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Neonatal hypoxic/ischemic brain injury induces production of calretinin-expressing interneurons in the striatum.

Ischemia-induced striatal neurogenesis from progenitors in the adjacent subventricular zone (SVZ) in young and adult rodents has been reported. However, it has not been established whether the precursors that reside in the SVZ retain the capacity to produce the full range of striatal neurons that has been destroyed. By using a neonatal rat model of hypoxic/ischemic brain damage, we show here that virtually all of the newly produced striatal neurons are calretinin (CR)-immunoreactive (+), but not DARPP-32(+), calbindin-D-28K(+), parvalbumin(+), somatostatin(+), or choline acetyltransferase(+). Retroviral fate-mapping studies confirm that these newly born CR(+) neurons are indeed descendants of the SVZ. Our studies indicate that, although the postnatal SVZ has the capacity to produce a range of neurons, only a subset of this repertoire is manifested in the brain after injury.

Pubmed ID: 18720478 RIS Download

Mesh terms: Animals | Animals, Newborn | Biomarkers | Calbindin 2 | Corpus Striatum | Dopamine and cAMP-Regulated Phosphoprotein 32 | Female | Humans | Hypoxia-Ischemia, Brain | Interneurons | Microtubule-Associated Proteins | Neuropeptides | Pregnancy | Rats | Rats, Wistar | S100 Calcium Binding Protein G | Tyrosine 3-Monooxygenase

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