Examining the proliferation and fate of new cells in the brain following chronic cerebral hypoperfusion

About time someone looked at new neurons after stroke. From the 2011 Canadian Stroke Congress.
page 119 here:
http://www.strokecongress.org/2011/wp-content/uploads/2011/12/CSC_Abstracts.pdf
Human and animal studies demonstrate that during stroke recovery the brain has a remarkable ability for innate repair. This is hypothesized to be partly due to newly dividing cells localized in the known neurogenic regions of the subgranular zone (SGZ) and subventricular zone (SVZ), as well as the infarct area. In rodents, this has primarily been shown following middle cerebral artery occlusion. Little is known whether a similar response occurs following cerebral hypoperfusion. To determine the proliferative response following cerebral hypoperfusion, we quantified proliferation one week following bilateral common carotid artery occlusion (2VO). Male Long Evans rats were randomly assigned to 2VO or sham surgery and compared to home cage controls. Proliferating cells were labeled with bromodeoxyuridine (BrdU, 2h) and brains were processed by immunohistochemistry for BrdU, doublecortin (DCX, immature neurons) and glial fibrillary acidic protein (GFAP, astrocytes). As expected BrdU+ cells were present in the SVZ and SGZ of all rats. However, qualitatively more BrdU+ cells were found in 2VO rats as compared to controls. In the SGZ, there was a 1.5 and 2.5 fold increase in BrdU+ cells in the 2VO animals compared to sham and home cage controls, respectively. BrdU+ cells were also observed in hypoperfused rats in the prefrontal cortex (bregma +2.96) and the striatum (bregma +1.18). The cells in these two regions were not positive for DCX or GFAP, suggesting that they are neither immature neurons nor astrocytes. Following 2VO there is an increase in proliferation in the known adult neurogenic regions and striatum, which is commonly observed
in other stroke models. To our knowledge, this is the first identification of cell division in the cortex following chronic hypoperfusion. This is exciting as these newly dividing cells may be able to be harnessed in order to enhance functional recovery.