Localization of a 42-kDa inositol 1,3,4,5-tetrakisphosphate receptor protein in retina and change in expression after optic nerve injury

Kreutz, Michael R.; Böckers, Tobias M.; Sabel, Bernhard A.; Stricker, Rolf; Hülser, E; Reiser, Georg

doi:10.1016/s0169-328x(96)00264-1

Cited by 16 publications

(9 citation statements)

References 40 publications

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“…Mild ONC is enough to shear but does not completely axotomize the nerve axons. Studies using this model have shown a loss of almost 70–80% retinal ganglion cells (RGCs) as a result of early necrosis and subsequent apoptosis within 2 weeks after injury (Sautter and Sabel, 1993; Kreutz et al, 1997; Bien et al, 1999; Kreutz et al, 1999). Near‐complete, spontaneous behavioral recovery was observed 2–3 weeks after the mild crush, but only 28% and 11% of RGCs survived at 2 and 14 days after crush, respectively, (Sautter and Sabel, 1993).…”

Section: Discussionmentioning

confidence: 99%

Protease‐activated receptor subtype expression in developing eye and adult retina of the rat after optic nerve crush

Rohatgi

Sedehizade

Sabel

et al. 2003

J of Neuroscience Research

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Protease-activated receptors (PARs), 7-transmembrane domain G protein-coupled receptors, are involved in tissue degeneration and repair upon injury. We demonstrate the expression of all four PAR subtypes in the postnatal eye and in retina of the adult rat by reverse transcription-polymerase chain reaction (RT-PCR). PAR-1 is regulated developmentally in the eye, with a decrease from P1, P9, to P16, whereas levels for PAR-2, PAR-3, and PAR-4 remain unchanged throughout. In the retina of the adult rat, PAR-1 is highly expressed, whereas PAR-2 and PAR-3 are moderately expressed, compared to low PAR-4 expression. To elucidate possible roles of PARs after trauma, we carried out semiquantitative RT-PCR analysis of expression of all 4 PAR subtypes, beginning 6 hr after partial optic nerve crush (ONC) in the adult rat until 3 weeks after the mild trauma. Levels of PAR mRNA for all four subtypes were upregulated as early as 6 hr after unilateral ONC, except PAR-3, which showed a delayed upregulation. PAR-1, PAR-3, and PAR-4 mRNA levels returned to almost basal levels at 3 weeks post-crush, whereas PAR-2 mRNA level was still high by the end of 3 weeks after crush. Although the lesion was unilateral, PAR mRNA expression in the contralateral, uninjured side was affected to levels almost comparable to those in the injured side. Previous studies have shown an increase in thrombin levels at the site of injury, retinal ganglion cell degeneration by necrosis and apoptosis, and PAR activation as consequences of nerve crush. PAR upregulation because of nerve crush in the mild trauma model could act as an effector of early cell death. Eventual return of receptor mRNA to basal levels is consistent with neuroprotection.

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Section: Discussionmentioning

confidence: 99%

Protease‐activated receptor subtype expression in developing eye and adult retina of the rat after optic nerve crush

Rohatgi

Sedehizade

Sabel

et al. 2003

J of Neuroscience Research

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“…2B). This label was not present on control sections treated with RNAse and was also not present on cryostat sections hybridized with other probes utilizing the same protocol (see Kreutz et al 1997Kreutz et al , 1998.…”

Section: Localization Of Caldendrin Transcripts and Proteins In The Amentioning

confidence: 95%

The cytoskeleton-associated neuronal calcium-binding protein caldendrin is expressed in a subset of amacrine, bipolar and ganglion cells of the rat retina

Menger¹,

Seidenbecher²,

Gundelfinger³

et al. 1999

Cell and Tissue Research

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Caldendrin is a novel calcium-binding protein confined to the somatodendritic compartment of neurons. Here we have studied the expression pattern of caldendrin in the rat retina. First we assessed the distribution of caldendrin transcripts in the adult and developing retina by in situ hybridization. In the adult retina, transcripts are expressed mainly in the inner half of the inner nuclear layer (INL) and to a lesser extent in the ganglion cell layer (GCL). During development labeling of the inner part of the cytoblast layer, where amacrine cells reside, is already present at postnatal day 1 (P1). The intensity of hybridization signal in this sublamina of the developing INL increases up to P8, whereas significant labeling in the GCL was first found at P14, coinciding with eye opening. Immunodetection with a polyclonal antibody revealed intensive staining of cells in the inner retina, which are presumably mainly amacrine and significantly fewer bipolar and ganglion cells. All parvalbumin-containing All amacrines were immunopositive for caldendrin. Colocalization with calbindin was found in cone bipolar cells, the majority of AII amacrines, and calbindin-positive cells in the GCL. In the GCL, caldendrin was also colocalized with calretinin-immunopositive cells. Most caldendrin-positive amacrine cells in the adult rat retina were glycinergic and only a few were GABAergic. In retinal flat mounts, it was confirmed that less than 10% of retrogradely labeled retinal ganglion cells (RGC) are caldendrin-positive. Caldendrin immunoreactivity does not colocalize with tyrosine hydroxylase, VIP, substance P and somatostatin immunoreactivity. In summary, caldendrin expression is regulated differentially in retinal cell types during development and is restricted to a subpopulation of amacrine, bipolar, and ganglion cells, suggesting specific functions in the developing and mature retina.

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“…Janssen, Mac Nair, Dietz, Schlamp, and Nickells () has reported the nuclear shrinkage of amacrine cells after optic nerve injury. In addition, 42‐kDa inositol 1, 3, 4, 5‐tetrakisphosphate receptor protein is upregulated in the photoreceptor's inner segments after optic nerve crush (Kreutz et al, ).…”

Section: Introductionmentioning

confidence: 99%

Change in phospholipid species of retinal layer in traumatic optic neuropathy model

Hirahara

Wakabayashi

Koike

et al. 2019

J of Neuroscience Research

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Injured optic nerves induce death in almost all retinal ganglion cells (RGC) and cause a loss of axons. To date, we have studied injured RGC axon regeneration by using a traumatic optic nerve injury (TONI) rodent model, and we revealed that axonal regeneration is induced by the graft of an autologous peripheral nerve. The efficient approach to the regeneration of axons thus needs an environmental adjustment of RGC. However, the RGC environment induced by TONI remains unknown. Here, we analyzed female and male C57BL/6 mouse retinal tissue alterations in detail after TONI and focused on the major phospholipid species that are enriched in the whole retina. Reactive astrocyte accumulation, glia scar formation, and demyelination were observed in the injured optic nerve area, while RGC cell death, astrocyte accumulation, and Glial fibrillary acidic protein (GFAP) positive Müller cell increases were detected in the retinal layer. Furthermore, phosphatidylinositol (PI) 18:0/20:4 was localized to three nuclear layer structures: the ganglion cell layer (GCL), the inner nuclear layer (INL), and the outer nuclear layer (ONL) in control retina; however, the localization of 18:0/20:4 PI in TONI was disturbed. Meanwhile, phosphatidylserine (PS) 18:0/22:6showed that the expression was specifically in the inner plexiform layer (IPL) with similar signal intensity in both cases. Other PS species and phosphatidylethanolamine (PE) were differentially localized in the retinal layer; however, the expressions of PE including docosahexaenoic acid (DHA) were affected by TONI. These results suggest that not only GCL but also other retinal layers were influenced by TONI.

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Localization of a 42-kDa inositol 1,3,4,5-tetrakisphosphate receptor protein in retina and change in expression after optic nerve injury

Cited by 16 publications

References 40 publications

Protease‐activated receptor subtype expression in developing eye and adult retina of the rat after optic nerve crush

Protease‐activated receptor subtype expression in developing eye and adult retina of the rat after optic nerve crush

The cytoskeleton-associated neuronal calcium-binding protein caldendrin is expressed in a subset of amacrine, bipolar and ganglion cells of the rat retina

Change in phospholipid species of retinal layer in traumatic optic neuropathy model

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