Stimulus-dependent modulation of spike burst length in cat striate cortical cells
Stimulus-dependent modulation of spike burst length in cat striate cortical cells
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DOI：
10.1152/jn.1997.78.1.199
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发表时间：
1997-07-01
影响因子：
2.5
通讯作者：
Bonds, AB
中科院分区：
文献类型：
--
作者：
DeBusk, BC;DeBruyn, EJ;Bonds, AB
突发活动由两个或多个间隔小于或等于 8 毫秒的尖峰组定义，分析了麻醉猫纹状皮层神经元引起的漂移正弦波光栅的响应。 507 个简单和复杂细胞群的爆发差异很大。该群体中有一半的峰值包含在爆发中，大于或等于 42%。爆发中的尖峰分数不随平均发射率的变化而变化，并且随着时间的推移保持稳定。在 3-5 ms 和 10-30 ms 处均发现峰间间隔直方图的峰值。在许多细胞中，这些峰的位置与放电速率无关，表明在两个不同时间尺度上对放电行为进行了量化控制。较短时间尺度上的活动很可能是由细胞膜的内在特性引起的，而较长时间尺度上的活动很可能是由循环网络激励引起的。突发频率（每秒突发数）和突发长度（每次突发峰值）均取决于发射率。爆发频率基本上与放电率呈线性关系，而爆发长度是放电率的非线性函数，并且也受刺激方向的控制。在给定的发射速率下，最佳方向的爆发长度大于非最佳方向的爆发长度。在外侧膝状核细胞的爆发中没有观察到有组织的方向依赖性。在低响应幅度下激活皮质对比度增益控制不会导致突发长度调制，但在以过饱和为特征的响应中发现最佳方向的突发缩短。在给定的放电速率下，显微注射γ-氨基丁酸（GABA）会缩短皮质爆发长度，而在存在GABA（A）受体阻滞剂N-甲基荷包牡丹碱的情况下，爆发会变得更长。这些结果与一个模型一致，在该模型中，非最佳方向的反应至少部分是由于 GABA 介导的突发缩短而减少的。类似的机制通过招募调节到相邻方向的抑制反应来导致高对比度下的反应过饱和。突发长度调制可以作为一种编码形式，支持动态的、依赖于刺激的单个网络连接有效性的重组。
Burst activity, defined by groups of two or more spikes with intervals of less than or equal to 8 ms, was analyzed in responses to drifting sinewave gratings elicited from striate cortical neurons in anesthetized cats. Bursting varied broadly across a population of 507 simple and complex cells. Half of this population had greater than or equal to 42% of their spikes contained in bursts. The fraction of spikes in bursts did not vary as a function of average firing rate and was stationary over time. Peaks in the interspike interval histograms were found at both 3-5 ms and 10-30 ms. In many cells the locations of these peaks were independent of firing rate, indicating a quantized control of firing behavior at two different time scales. The activity at the shorter time scale most likely results from intrinsic properties of the cell membrane, and that at the longer scale from recurrent network excitation. Burst frequency (bursts per s) and burst length (spikes per burst) both depended on firing rate. Burst frequency was essentially linear with firing rate, whereas burst length was a nonlinear function of firing rate and was also governed by stimulus orientation. At a given firing rate, burst length was greater for optimal orientations than for nonoptimal orientations. No organized orientation dependence was seen in bursts from lateral geniculate nucleus cells. Activation of cortical contrast gain control at low response amplitudes resulted in no burst length modulation, but burst shortening at optimal orientations was found in responses characterized by supersaturation. At a given firing rate, cortical burst length was shortened by microinjection of gamma-aminobutyric acid (GABA), and bursts became longer in the presence of N-methyl-bicuculline, a GABA(A) receptor blocker. These results are consistent with a model in which responses are reduced at nonoptimal orientations, at least in part, by burst shortening that is mediated by GABA. A similar mechanism contributes to response supersaturation at high contrasts via recruitment of inhibitory responses that are tuned to adjacent orientations. Burst length modulation can serve as a form of coding by supporting dynamic, stimulus-dependent reorganization of the effectiveness of individual network connections.