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Presynaptic activity regulates Na+ channel distribution at the axon initial segment

Author

Listed:
  • Hiroshi Kuba

    (Career-Path Promotion Unit for Young Life Scientists,)

  • Yuki Oichi

    (Career-Path Promotion Unit for Young Life Scientists,)

  • Harunori Ohmori

    (Kyoto University Graduate School of Medicine, Kyoto 606-8501, Japan)

Abstract

A centre for neural control The axon initial segment (AIS) at the base of each nerve fibre, where clusters of sodium channels generate the action potential that then propagates along the axon, is a focus of much attention from neuroscientists working on the nature of neuronal excitability. As the source of a nerve impulse, it seems a logical point at which to regulate neural activity. Two papers in this issue confirm that the AIS is a source of intrinsic neuronal plasticity. Matthew Grubb and Juan Burrone show that electrical activity reversibly alters the position of the AIS in cultured hippocampal neurons. They suggest that the resulting increase in intrinsic excitability may fine-tune neuronal excitability during development, and point to potential targets for the control of epilepsy. Hiroshi Kuba, Yuki Oichi and Harunori Ohmori show that the size of the AIS increases in bird auditory neurons deprived of sound stimulation. Again intrinsic excitability increases, possibly contributing to the maintenance of the auditory pathway. Such neuronal plasticity may compensate some forms of hearing loss.

Suggested Citation

  • Hiroshi Kuba & Yuki Oichi & Harunori Ohmori, 2010. "Presynaptic activity regulates Na+ channel distribution at the axon initial segment," Nature, Nature, vol. 465(7301), pages 1075-1078, June.
  • Handle: RePEc:nat:nature:v:465:y:2010:i:7301:d:10.1038_nature09087
    DOI: 10.1038/nature09087
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    Cited by:

    1. Hyoseon Oh & Suho Lee & Yusang Oh & Seongbin Kim & Young Seo Kim & Yeji Yang & Woochul Choi & Ye-Eun Yoo & Heejin Cho & Seungjoon Lee & Esther Yang & Wuhyun Koh & Woojin Won & Ryunhee Kim & C. Justin , 2023. "Kv7/KCNQ potassium channels in cortical hyperexcitability and juvenile seizure-related death in Ank2-mutant mice," Nature Communications, Nature, vol. 14(1), pages 1-20, December.

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