Impaired electrical signaling disrupts gamma frequency oscillations in connexin 36-deficient mice

被引:409
作者
Hormuzdi, SG
Pais, I
LeBeau, FEN
Towers, SK
Rozov, A
Buhl, EH
Whittington, MA
Monyer, H
机构
[1] Univ Hosp Neurol, Dept Clin Neurobiol, Heidelberg, Germany
[2] Univ Leeds, Sch Biomed Sci, Leeds LS2 9NQ, W Yorkshire, England
[3] Max Planck Inst Med Res, D-69120 Heidelberg, Germany
基金
英国医学研究理事会;
关键词
D O I
10.1016/S0896-6273(01)00387-7
中图分类号
Q189 [神经科学];
学科分类号
071006 ;
摘要
Neural processing occurs in parallel in distant cortical areas even for simple perceptual tasks. Associated cognitive binding is believed to occur through the interareal synchronization of rhythmic activity in the gamma (30-80 Hz) range. Such oscillations arise as an emergent property of the neuronal network and require conventional chemical neurotransmission. To test the potential role of gap junction-mediated electrical signaling in this network property, we generated mice lacking connexin 36, the major neuronal connexin. Here we show that the loss of this protein disrupts gamma frequency network oscillations in vitro but leaves high frequency (150 Hz) rhythms, which may involve gap junctions between principal cells (Schmitz et al., 2001), unaffected. Thus, specific connexins differentially deployed throughout cortical networks are likely to regulate different functional aspects of neuronal information processing in the mature brain.
引用
收藏
页码:487 / 495
页数:9
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