Potashner S J, Suneja S K, Benson C G
Department of Anatomy, University of Connecticut Health Center, Farmington 06030, USA.
Exp Neurol. 1997 Nov;148(1):222-35. doi: 10.1006/exnr.1997.6641.
In young adult guinea pigs, the effects of unilateral ossicle removal and cochlear ablation were determined on transmitter release from glutamatergic presynaptic endings and glutamate inactivation via uptake. (i) D-[3H]Aspartate release and uptake were measured in subdivisions of the cochlear nucleus (CN) and in nuclei of the superior olive (SOC) and auditory midbrain (MB) up to 145 days after placing the lesions. Activities were compared to those from age-matched unlesioned controls. Fiber degeneration was visualized histologically. (ii) In the ipsilateral CN, changes in release and uptake were governed by the type of lesion. Ossicle removal produced sparse pruning of fibers only after 112 days and decreased release and uptake at 145 days, consistent with regulatory weakening of excitatory glutamatergic transmission. Cochlear ablation deafferented the CN, producing deficient release and uptake at 2 days and abundant fiber degeneration at 7 days. Subsequently, the residual release and uptake increased in magnitude, consistent with strengthening of excitatory glutamatergic transmission. (iii) In the contralateral CN, after either lesion, changes in release and uptake usually matched those in the ipsilateral CN. Thus, the auditory pathway associated with the lesioned ear probably provided cues for the regulation of synaptic strength in the contralateral CN. (iv) Both lesions increased release in the SOC and MB, and uptake in the SOC, consistent with strengthening of excitatory glutamatergic transmission. Sparse fiber degeneration, suggesting axonal pruning, appeared in the SOC and MB after cochlear ablation. (v) The strengthening of excitatory glutamatergic transmission may facilitate and maintain symptoms such as loudness recruitment and tinnitus which often accompany hearing loss.
在年轻成年豚鼠中，研究了单侧听小骨切除和耳蜗损毁对谷氨酸能突触前末梢递质释放及通过摄取实现的谷氨酸失活的影响。(i) 在损伤后长达145天的时间里，测量了耳蜗核（CN）各亚区、上橄榄核（SOC）和听觉中脑（MB）中D-[3H]天冬氨酸的释放和摄取。将这些活性与年龄匹配的未损伤对照组的活性进行比较。通过组织学观察纤维变性情况。(ii) 在同侧CN中，释放和摄取的变化取决于损伤类型。听小骨切除仅在112天后导致纤维稀疏修剪，并在145天时使释放和摄取减少，这与兴奋性谷氨酸能传递的调节减弱一致。耳蜗损毁使CN传入神经缺失，在2天时导致释放和摄取不足，在7天时出现大量纤维变性。随后，残余的释放和摄取量增加，这与兴奋性谷氨酸能传递的增强一致。(iii) 在对侧CN中，无论哪种损伤后，释放和摄取的变化通常与同侧CN中的变化相匹配。因此，与受损耳相关的听觉通路可能为对侧CN中突触强度的调节提供了线索。(iv) 两种损伤均增加了SOC和MB中的释放，以及SOC中的摄取，这与兴奋性谷氨酸能传递的增强一致。耳蜗损毁后，SOC和MB中出现了提示轴突修剪的稀疏纤维变性。(v) 兴奋性谷氨酸能传递的增强可能会促进和维持响度重振和耳鸣等通常伴随听力损失出现的症状。
