Deafness-induced plasticity in the mature central auditory system
Deafness-induced plasticity in the mature central auditory system
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DOI：
10.1097/00001756-199512000-00054
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发表时间：
1995-12-29
期刊：
影响因子：
1.7
通讯作者：
Altschuler, RA
中科院分区：
文献类型：
--
作者：
Bledsoe, SC;Nagase, S;Altschuler, RA
大鼠和豚鼠的研究表明，抑制性递质的局部变化可能是麻醉诱导的成熟中枢听觉系统细胞电生理反应性可塑性变化的基础。双侧耳聋21天后，对侧耳蜗电刺激诱发下丘中央核（CIC）Fos免疫反应神经元的增加，与正常或1天的耳聋动物相比。耳聋还与CIC神经元数量的急剧减少有关，CIC神经元对电刺激的活性抑制作出反应。此外，在体内微透析揭示了一个显着减少γ-氨基丁酸（GABA）的释放从CIC细胞在rephened动物。这些结果可能对感觉输入去传入引起的中枢神经系统可塑性的调节具有普遍意义。
STUDIES in rats and guinea pigs indicate that local changes in inhibitory transmitters may underlie deafness-induced plastic changes in electrophysiological responsiveness of cells of the mature central auditory system. Following 21 days of bilateral deafness there is an increase in evoked Fos-immunoreactive neurones in the central nucleus of the inferior colliculus (CIC) to contralateral cochlear electrical stimulation, compared with normal or 1-day deafened animals. Deafness is also associated with a dramatic reduction in the population of CIC neurones that respond with suppression of activity to electrical stimulation. Moreover, in vivo microdialysis reveals a marked decrease in gamma-aminobutyric acid (GABA) release from the CIC cells in deafened animals. The results may have general implications for the mediation of central nervous system plasticity induced by deafferentation of sensory input.