Loss of melanopsin-containing retinal ganglion cells in a rat glaucoma model

Intrinsically Photosensitive Retinal Ganglion Cells

“…A mutation in melanopsin may be associated with seasonal affective disorder (165), an effective treatment of which is to deliver intense light to the eyes, particularly light enriched in blue, which drives ipRGCs effectively (194). IpRGCs are also compromised in glaucoma (110, 215), a disease that affects circadian rhythms secondary to compromising vision (42). Finally, melanopsin itself has been delivered to the eyes of mice with degenerated rods and cones as one experimental strategy to restore vision (Fig.…”

Intrinsically Photosensitive Retinal Ganglion Cell Activity Is Associated with Decreased Sleep Quality in Patients with Glaucoma

“…However, a recent study reported the opposite results, concluding that these cells could be lost over the course of the disease. 22 In addition, previous studies have shown that the pupillary reflex could be used to isolate ipRGCs, demonstrating that the numbers of these cells were decreased in advanced glaucoma cases. Furthermore, previous studies have shown that melatonin was a good marker of the circadian phase.…”

“…Nevertheless, a few preliminary studies in animal models of glaucoma have suggested that a loss of ipRGCs impairs circadian rhythm regulation. 21,22 A few human studies have described abnormal circadian rhythms for melatonin secretion and light-induced melatonin suppression in subjects with glaucoma. 23 However, no previous studies have investigated sleep quality or circadian rhythm abnormalities using polysomnography parameters and correlated them with the pupillary light reflex and structural damage parameters in patients with glaucoma.…”

Retinal neurodegeneration in experimental glaucoma

“…RGC survival after 2 weeks of LP was roughly 50% for the Brn3a + RGCs or m + RGCs, both in pigmented mice (Valiente-Soriano et al, 2015a) and albino rats (Valiente-Soriano et al, 2015b). Although m + RGCs have been shown to be more resistant to ON axotomy (Pérez de Sevilla Müller et al, 2014; Robinson and Madison, 2004), NMDA-induced RGC degeneration (DeParis et al, 2012), and inherited optic neuropathies (La Morgia et al, 2010), it is not clear yet if they are also more resistant to OHT-induced retinal injury (de Zavalía et al, 2011;El-Danaf and Huberman, 2015;Jakobs et al, 2005;Li et al, 2006;Wang et al, 2008;Zhang et al, 2013), but our studies do not support such conclusion. However, when compared to the general population of RGCs, the responses of m + RGCs to OHT-induced retinal degeneration differed in two important aspects: (i) the distribution of surviving m + RGCs within the retinas did not show the typical sectorial pattern observed for the general population of Brn3a + RGCs, but rather a diffuse pattern of m + RGCs loss (Fig.…”