by 3 weeks of age, 84.17±3.24 by 4 weeks, and 66.67±4.17 by 8 weeks. Shortly after auditory deprivation by oto?toxicity, GAP-43 expression was dramatically boosted in the AC. Conclusions GAP-43 shows a close correlation with the growth and plasticity of the AC, which can be a significant marker for auditory plasticity.
出处
《中华耳科学杂志》
CSCD
北大核心
2014年第4期638-642,共5页
Chinese Journal of Otology
关键词
幼鼠
听觉剥夺
GAP-43
听皮层
可塑性
Immature rats Auditory deprivation GAP-43 Auditory cortex Plasticity