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Action potential broadening in a presynaptic channelopathy

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Listed:
  • Rahima Begum

    (UCL Institute of Neurology, University College London, Queen Square)

  • Yamina Bakiri

    (UCL Institute of Neurology, University College London, Queen Square)

  • Kirill E. Volynski

    (UCL Institute of Neurology, University College London, Queen Square)

  • Dimitri M. Kullmann

    (UCL Institute of Neurology, University College London, Queen Square)

Abstract

Brain development and interictal function are unaffected in many paroxysmal neurological channelopathies, possibly explained by homoeostatic plasticity of synaptic transmission. Episodic ataxia type 1 is caused by missense mutations of the potassium channel Kv1.1, which is abundantly expressed in the terminals of cerebellar basket cells. Presynaptic action potentials of small inhibitory terminals have not been characterized, and it is not known whether developmental plasticity compensates for the effects of Kv1.1 dysfunction. Here we use visually targeted patch-clamp recordings from basket cell terminals of mice harbouring an ataxia-associated mutation and their wild-type littermates. Presynaptic spikes are followed by a pronounced afterdepolarization, and are broadened by pharmacological blockade of Kv1.1 or by a dominant ataxia-associated mutation. Somatic recordings fail to detect such changes. Spike broadening leads to increased Ca2+ influx and GABA release, and decreased spontaneous Purkinje cell firing. We find no evidence for developmental compensation for inherited Kv1.1 dysfunction.

Suggested Citation

  • Rahima Begum & Yamina Bakiri & Kirill E. Volynski & Dimitri M. Kullmann, 2016. "Action potential broadening in a presynaptic channelopathy," Nature Communications, Nature, vol. 7(1), pages 1-9, November.
    • Handle: RePEc:nat:natcom:v:7:y:2016:i:1:d:10.1038_ncomms12102
    DOI: 10.1038/ncomms12102
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