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Editors Selection IGR 15-2

Basic Research: Reduction in neuronal function in LGN

Comment by Ronald Harwerth on:

27908 Dendrite plasticity in the lateral geniculate nucleus in primate glaucoma, Ly T; Gupta N; Weinreb RN et al., Vision Research, 2011; 51: 243-250

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Although glaucoma is an optic neuropathy caused by the death of retinal ganglion cells, recent work by this group has provided evidence of neuropathy in higher centers of the afferent visual pathway, especially the lateral geniculate nucleus (LGN). Such alterations suggest an activity-dependent reduction in neuronal function in the LGN that should be considered in treatment and/or neuro-protection paradigms. In order to explore these effects farther, an investigation by Ly et al. (116) was undertaken to determine whether the characteristics of the dendrites of the LGN relay neurons were modified by experimental glaucoma in primates and, if so, were the changes modifiable by memantine. Measurements of dendritic field size and complexity were compared across groups of macaque monkeys with either normal intraocular pressures (controls) or elevated intraocular pressures from laser scarification of the trabecular meshwork (experimental glaucoma). The monkeys with experimental glaucoma were subdivided into vehicle and memantine treatment groups. Methods of immunohistochemistry were used to identify the relay neurons and their dendrites for comparison across the three groups.

It has been suggested that there is an activity-dependent reduction in neuronal function in the lateral geniculate nucleus that should be considered in treatment and/or neuro-protection paradigms

The results of the study showed a pressure-related reduction in the mean complexity and length of the dendrites of LGN relay neurons in the monkeys with experimental glaucoma, compared to controls, but the dendrite changes were less in the monkeys treated with memantine, compared to the vehicle treated animals. The experimental results are interesting and demonstrate a greater level of preservation of neuronal structure with memantine, but as the authors point out, it is not clear whether there is preservation of neuronal function or how long the treatment effect might last. However, the important point of the study is that there may be a form of neuroprotection that maintains neuronal structure for a period of time until the disease is treated to retain the health of the retinal ganglion cells.

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