To cite this article: Neuroendocrinol Lett 2010; 31(4):530–537 ORIGINAL ARTICLE Neuroendocrinology Letters Volume 31 No. 4 2010 Ultra structural evidence of axonal regeneration following intracranial transection of optic nerve Rasha Ahmad Elmansy 1 , Abdel Rahman El Shahat 2 , Masood Ahmed Shaikh 3 1 Department of Anatomy, Faculty of Medicine, Ainshamas University, Egypt 2 Department of Anatomy, Faculty of Medicine, Cairo University, Egypt 3 Department of Anatomy & Histology, College of Medicine, Qassim University, Al-Qassim, Saudi Arabia Correspondence to: Prof. Masood Ahmed, MBBS., MPhil., PhD. Department of Anatomy & Histology, College of Medicine, Qassim University P. O. BOX #6666, 51452, AL-Qassim, Saudi Arabia. tel: +966-6-3800050 ext. 2503; fax: +966-6-3802275; e-mail: shaikhm_63@hotmail. com Submitted: 2010-07-10 Accepted: 2010-07-18 Published online: 2010-08-27 Key words: optic nerve; regeneration; axonal injury; axonal growth Neuroendocrinol Lett 2010; 31(4):530–537 PMID: 20802438 NEL310410A16 © 2010 Neuroendocrinology Letters • www. nel. edu Abstract OBJECTIVE: The present work was aimed at studying the ultra structural changes of the proximal (retinal) stump of the intracranially transected optic nerve of the rat for any possible regenerative ability. METHODS: Specimens were collected one (1 wpo) and four weeks(4 wpo) after the transection and the cross sections of the stumps were studied by electron micros- copy by dividing them into three zones, (1) the central zone, (2) the intermediate zone, and (3) the peripheral zone. RESULTS: The present results showed evident morphological changes in these zones both in the 1 wpo and 4 wpo groups. The signs of degeneration were more marked in the central zone than in the peripheral zone and they were more promi- nent in the 1 wpo group than in the 4 wpo group. The most prominent sign of the degeneration was loss or lack of the healthy myelinated axons. The main evidence of the regenerative ability was the reappearance of the apparently healthy myelin- ated axonal profiles, with a parallel decrease of the non myelinated ones. This regenerative feature was more prominent peripherally and might be an indication that ischemia was the cause of optic nerve degeneration. CONCLUSION: The present work revealed a clear morphological evidence of the regenerative capability of the intracranially transected optic nerve though it is considered as a part of the CNS. INTRODUCTION Most neurons in the mammalian brain are gener- ated embryonically during the restricted phases and the mature mammalian brain is character- ized by a relatively constant number of neurons. There is still a low rate of constitutive gliogenesis and a more restricted neurogenesis in the adult mammalian central nervous system (CNS) (Rakic 2002). It has long been thought that neurons gen- erally are not replaced in the mammalian brain after injury or during the course of a disease. Interestingly, several recent studies have reported compensatory proliferation and neurogenesis in response to injury or disease in the mammalian brain (Emsley et al. 2005). Axon growth is a highly