UP-REGULATION OF L-TYPE CA2+ CHANNELS IN REACTIVE ASTROCYTES AFTER BRAIN INJURY, HYPOMYELINATION, AND ISCHEMIA

Anti-peptide antibodies that specifically recognize the alpha(1) subun it of class A-D voltage-gated Ca2+ channels and a monoclonal antibody (MANC-1) to the alpha(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 epi lepsy in the hippocampus, mechanical and thermal lesions in the forebr ain, hypomyelination in white matter, and ischemia. immunostaining of the alpha(2) subunit of L-type Ca2+ channels by the MANC-1 antibody wa s increased in reactive astrocytes in each of these forms of brain inj ury. The alpha(1C) subunits of class C L-type Ca2+ channels were upreg ulated in reactive astrocytes located in the affected regions in each of these models of brain injury. although staining for the alpha(1) su bunits of class D L-type. class A P/Q-type, and class B N-type Ca2+ ch annels did not change from patterns normally observed in control anima ls. In all of these models of brain injury, there was no apparent redi stribution or upregulation of the voltage-gated Ca2+ channels in neuro ns. The upregulation of L-type Ca2+ channels in reactive astrocytes ma y contribute to the maintenance of ionic homeostasis in injured brain legions, enhance the release of neurotrophic agents to promote neurona l survival and differentiation, and/or enhance signaling in astrocytic networks in response to injury.