Quantification of the Effect of Different Levels of IOP in the Astroglia of the Rat Retina Ipsilateral and Contralateral to Experimental Glaucoma

Abstract

OHT induces changes in the macroglia of contralateral eyes; thus, these fellow eyes should not be used as control. In eyes with OHT, there is a close relationship between IOP values and decreased AROA.

Different Ipsi- and Contralateral Glial Responses to Anti-VEGF and Triamcinolone Intravitreal Injections in Rats

“…Glial cells and especially microglial cells are the first cells of the central nervous system to react to local and systemic insults such as intraocular pressure increase, systemic infections, and blood glucose levels, [57][58][59][60][62][63][64][65][72][73][74][75][76]93 thus supporting the notion that microglial cells are the sentries of the system and that they react promptly, maybe in order to prepare the system for a further challenge or damage. In this work we observed that unilateral IVI triggers a general glial cell reaction in both eyes that does not fully depend on the substance injected.…”

“…For example, topical instillation of saline to one eye resulted in marked upregulation of the mRNA expression levels of fibroblast growth factor 2 (FGF2) in the intact, contralateral fellow retina. 57 More recently, a detailed study of the macro-and microglia has shown that following elevation of the intraocular pressure in one eye, there are marked changes in the contralateral fellow intact eye, [58][59][60][61][62] highlighting the observation that activation of the retinal macro-and microglia in the uninjured eye may result as a consequence of injury to the contralateral fellow eye-thus confirming original observations that unilateral injury to one adult rat optic nerve may cause multiple cellular responses in the contralateral site. 63 In this work we studied the retinal glial response (microglia, astrocytes and Müller cells) of the rodent retina after single or repeated IVI of the substances most used at present in ophthalmology, anti-VEGF and corticosteroids, and their respective vehicles.…”

“…Recent studies have shown that certain stimuli applied to one eye may trigger molecular and cellular responses in the contralateral untouched retina. This was the case after optic nerve axotomy, 37,63 topical instillation of saline drops, 57 ocular hypertension induced by laser photocoagulation to the limbal tissues, 58,[60][61][62] or after anti-VEGF injection. [29][30][31] At present we do not know the mechanism responsible for the response in the contralateral fellow eyes, but one possibility is the limited systemic absorption of the injected substances, and, alternatively, that retinal or eye injury results in systemic inflammatory or paracrine-mediated effects that reach the fellow eye.…”

Retinal neurodegeneration in experimental glaucoma

“…In addition, there are several spontaneous models of experimental glaucoma in mice with a targeted type I collagen mutation (Aihara et al, 2003) or the DBA/2J mice which develops a pigmentary glaucoma Danias et al, 2003;Filippopoulos et al, 2006;Panagis et al, 2010;Pérez de Lara et al, 2014;Reichstein et al, 2007). In our laboratory, laser photocoagulation (LP) of the limbar tissues has been the method of choice to induce OHT in adult albino rats Ramírez et al, 2010;Salinas-Navarro et al, 2010;Schnebelen et al, 2009;Valiente-Soriano et al, 2015b) and in albino de Hoz et al, 2013;Dekeyster et al, 2015;Gallego et al, 2012;Rojas et al, 2014;Salinas-Navarro et al, 2009c) or pigmented (Nguyen et al, 2011;Valiente-Soriano et al, 2015a) mice. In the LP-OHT models, typical observations are a sectorial loss of RGCs, an initial damage to RGC axons somewhere near the ON head, and an alteration of the retrograde axoplasmic transport that precedes RGC death (Chidlow et al, 2011;Martin et al, 2006;Soto et al, 2011;Vidal-Sanz et al, 2012) all of which are also found in a classic model of glaucoma, the DBA/2J mouse Crish et al, 2010;Filippopoulos et al, 2006;Jakobs et al, 2005), thus making this model relevant to advance our knowledge on the retinal pathology induced by OHT.…”

Topical Treatment With Bromfenac Reduces Retinal Gliosis and Inflammation After Optic Nerve Crush

“…[22][23][24][25][26][27][28] Macroglial retinal cells, astrocytes, and Müller cells readily respond to intravitreral injections, 29 injury, or disease. [30][31][32][33] A very well characterized model of retinal damage and degeneration is optic nerve axotomy in rodents. [34][35][36][37][38][39] Complete intraorbital optic nerve crush (ONC) is an acute insult that kills the vast majority of retinal ganglion cells (RGCs) within the first 2 weeks after injury.…”