[Skip to Content]
Access to paid content on this site is currently suspended due to excessive activity being detected from your IP address Please contact the publisher to request reinstatement.
[Skip to Content Landing]
September 2003

Mitochondrial Function and Dysfunction Within the Optic Nerve

Arch Ophthalmol. 2003;121(9):1342-1343. doi:10.1001/archopht.121.9.1342-a

We read with great interest and satisfaction the report by Bristow et al in the June 2002 issue of the ARCHIVES.1 The authors use 3 different models (human, pig, and rabbit optic nerve) and histochemical and immunocytochemical techniques to demonstrate that the pattern of mitochondrial distribution is inversely related to that of myelination; they conclude that mitochondria build up where energy is needed. We certainly agree. We would like to point out previous studies that have come to similar conclusions. In 1998, we published findings from a horizontal sagittal section of a normal human optic nerve stained for cytochrome-c oxidase and concluded that the accumulation at the lamina cribrosa was due to higher respiratory activity anterior to the point of myelination.2 In that article, we also refer to the work of Brady, 3 who describes the transport of mitochondria as being irregular and a reflection of the local metabolic needs. For example, he observed that mitochondria can accumulate at the nodes of Ranvier.

First Page Preview View Large
First page PDF preview
First page PDF preview