Limiting photoreceptor death and deconstruction during experimental retinal detachment: the value of oxygen supplementation

Animal models of retinal detachment and reattachment: identifying cellular events that may affect visual recovery

“…The cellular 'degeneration' that ensues is limited to photoreceptors and this usually does not result in complete destruction of these cells, but rather a process that we have termed 'deconstruction' of all, and the death of some. 7 We have preferred the term 'retinopathy,' to describe the results of detachment because it involves a variety of complex but characteristic cellular responses in many different retinal cell types. 8 Most importantly, many of the events initiated by detachment can be halted or reversed by reattachment, or by providing certain specific biological factors such as the trophic factor known as 'brain-derived neurotrophic factor' (BDNF), 9 or an increase in environmental oxygen (hyperoxia).…”

Changes in Membrane Conductance Play a Pathogenic Role in Osmotic Glial Cell Swelling in Detached Retinas

“…Moreover, we show that various purinergic receptor agonists such as ATP and UTP may inhibit osmotic Mü ller cell swelling as well. UTP may act on UTP-sensitive purinergic receptors, ie, P2Y 2 and P2Y 4 . 42 Pharmacological activation of P2Y 2 receptors has been shown to stimulate the subretinal fluid reabsorption and reattachment of experimentally detached retinas 43 via activation of ion and water transport through the pigment epithelium.…”

“…Experimental detachment causes complex cellular responses in the neural retina. 2 The damage to the outer segments and the apoptotic death of photoreceptor cells, 3,4 as well as the morphological and biochemical alterations of inner retinal neurons, [5][6][7][8] are associated with activation of macro-and microglial cells. 9 -13 Among the various gliotic responses being characteristic for the detached retina, Mü ller glial cells display a decrease in their K ϩ conductance.…”

Deficiency of Bax and Bak protects photoreceptors from light damage in vivo

“…5 The cell death in this model is most likely hypoxia induced, as breathing high oxygen content air can partially protect photoreceptors. 6,7 Similarly, hypoxia-induced activation of the apoptotic pathway in vitro is rescued by Bax deficiency, and Bak activation in this system is dependent upon the presence of Bax. 8 In contrast to the cell death induced by hypoxia, Bak can be activated in the absence of Bax when cell death is induced by staurosporine exposure, growth factor withdrawal, and UV irradiation.…”