Spreading acidification and depression in the cerebellar cortex

Timothy J. Ebner, Gang Chen

Research output: Contribution to journalReview articlepeer-review

21 Scopus citations

Abstract

Optical imaging of activity-dependent pH changes using neutral red has revealed a novel form of propagated activity in the cerebellar cortex: spreading acidification and depression (SAD). Evoked by surface stimulation, SAD is characterized by a propagation geometry that reflects the parasagittal architecture of the cerebellum, high speed of propagation across several folia, and a transient depression of the molecular layer circuitry. The properties of SAD differentiate it from other forms of propagating activity in the nervous system including spreading depression and Ca++ waves. Involving several factors, SAD is hypothesized to be a regenerative process that requires a functioning parallel fibers-Purkinje cell circuit, glutamatergic neurotransmission, and is initiated by increased neuronal excitability. Three possible neuronal and glia substrates in the cerebellar cortex could account for the propagation geometry of SAD. Recently, the authors demonstrated that blocking voltage-gated Kv1.1 potassium channels plays a major role in the generation of SAD. This observation has lead to the hypothesis that the episodic and transient disruption in cerebellar function that characterizes episodic ataxia type 1, a Kv1.1 channelopathy, is due to SAD occurring in the cerebellar cortex.

Original languageEnglish (US)
Pages (from-to)37-45
Number of pages9
JournalNeuroscientist
Volume9
Issue number1
DOIs
StatePublished - Feb 1 2003

Keywords

  • Channelopathy
  • Episodic ataxia
  • Parallel fibers
  • Potassium channels
  • Purkinje cells
  • Spreading acidification

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