Increased Bcl-w expression following focally evoked limbic seizures in the rat.

Autor: Henshall DC; Robert S. Dow Neurobiology Laboratories, Legacy Clinical Research & Technology Center, 1225 NE 2nd Avenue, Portland, OR, 97232, USA. dhenshall@DowNeurobiology.org, Skradski SL, Lan JQ, Ren T, Simon RP
Jazyk: angličtina
Zdroj: Neuroscience letters [Neurosci Lett] 2001 Jun 15; Vol. 305 (3), pp. 153-6.
DOI: 10.1016/s0304-3940(01)01849-3
Abstrakt: 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-apoptotic member of this family that may confer neuroprotective effects. We therefore investigated Bcl-w expression in rat brain following focally evoked limbic seizures. Seizures were induced by unilateral microinjection of kainic acid into the amygdala of the rat and terminated after 40 min by diazepam. Constitutive Bcl-w expression was detected by Western blotting and immunohistochemistry. Bcl-w expression was increased 4-72 h following seizures within the injured hippocampus. Immunohistochemistry determined Bcl-w was predominantly expressed in neurons and seizures increased Bcl-w immunoreactivity within piriform cortex and surviving regions of the injured hippocampus. These data suggest Bcl-w may be involved in the modulation of seizure-induced brain injury.
Databáze: MEDLINE