Spreading Acidification and Depression in the Cerebellar Cortex  

Oleh:

Ebner, Timothy J. ; Gang, Chen

Jenis: Article from Journal - ilmiah internasional
Dalam koleksi: The Neuroscientist vol. 9 no. 1 (Feb. 2003), page 37–45.
Topik: Spreading acidification; Parallel fibers; Purkinje cells; Channelopathy; Episodic ataxia; Potassium channels
Fulltext: 37TN91.pdf (164.5KB)

Isi artikel

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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