Immunohistochemical evidence for dysregulation of the GABAergic system ipsilateral to photochemically induced cortical infarcts in rats.

摘要: Abstract Deficits of GABAergic transmission have been reported to occur in tissue surrounding ischemic cortical lesions between a few days and several weeks after the insult. In present experiments, we used immunohistochemistry with antibodies aagainst parvalbumin two major subunits GABAA receptor (α1, α2) characterize events that underlie these changes at different levels circuit organization. Neocortical infarcts (∼2 mm diameter) consistently affecting medial parts primary somatosensory cortex were induced photochemically adult male Wistar rats; animals allowed recover for one week before perfusion–fixation. When compared controls pattern immunoreactivity had changed α1 subunit seven Ipsilateral lesions, found decrease staining intensity reaching up 4 mm laterally, resulting partial or complete absence normal laminar pattern. No consistent observed α2 subunit. Parvalbumin revealed pathological alterations rim infarct, measuring 1 mm from border infarcts. Parvalbumin-positive interneurons this region showed signs degeneration; both reduction number dendrites and, lesser extent only immediately adjacent parvalbumin-positive neurons was readily apparent. The results provide evidence differential regulation degenerative parvalbumin-containing ipsilateral relevance findings mechanisms underlying long-term recovery, transient functional deficits postinfarct seizures warrants further investigation.