COMPARISON OF EVOKED-POTENTIALS AND HIGH-FREQUENCY (GAMMA-BAND) OSCILLATING-POTENTIALS IN RAT AUDITORY-CORTEX
COMPARISON OF EVOKED-POTENTIALS AND HIGH-FREQUENCY (GAMMA-BAND) OSCILLATING-POTENTIALS IN RAT AUDITORY-CORTEX
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DOI：
10.1152/jn.1995.74.1.96
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发表时间：
1995-07-01
影响因子：
2.5
通讯作者：
BARTH, DS
中科院分区：
文献类型：
--
作者：
FRANOWICZ, MN;BARTH, DS
1.方法1.在15只轻度麻醉大鼠的听觉皮层及其邻近区域，用8 × 8电极的外膜阵列记录瞬态和稳态（40 Hz）诱发电位，以及自发和咔哒声诱发的γ波段振荡，以确定和比较这四种现象的时空分布.瞬态诱发反应复制了我们实验室的早期发现，包括41区的初始双相尖波，36区的类似但延迟的双相尖波，以及更广泛分布的慢波成分。时空分析支持丘脑皮质投射的平行和异步激活的模型，这些投射是中潜伏期听觉诱发电位（MAEP）复合体的这些颞叶成分的神经发生的基础. 40赫兹的点击列车的反应叠加在一个稳定的电位移动（SP），这两个都是本地化的初级听觉皮层。SP的Epipial分布与在同一动物中记录的41区的最短潜伏期负峰相似，表明类似的神经发生器。40-Hz反应更集中，与SP和MAEP复合体的任何其他时间成分不同，表明其神经发生的细胞亚群是独特的。自发的γ-波段活动，功率谱分析评估，本地化的初级和次级听觉皮层，但有一个变量之间的分布不符合该地区的细分内的cytoarchitectonic边界的大鼠。数字电影计算的个别突发的伽玛活动表明，一个高度的时空变化内和突发之间。点击反应的单次试验光谱分析表明，在大多数的MAEP复合物的抑制γ-波段振荡，随后增强的γ-活性在300- 350-ms的慢波组件，持续时间超过了MAEP类似500毫秒。epipial分布的prestimulus和增强的poststimulus γ-振荡是相同的。与40 Hz的点击序列反应相反，单次点击刺激的γ振荡锁相并没有被抑制。这些结果表明，无论是MAEP复合物和稳态40 Hz的响应与其相关的SP是高度刻板的轻度麻醉啮齿动物皮层。它们的时空分布可能在很大程度上是由并行丘脑皮质投射系统的异步激活决定的。我们的数据表明，无论是MAEP或稳态40赫兹的响应自发或诱发的伽玛波段振荡的听觉皮层之间没有直接的联系。在41、36和20区内迅速传播的γ振荡的显著时空变异性表明，皮质内的神经发生器独立于直接丘脑皮质起搏器的影响。这一假设得到了以下观测结果的进一步支持：持续伽马振荡的空间分布和相位都不受MAEP的影响。然而，听觉刺激后γ-突触的后抑制增强可能表明听觉信息处理中的作用，这并不反映在刺激特定的空间分布或相位关系。
1. Transient and steady-state (40 Hz) evoked potentials, as well as spontaneous and click-evoked gamma-band oscillations, were recorded from 15 lightly anesthetized rats using an 8 x 8 electrode epipial array covering auditory cortex and adjacent areas to determine and compare the spatiotemporal distributions of these four phenomena.2. The transient evoked response replicated earlier findings in our laboratory, consisting of an initial biphasic sharp wave in area 41, a similar but delayed biphasic sharp wave in area 36, and more widely distributed slow-wave components. Spatiotemporal analysis supported a model of parallel and asynchronous activation of distinct groups of thalamocortical projections underlying the neurogenesis of these temporal components of the middle-latency auditory evoked potential (MAEP) complex.3. The 40-Hz response to click trains was superimposed on a steady potential shift (SP), both of which were localized within primary auditory cortex. Epipial distributions of the SP were similar to those of the shortest-latency negative peak in area 41 recorded in the same animals, suggesting similar neural generators. The 40-Hz response was more focal and dissimilar from the SP and any other temporal components of the MAEP complex, suggesting that a unique subpopulation of cells underlies its neurogenesis.4. Spontaneous gamma-band activity, as assessed by power spectrum analysis, was localized to primary and secondary auditory cortex but had a variable distribution between rats that did not conform to the cytoarchitectonic boundaries within subdivisions of this region. Digital movies computed for individual bursts of gamma-activity indicated a high degree of spatiotemporal variability within and between bursts.5. Single-trial spectral analysis of click responses indicated an inhibition of gamma-band oscillations during most of the MAEP complex, with subsequent enhanced gamma-activity during the 300- to 350-ms slow-wave component that outlasted the MAEP by similar to 500 ms. The epipial distributions of prestimulus and enhanced poststimulus gamma-oscillations were the same. In contrast to the 40-Hz response to click trains, phase-locking of gamma-oscillations by the single click stimulus was not observed.6. These results suggest that both the MAEP complex and the steady-state 40-Hz response with its associated SP are highly stereotyped in lightly anesthetized rodent cortex. Their spatiotemporal distributions are probably determined in large part by asynchronous activation of parallel thalamocortical projection systems. Our data suggest no direct link between either the MAEP or the steady-state 40-Hz response to spontaneous or evoked gamma-band oscillations in auditory cortex. The notable spatiotemporal variability of gamma-oscillations, with rapid spread within areas 41, 36, and 20, suggests a neural generator within the cortex independent of direct thalamocortical pacemaker influence. This hypothesis is further supported by the observation that neither the spatial distribution nor the phase of ongoing gamma-oscillations is influenced by the MAEP. However, postinhibitory enhancement of gamma-oscilla tions after auditory stimulation may indicate a role in auditory information processing that is not reflected in either a stimulus-specific spatial distribution or phase relationship.