Differential Expression of Pax6 Following Bilateral Common Carotid Artery Occlusion

Abstract

Background/aim: Chronic cerebral hypoperfusion causes neuronal damage involving cognitive impairment and development of dementia. Permanent bilateral common carotid artery occlusion (BCCAO) in rat models is used to study chronic cerebral hypoperfusion. Pax6 is used as an early neurogenesis marker which affects the maturation of neuronal cells. However, the expression of PAX 6 after BCCAO is not well understood. In this study, we investigated the expression of PAX6 in the neurogenic zones after BCCAO to evaluate the effects of Pax6 on chronic hypoperfusion.

Materials and methods: Chronic hypoperfusion was induced by BCCAO. Common carotid artery was laid parallel to the vagus nerve and separated from it. Both arteries were occluded using 4-0 silk sutures. Rats who underwent bi-common carotid artery occlusion formed in the BCCAO group, while unoperated rats served as the control group. Brain samples were obtained on days 3 and 14 after BCCAO and subjected to immunohisto-chemistry with NeuN and western blotting for Pax6 and HIF1α.

Results: Compared to the control, the expression of Pax6 increased three days after surgery but did not differ on day 14, while that of NeuN showed the opposite trend. The expression of HIF1α increased three days after surgery.

Conclusion: Bilateral common carotid artery occlusion induced early neurogenesis at three days after BCCAO but this result was not maintained at fourteen days after BCCAO.

Keywords: BCCAO; Pax6; hypoperfusion; neurogenesis.