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

Neuron. 2001 Aug 16;31(3):487-95. doi: 10.1016/s0896-6273(01)00387-7.

Abstract

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.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Aging
  • Animals
  • Brain / growth & development
  • Brain / physiology*
  • Carbachol / pharmacology
  • Cerebral Cortex / physiology
  • Connexins / deficiency
  • Connexins / genetics
  • Connexins / physiology*
  • Electroencephalography
  • Gap Junctions / physiology
  • Gene Expression Regulation, Developmental
  • Hippocampus / drug effects
  • Hippocampus / physiology*
  • In Vitro Techniques
  • Kainic Acid / pharmacology
  • Mice
  • Mice, Knockout
  • Nerve Net / physiology*
  • Neurons / drug effects
  • Neurons / physiology*
  • Oscillometry
  • RNA, Messenger / analysis
  • Reverse Transcriptase Polymerase Chain Reaction
  • Signal Transduction
  • Transcription, Genetic

Substances

  • Connexins
  • RNA, Messenger
  • connexin 36
  • Carbachol
  • Kainic Acid