MIDDLE-LATENCY AND LONG-LATENCY AUDITORY EVOKED-RESPONSES RECORDED FROM THE VERTEX OF NORMAL AND CHRONICALLY LESIONED CATS
MIDDLE-LATENCY AND LONG-LATENCY AUDITORY EVOKED-RESPONSES RECORDED FROM THE VERTEX OF NORMAL AND CHRONICALLY LESIONED CATS
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DOI：
10.1016/0006-8993(81)90722-8
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发表时间：
1981-01-01
期刊：
影响因子：
2.9
通讯作者：
BROWN, KA
中科院分区：
文献类型：
--
作者：
BUCHWALD, JS;HINMAN, C;BROWN, KA
从清醒的受限制的猫的顶点记录了一个潜伏期为1-250 ms的听觉诱发电位延长序列。该序列在受试者内部和受试者之间可重复，并且不因神经肌肉完全麻痹而改变。研究了点击率、戊巴比妥和慢性损伤对不同脑区电位的影响。顶点波1-5之前起源于脑干初级听觉通路的发生器，随后是较小且定义不明确的波6和7，其峰值潜伏期分别在6-8 ms和10-12 ms范围内。这些潜力不会被快速点击率（即高达50/s）或中等水平的戊巴比妥所消除。相关的颅外和颅内研究表明，波6与内侧膝状体，主部电位在相同的潜伏期范围内发生，波7与初级外脑皮层电位在相同的潜伏期范围内发生。颅内电位表现出与第6波和第7波相似的咔嗒恢复功能和巴比妥耐药，第7波在抽吸后消失。波6和波7明显反映内侧膝状体和外脑回的发生器。与电位1-7的稳定性相反，较长的潜伏期波相对不稳定。波A的潜伏期为17- 25ms，波B为35- 45ms，波C为50- 75ms，波D为150- 200ms。所有这些波都表现出明显的幅度波动，当点击率增加到10/s时消失，并被中等水平的戊巴比妥消除。双侧中背上回、外脑回或额叶抽吸后，A波继续出现。在切除了所有皮质、基底节区和边缘叶的半脑切除术后，1只动物的A波没有消失，反而出现增强。波A的产生系统似乎在很大程度上独立于听觉皮层和邻近的联想皮层，但可能受到其他前脑系统的调节。脑波C在上、外脑回抽吸后和额叶切除后继续出现；然而，在半脑切除术后，它消失了。波C反映了一个不同于波a的产生系统，但它似乎也在很大程度上独立于初级膝小叶皮层听觉通路。波1到波7表现出高保真度、抗速率、巴比妥酸盐不敏感的声音传输，明显反映了从听神经到听觉皮层的初级听觉系统的激活。随后，较长潜伏期的顶点电位似乎是通过其他接收听觉信息的前脑系统产生的，这些系统平行地从干接收听觉信息，而不是依次地从初级膝丘-皮层通路和关联皮层中继接收。讨论了cat模型中数据与人体顶点电位的相关性。
A prolonged sequence of auditory-evoked potentials with latencies ranging from 1-250 ms was recorded from the vertex of the awake restrained cat. This sequence was reproducible within and across subjects, and was not altered by complete neuromuscular paralysis. The effects of click rate, pentobarbital and chronic lesions of a number of different brain areas were evaluated for each of the potentials. Vertex waves 1-5, previously originating from generators in the primary auditory pathway of the brain stem, were followed by smaller and less well-defined waves, 6 and 7, with peak latencies in the 6-8 ms and 10-12 ms range, respectively. These potentials were not abolished by fast click rates (i.e., up to 50/s) nor by moderate levels of pentobarbital. Correlative extra- and intracranial studies indicated that wave 6 occurred in the same latency range as the medial geniculate body, pars principalis potential, and that wave 7 occurred in the same latency range as the primary ectosylvian cortical potential. The intracranial potentials showed click recovery functions and barbiturate resistance which were similar to those of waves 6 and 7, and wave 7 disappeared following aspiration of ectosylvian cortex. Waves 6 and 7 apparently reflect generators in medial geniculate body and ectosylvian gyrus. In contrast to the stability of potentials 1-7, the longer latency waves were relatively unstable. Wave A occurred in a latency range of 17-25 ms, wave B, 35-45 ms, wave C, 50-75 ms, and wave D, 150-200 ms. All of these waves showed marked amplitude fluctuations, disappeared as click rates increased to 10/s, and were abolished by moderate levels of pentobarbital. After bilateral aspiration of middle suprasylvian gyrus, ectosylvian gyrus or frontal lobes, wave A continued to appear. After hemispherectomy, which removed all cortex, basal ganglia and limbic lobes, wave A was not abolished and appeared enhanced in 1 animal. The generator system of wave A appears to be largely independent of auditory cortex and adjacent association cortex, but may be modulated by other forebrain systems. Wave C continued to appear after aspiration of suprasylvian and ectosylvian gyri and after frontal lobectomy; it disappeared, however, after hemispherectomy. Wave C reflects a generator system which differs from that of wave A, but which also appears to be largely independent of the primary geniculo-cortical auditory pathway. Waves 1 through 7, which show high fidelity, rate-resistant, barbiturate-insensitive acoustic transmission, apparently reflect activation of the primary auditory system from acoustic nerve to auditory cortex. Subsequent, longer-latency vertex potentials seem to be generated through other forebrain systems, which receive auditory information, in parallel from the stem, rather than serially from the primary geniculo-cortical pathway and association cortex relays. The relevance of data in the cat model to the human vertex potentials is discussed.