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Adenosine triphosphate-induced photoreceptor death and retinal remodeling in rats.

Vessey KA, Greferath U, Aplin FP, Jobling AI, Phipps JA, Ho T, De Iongh RU, Fletcher EL - J. Comp. Neurol. (2014)

Bottom Line: Intravitreal administration of adenosine triphosphate (ATP) has recently been found to induce acute photoreceptor death.ATP caused significant loss of visual function within 1 day and loss of 50% of the photoreceptors within 1 week.These extreme changes were also observed in the 2-year-old P23H rhodopsin transgenic rat model of retinitis pigmentosa.

View Article: PubMed Central - PubMed

Affiliation: Department of Anatomy and Neuroscience, The University of Melbourne, Melbourne, Victoria, 3010, Australia.

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Related in: MedlinePlus

Amacrine and ganglion cell morphology following ATP-induced photoreceptor degeneration. Sections of retinae from saline- and ATP-treated eyes were labelled for a subset of amacrine and ganglion cells (calretinin, green) and cell nuclei (DAPI, blue) at 3 months (A: saline; B,C: ATP) and 6 months (D: saline; E,F: ATP) post-injection. For each time point, two example regions of ATP-treated retinae are presented. Arrowheads in F indicate extreme remodeling events of amacrine cell processes displaced into the choroid. ONL, outer nuclear layer; OPL, outer plexiform layer; INL, inner nuclear layer; IPL, inner plexiform layer; GCL, ganglion cell layer. Scale bars = 20 μm.
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fig07: Amacrine and ganglion cell morphology following ATP-induced photoreceptor degeneration. Sections of retinae from saline- and ATP-treated eyes were labelled for a subset of amacrine and ganglion cells (calretinin, green) and cell nuclei (DAPI, blue) at 3 months (A: saline; B,C: ATP) and 6 months (D: saline; E,F: ATP) post-injection. For each time point, two example regions of ATP-treated retinae are presented. Arrowheads in F indicate extreme remodeling events of amacrine cell processes displaced into the choroid. ONL, outer nuclear layer; OPL, outer plexiform layer; INL, inner nuclear layer; IPL, inner plexiform layer; GCL, ganglion cell layer. Scale bars = 20 μm.

Mentions: Amacrine and ganglion cells were identified with an antibody against calretinin (Fig. 7). At 3 months following ATP, calretinin-positive amacrine cells in the inner nuclear layer and ganglion cells/amacrine cells in the ganglion cell layer were generally well preserved (Fig. 7B,C) and of similar morphology to saline-injected retinae (Fig. 7A). Furthermore, in regions of ATP-injected eyes with remnant photoreceptors, the processes of these cells were found to laminate in three layers within the inner plexiform layer (Fig. 7B), similar to control retinae (Fig. 7A) and consistent with healthy rodent retinae (Sherry et al., 2003). In regions where photoreceptor nuclei were absent, calretinin-positive processes appeared irregular yet still formed three distinct laminae (Fig. 7C). By 6 months after ATP injection, calretinin-positive cells were less regular in number and spacing, and their processes were frequently disorganized (Fig. 7E). In some regions, severe remodeling had occurred, with processes found to extend into the choroid (Fig. 7F, arrowheads). Overall, the effects of ATP treatment on neuronal remodeling correlate well with events common to retinal degenerations (Marc et al., 2003). However, there were instances of neurons and process connections outside the neural retinae, an extreme and unusual remodeling event that is not commonly described for retinal degenerations but was also found to be apparent in the 2-year-old P23H rat retina.


Adenosine triphosphate-induced photoreceptor death and retinal remodeling in rats.

Vessey KA, Greferath U, Aplin FP, Jobling AI, Phipps JA, Ho T, De Iongh RU, Fletcher EL - J. Comp. Neurol. (2014)

Amacrine and ganglion cell morphology following ATP-induced photoreceptor degeneration. Sections of retinae from saline- and ATP-treated eyes were labelled for a subset of amacrine and ganglion cells (calretinin, green) and cell nuclei (DAPI, blue) at 3 months (A: saline; B,C: ATP) and 6 months (D: saline; E,F: ATP) post-injection. For each time point, two example regions of ATP-treated retinae are presented. Arrowheads in F indicate extreme remodeling events of amacrine cell processes displaced into the choroid. ONL, outer nuclear layer; OPL, outer plexiform layer; INL, inner nuclear layer; IPL, inner plexiform layer; GCL, ganglion cell layer. Scale bars = 20 μm.
© Copyright Policy - open-access
Related In: Results  -  Collection

License
Show All Figures
getmorefigures.php?uid=PMC4265795&req=5

fig07: Amacrine and ganglion cell morphology following ATP-induced photoreceptor degeneration. Sections of retinae from saline- and ATP-treated eyes were labelled for a subset of amacrine and ganglion cells (calretinin, green) and cell nuclei (DAPI, blue) at 3 months (A: saline; B,C: ATP) and 6 months (D: saline; E,F: ATP) post-injection. For each time point, two example regions of ATP-treated retinae are presented. Arrowheads in F indicate extreme remodeling events of amacrine cell processes displaced into the choroid. ONL, outer nuclear layer; OPL, outer plexiform layer; INL, inner nuclear layer; IPL, inner plexiform layer; GCL, ganglion cell layer. Scale bars = 20 μm.
Mentions: Amacrine and ganglion cells were identified with an antibody against calretinin (Fig. 7). At 3 months following ATP, calretinin-positive amacrine cells in the inner nuclear layer and ganglion cells/amacrine cells in the ganglion cell layer were generally well preserved (Fig. 7B,C) and of similar morphology to saline-injected retinae (Fig. 7A). Furthermore, in regions of ATP-injected eyes with remnant photoreceptors, the processes of these cells were found to laminate in three layers within the inner plexiform layer (Fig. 7B), similar to control retinae (Fig. 7A) and consistent with healthy rodent retinae (Sherry et al., 2003). In regions where photoreceptor nuclei were absent, calretinin-positive processes appeared irregular yet still formed three distinct laminae (Fig. 7C). By 6 months after ATP injection, calretinin-positive cells were less regular in number and spacing, and their processes were frequently disorganized (Fig. 7E). In some regions, severe remodeling had occurred, with processes found to extend into the choroid (Fig. 7F, arrowheads). Overall, the effects of ATP treatment on neuronal remodeling correlate well with events common to retinal degenerations (Marc et al., 2003). However, there were instances of neurons and process connections outside the neural retinae, an extreme and unusual remodeling event that is not commonly described for retinal degenerations but was also found to be apparent in the 2-year-old P23H rat retina.

Bottom Line: Intravitreal administration of adenosine triphosphate (ATP) has recently been found to induce acute photoreceptor death.ATP caused significant loss of visual function within 1 day and loss of 50% of the photoreceptors within 1 week.These extreme changes were also observed in the 2-year-old P23H rhodopsin transgenic rat model of retinitis pigmentosa.

View Article: PubMed Central - PubMed

Affiliation: Department of Anatomy and Neuroscience, The University of Melbourne, Melbourne, Victoria, 3010, Australia.

Show MeSH
Related in: MedlinePlus