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      Spreading acidification and depression in the cerebellar cortex.

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          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.

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          Author and article information

          Journal
          Neuroscientist
          The Neuroscientist : a review journal bringing neurobiology, neurology and psychiatry
          SAGE Publications
          1073-8584
          1073-8584
          Feb 2003
          : 9
          : 1
          Affiliations
          [1 ] Department of Neuroscience, University of Minnesota, Minneapolis 55455, USA. ebner001@umn.edu
          Article
          10.1177/1073858402239589
          12580338
          adb9f3c8-88f7-47c2-bd19-701a67dd3c6e
          History

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