Stanton S G, Harrison R V
Auditory Science Laboratory, Otolaryngology/Brain and Behavior, The Hospital for Sick Children, Toronto, Ontario M5G 1X8, Canada.
J Comp Neurol. 2000 Oct 9;426(1):117-29. doi: 10.1002/1096-9861(20001009)426:1<117::aid-cne8>3.0.co;2-s.
In the present study, anatomical projections from the medial geniculate body (MGB) to primary auditory cortex (AI) were investigated in normal adult cats and in animals that were neonatally deafened with the ototoxic drug amikacin. Cochleotopic/tonotopic maps in AI (based on neural response characteristic frequency) were obtained with microelectrode recording techniques, and single or multiple injections of retrograde tracers (horseradish peroxidase and fluorescent dyes) were introduced into AI. The AI maps of the amikacin-treated cats had an abnormal cochleotopic organization, such that deprived cortical areas exhibited an expanded representation of intact regions of the damaged cochlea. However, retrograde tracer injections into different regions of AI produced a normal pattern of labeling in the ventral division of the medial geniculate body (MGBv). In both experimental and control animals, the main mass of labeled thalamic cells was found in the MGBv. Different isofrequency contours in AI receive input from different portions of the MGBv. Thus, cell arrays labeled by anterior AI injections were situated medially in MGBv, and injections into posterior AI labeled MGBv more laterally. Furthermore, the deafened cats did not develop a more divergent thalamocortical projection compared with normal control animals, indicating that an abnormal spread of the thalamocortical afferents across the frequency domain in AI (anterior-posterior axis) is not responsible for the altered cochleotopic map in these neonatally deafened animals. The relatively normal thalamocortical projection pattern suggests that, after neonatal cochlear lesions, the major reorganization of cochleotopic maps occurs at subthalamic levels.
在本研究中，对正常成年猫以及新生期用耳毒性药物阿米卡星致聋的动物，研究了内侧膝状体（MGB）至初级听觉皮层（AI）的解剖投射。采用微电极记录技术获得了AI中的耳蜗拓扑/音调拓扑图（基于神经反应特征频率），并将逆行示踪剂（辣根过氧化物酶和荧光染料）单次或多次注入AI。阿米卡星处理的猫的AI图具有异常的耳蜗拓扑组织，使得被剥夺的皮层区域呈现出受损耳蜗完整区域的扩大表征。然而，将逆行示踪剂注入AI的不同区域，在内侧膝状体腹侧部（MGBv）产生了正常的标记模式。在实验动物和对照动物中，标记的丘脑细胞主要集中在MGBv。AI中不同的等频率轮廓接收来自MGBv不同部分的输入。因此，由AI前部注射标记的细胞阵列位于MGBv的内侧，而注入AI后部则标记MGBv更靠外侧的区域。此外，与正常对照动物相比，致聋的猫并未形成更分散的丘脑皮质投射，这表明AI中丘脑皮质传入纤维在频域（前后轴）上的异常扩散并非这些新生期致聋动物耳蜗拓扑图改变的原因。相对正常的丘脑皮质投射模式表明，新生期耳蜗损伤后，耳蜗拓扑图的主要重组发生在丘脑下水平。
