Purchase this article with an account.
Tsung-Han Chou, Xu Yang, Vittorio Porciatti; Retrograde Signaling In The Optic Nerve Is Necessary For Normal Electrical Responsiveness Of Retinal Ganglion Cells. Invest. Ophthalmol. Vis. Sci. 2012;53(14):1956.
Download citation file:
© ARVO (1962-2015); The Authors (2016-present)
To investigate the role of retrograde signaling on retinal ganglion cell (RGC) function in an in vivo mouse model.
Electrical response of RGC was measured by pattern electroretinogram (PERG) in 16 C57BL/6J mice (B6) 4-6 months old under ketamine/xylazine anesthesia. Outer retina response was measured by photopic flash ERG (FERG). PERGs and FERGs were recorded before and at different times after A) blockade of optic nerve axon transport by means of retrobulbar injections of Lidocaine (40 µg/µl), B) removal of the main target of RGC axons by means of surgical ablation of the superior colliculus (SC).
After Lidocaine injection, the PERG amplitude progressively decreased within 30 min to a plateau ~ 50% smaller than baseline (n=5, P<0.001). The PERG amplitude fully recovered the next day. The FERG was unaltered throughout the procedure. Two hours after SC-lesion, the PERG amplitude decreased in the eye contralateral to the lesion to a level ~ 50% smaller than baseline. PERG loss after SC lesion remained stable up to three months (n=11, P<0.01). Brn3b immunohistochemistry of excised retinas did not reveal reduction of RGC counts from normal, but did reveal shrinkage of RGC somas (P<0.05).
Blockade of axon transport or removal of the main target of RGC axons causes loss PERG signal of similar magnitude but with different time constants. This implies that retrograde transport of target-derived molecules is necessary for normal RGC electrical responsiveness. Shrinkage of RGC somas after SC-lesion suggests a neurotrophic component. Overall, results are compatible with neurotrophin-mediated regulation of RGC function.
This PDF is available to Subscribers Only