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The Journal of Neuroscience, April 1, 1998, 18(7):2321-2334

Upregulation of L-Type Ca²⁺ Channels in Reactive Astrocytes after Brain Injury, Hypomyelination, and Ischemia

Ruth E. Westenbroek¹, Suzanne B. Bausch¹, Richard C. S. Lin³, Joanne E. Franck², Jeffery L. Noebels⁴, and William A. Catterall¹

Departments of ¹ Pharmacology and ² Neurological Surgery, University of Washington, Seattle, Washington 98195, ³ Allegheny University of the Health Sciences, Philadelphia, Pennsylvania 19102, and ⁴ Developmental Neurogenetics Laboratory, Department of Neurology, Baylor College of Medicine, Houston, Texas 77030

Anti-peptide antibodies that specifically recognize the ₁ subunit of class A-D voltage-gated Ca²⁺ channels and a monoclonal antibody (MANC-1) to the ₂ subunit of L-type Ca²⁺ channels were used to investigate the distribution of these Ca²⁺ channel subtypes in neurons and glia in models of brain injury, including kainic acid-induced epilepsy in the hippocampus, mechanical and thermal lesions in the forebrain, hypomyelination in white matter, and ischemia. Immunostaining of the ₂ subunit of L-type Ca²⁺ channels by the MANC-1 antibody was increased in reactive astrocytes in each of these forms of brain injury. The _1C subunits of class C L-type Ca²⁺ channels were upregulated in reactive astrocytes located in the affected regions in each of these models of brain injury, although staining for the ₁ subunits of class D L-type, class A P/Q-type, and class B N-type Ca²⁺ channels did not change from patterns normally observed in control animals. In all of these models of brain injury, there was no apparent redistribution or upregulation of the voltage-gated Ca²⁺ channels in neurons. The upregulation of L-type Ca²⁺ channels in reactive astrocytes may contribute to the maintenance of ionic homeostasis in injured brain regions, enhance the release of neurotrophic agents to promote neuronal survival and differentiation, and/or enhance signaling in astrocytic networks in response to injury.

Key words: L-type Ca²⁺ channels; reactive astrocytes; brain injury; hypomyelination; ischemia; rat CNS

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Copyright © 1998 Society for Neuroscience  0270-6474/98/1872321-14$05.00/0

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