Although the authors claim that “there are as of yet no reports on the effect of these used anesthetic regimen (ketamine and xylazine) on RD (retinal degeneration)” and the paper presents “novel evidence that anesthesia with katamine-xylazine has a protective effect on photoreceptor cell death caused by light exposure in rats”, this finding is NOT novel at all. Many previous studies demonstrated the protective effects. It is unfortunate that these studies are not cited by the authors of this paper.

The neuroprotective effect of xylazine, an α-2 adrenergic agonist, was first discovered by Wen et al (J Neurosci 1996 16:5986) while using ketamin/xylazine in their studies. They demonstrated that it was xylazine, not ketamine, that protects photoreceptors from light damage in rats. They further showed that xylazine and clonidine, another α-2 adrenergic agonists specifically induce bFGF expression in retinal Müller cells. Subsequent studies demonstreated that systemic application of α-2 adrenergic agonists selectively activates ERK kinase in retinal Müller cells (Peng et al, IOVS 1998 39:1721). Thus, it is believed that the neuroprotective effects of α-2 adrenergic agonists is mediated by Müller cells and perhaps through autocrine of bFGF and the ERK kinase pathway.

Further studies demonstrated that α-2 adrenergic agonist brimonidine protects retinal function, assessed by ERG, after acute retinal ischemic injury in the rat (Lai et al, 2002Vis Neurosci 19:175), and prevents axonal and somatic degeneration of retinal ganglion cells (Lambert et al, 2011 Mol Neurodegeneration 6:4). Xylazine also has been shown to promote xonal regnereation in the crushed optic nerve model (Kurimoto et al, 2006 Nerureport 17:1525).