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Editors Selection IGR 11-3

Basic science: Axotomy

Comment by Harry Quigley on:

14598 Examination of cellular and molecular events associated with optic nerve axotomy, Nitzan A; Kermer P; Shirvan A et al., GLIA, 2006; 54: 545-556

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Nitzan et al. (1049) have transected the optic nerve in rats and report some details of the effect on the area of injury that have not previously been reported regarding the semaphorin 3A molecule. In non-ocular, nervous tissues this molecule has been thought to be associated with the guidance of axons during development. In lay terms, it is like a 'stop' signal that tells an axon not to go its way. The present experiments show that there is a huge increase in semaphorin at the site of the nerve transection, apparently produced by invading microglia, or the altered astrocytes and oligodendrocytes at the wound site. Since this has previously been seen in other central nervous system tissues, the finding is not unexpected. Unfortunately, the experiment was not accompanied by the corroborating evidence of inhibiting this molecule's expression or blocking its action to determine if this would lead to longer survival of retinal ganglion cells, greater time to axonal degeneration, or even, most hopefully, actual regenerative attempts by the axons. There are many potential ways in which such an experiment could have been done.

The finding that p38 is activated in the ganglion cell layer in these rats was included in the Results. This has been reported in many past studies of optic nerve injury, none of which were cited by the authors. Levkovitch-Verbin and others recently have studied the MAP kinase pathways and other changes in the retina after injury, by gene array and RT-PCR, including in experimental glaucoma in much more detail that did Nitzan et al.

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