Increased Bcl-w expression following focally evoked limbic seizures in therat

Control of seizure-induced neuronal death may involve members of the Bcl-2 family of cell death regulating proteins. Bcl-w is a newly described anti-a poptotic member of this family that may confer neuroprotective effects. We therefore investigated Bcl-w expression in rat brain following focally evok ed limbic seizures. Seizures were induced by unilateral microinjection of k ainic acid into the amygdala of the rat and terminated after 40 min by diaz epam. Constitutive Bcl-w expression was detected by Western blotting and im munohistochemistry. Bcl-w expression was increased 4-72 h following seizure s within the injured hippocampus. Immunohistochemistry determined Bcl-w was predominantly expressed in neurons and seizures increased Bcl-w immunoreac tivity within piriform cortex and surviving regions of the injured hippocam pus. These data suggest Bcl-w may be involved in the modulation of seizure- induced brain injury. (C) 2001 Elsevier Science Ireland Ltd. All rights res erved.