Kim J J, Gross J, Morest D K, Potashner S J
Department of Neuroscience, The University of Connecticut Health Center, Farmington, Connecticut 06030, USA.
J Neurosci Res. 2004 Sep 15;77(6):829-42. doi: 10.1002/jnr.20211.
To determine if acoustic overstimulation altered synaptic connections in the cochlear nucleus, anesthetized adult chinchillas, with one ear protected by a silicone plug, were exposed for 3 hr to a 108-dB octave-band noise, centered at 4 kHz, and allowed to survive for periods up to 32 weeks. This exposure led to cochlear damage in the unprotected ear, mainly in the basal regions of the organ of Corti. The anterior part of the ipsilateral posteroventral cochlear nucleus consistently contained a band of degenerating axons and terminals, in which electron microscopic analysis revealed substantial losses of axons and synaptic terminals with excitatory and inhibitory cytology. The losses were significant after 1 week's survival and progressed for 16-24 weeks after exposure. By 24-32 weeks, a new growth of these structures produced a resurgence in the number of axons and terminals. The net number of excitatory endings fully recovered, but the quantity with inhibitory cytology was only partially recouped. Neuronal somata lost both excitatory and inhibitory endings at first and later recovered a full complement of excitatory but not inhibitory terminals. Dendrites suffered a net loss of both excitatory and inhibitory endings. Excitatory and inhibitory terminals with unidentified postsynaptic targets in the neuropil declined, then increased in number, with excitatory terminals exhibiting a greater recovery. These findings are consistent with a loss and regrowth of synaptic endings and with a reorganization of synaptic connections that favors excitation.
为了确定听觉过度刺激是否会改变耳蜗核中的突触连接,对成年龙猫进行麻醉,用硅胶塞保护一只耳朵,将另一只耳朵暴露于以4kHz为中心的108分贝倍频程噪声中3小时,并使其存活长达32周。这种暴露导致未受保护耳朵的耳蜗损伤,主要位于柯蒂氏器的基部区域。同侧后腹侧耳蜗核的前部始终包含一条退化轴突和终末带,电子显微镜分析显示,具有兴奋性和抑制性细胞学特征的轴突和突触终末大量丢失。暴露后1周,这些损失显著,并在暴露后16 - 24周持续进展。到24 - 32周时,这些结构的新生长导致轴突和终末数量的回升。兴奋性终末的净数量完全恢复,但具有抑制性细胞学特征的数量仅部分恢复。神经元胞体最初同时失去兴奋性和抑制性终末,后来恢复了完整的兴奋性终末,但抑制性终末未完全恢复。树突在兴奋性和抑制性终末方面都有净损失。神经毡中具有未识别突触后靶点的兴奋性和抑制性终末数量先减少,然后增加,其中兴奋性终末的恢复更为明显。这些发现与突触终末的丢失和再生以及有利于兴奋的突触连接重组一致。