Wickesberg R E
Department of Psychology, University of Illinois at Urbana-Champaign 61820, USA.
J Acoust Soc Am. 1996 Sep;100(3):1691-702. doi: 10.1121/1.416067.
This study examined responses to pairs of clicks recorded extracellularly from single units in ventral cochlear nuclei (VCN) of ketamine-anesthetized chinchillas. The response to the trailing click was suppressed for interclick intervals of 1 and 2 ms, but little suppression was observed for an interclick interval of 4 ms. To determine whether any suppression originated in the dorsal cochlear nucleus (DCN), responses to click pairs were recorded before and after injecting lidocaine in the deep layer of the DCN. For 19% of the neurons (7/37), the response to the trailing click increased following the injection, which is consistent with lidocaine reducing delayed inhibition from the DCN. Unexpectedly, for 62% of the units (23/37) the response to the initial click decreased after lidocaine administration. Three units (3/37 or 8%) showed a combination of both responses. For 52% of the units with a decreased response (12/23), the reduction occurred only for loud clicks (> or = 30 dB above threshold), while at intensities 20 dB lower, responses to pairs of clicks were unchanged. No changes in spontaneous rate were observed. Following lidocaine injections, the tuning curves of 7/12 neurons tested had increased thresholds, but only around the characteristic frequency. These results indicate the presence of two rapid inhibitory inputs onto VCN neurons.
本研究检测了氯胺酮麻醉的龙猫腹侧耳蜗核（VCN）中单个神经元细胞外记录到的对成对点击声的反应。对于1毫秒和2毫秒的点击间隔，对尾随点击声的反应受到抑制，但对于4毫秒的点击间隔，几乎未观察到抑制现象。为了确定是否有任何抑制作用起源于背侧耳蜗核（DCN），在DCN深层注射利多卡因之前和之后记录对点击对的反应。对于19%的神经元（7/37），注射后对尾随点击声的反应增强，这与利多卡因减少来自DCN的延迟抑制作用一致。出乎意料的是，对于62%的单位（23/37），利多卡因给药后对初始点击声的反应减弱。三个单位（3/37或8%）表现出两种反应的组合。对于52%反应减弱的单位（12/23），仅在高声强点击（高于阈值30分贝或更高）时反应降低，而在低20分贝的强度下，对成对点击声的反应未改变。未观察到自发发放率的变化。利多卡因注射后，测试的12个神经元中有7个的调谐曲线阈值升高，但仅在特征频率附近。这些结果表明在VCN神经元上存在两种快速抑制性输入。
