Types and density of calretinin-containing retinal ganglion cells in mouse

Lee, Eun-Shil; Lee, Jea-Young; Jeon, Chang‐Jin

doi:10.1016/j.neures.2009.10.008

Cited by 40 publications

(67 citation statements)

References 57 publications

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“…Retinal slices were immunolabeled for the marker proteins calretinin (ganglion cells, ACs), 29, 45 calbindin (amacrine and horizontal cells), protein kinase C α (PKC α ; bipolar cells) and cellular retinaldehyde-binding protein (CRALBP; Müller cells) to quantify the respective cell types. Calretinin immunostaining revealed positive cell bodies in the GCL and INL and three positive bands in the IPL (Figure 4a).…”

Section: Resultsmentioning

confidence: 99%

Differential effects of P2Y1 deletion on glial activation and survival of photoreceptors and amacrine cells in the ischemic mouse retina

et al. 2014

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Gliosis of retinal Müller glial cells may have both beneficial and detrimental effects on neurons. To investigate the role of purinergic signaling in ischemia-induced reactive gliosis, transient retinal ischemia was evoked by elevation of the intraocular pressure in wild-type (Wt) mice and in mice deficient in the glia-specific nucleotide receptor P2Y1 (P2Y1 receptor-deficient (P2Y1R-KO)). While control retinae of P2Y1R-KO mice displayed reduced cell numbers in the ganglion cell and inner nuclear layers, ischemia induced apoptotic death of cells in all retinal layers in both, Wt and P2Y1R-KO mice, but the damage especially on photoreceptors was more pronounced in retinae of P2Y1R-KO mice. In contrast, gene expression profiling and histological data suggest an increased survival of amacrine cells in the postischemic retina of P2Y1R-KO mice. Interestingly, measuring the ischemia-induced downregulation of inwardly rectifying potassium channel (Kir)-mediated K+ currents as an indicator, reactive Müller cell gliosis was found to be weaker in P2Y1R-KO (current amplitude decreased by 18%) than in Wt mice (decrease by 68%). The inner retina harbors those neurons generating action potentials, which strongly rely on an intact ion homeostasis. This may explain why especially these cells appear to benefit from the preserved Kir4.1 expression in Müller cells, which should allow them to keep up their function in the context of spatial buffering of potassium. Especially under ischemic conditions, maintenance of this Müller cell function may dampen cytotoxic neuronal hyperexcitation and subsequent neuronal cell loss. In sum, we found that purinergic signaling modulates the gliotic activation pattern of Müller glia and lack of P2Y1 has janus-faced effects. In the end, the differential effects of a disrupted P2Y1 signaling onto neuronal survival in the ischemic retina call the putative therapeutical use of P2Y1-antagonists into question.

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Section: Resultsmentioning

confidence: 99%

Differential effects of P2Y1 deletion on glial activation and survival of photoreceptors and amacrine cells in the ischemic mouse retina

et al. 2014

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“…The fundamental procedure for single-cell injection following immunocytochemistry on whole mount retina has been previously described in detail [19, 20, 22] and therefore will be presented in a brief outlined. The FITC- and dextran-labeled neurons were viewed with a microscope equipped with a Zeiss 40X Plan Achroplan (NA 0.80) water-immersion lens and Zeiss filter set 09 (excitation, 450–490 nm; emission, 515 nm).…”

Section: Methodsmentioning

confidence: 99%

“…Recently, Völgyi et al [44] have morphologically analyzed 22 RGC subtypes based on soma-dendritic parameters in the mouse. Furthermore, our previous studies have shown the morphology of RGCs with the expression of parvalbumin (PV) [20] and calretinin [22] by using a newly developed single-cell injection method following immunocytochemistry.…”

Section: Introductionmentioning

confidence: 99%

“…Recently, neural circuits with PV-immunoreactive (IR) neurons have been studied in the brain and gradually were shown to function in the neural circuity. Although the systematic study of RGC types with its expression of a particular protein has been previously accomplished for PV and calretinin in the mouse [22, 26], the types of RGCs that project to the superior colliculus (SC), and their expression of specific proteins, have not been studied.…”

Section: Introductionmentioning

confidence: 99%

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Types of Parvalbumin-Containing Retinotectal Ganglion Cells in Mouse

Lee

et al. 2012

Acta Histochem. Cytochem

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The calcium-binding protein parvalbumin (PV) occurs in the retinal ganglion cells (RGCs) of various vertebrate species. In the present study, we aimed to identify the types of PV-containing RGCs that project to the superior colliculus (SC) in the mouse. We injected retrograde tracer dextran into the mouse SC to label RGCs. PV-containing RGCs were first identified by immunocytochemistry and then neurons double-labeled with dextran and PV were iontophoretically injected with a lipophilic dye, DiI. Subsequently, confocal microscopy was used to characterize the morphologic classification of the PV-immunoreactive (IR) retinotectal ganglion cells on the basis of dendritic field size, branching pattern, and stratification within the inner plexiform layer. Among the 8 different types of PV-containing RGCs in the mouse retina, we found all 8 types of RGCs projecting to the SC. The RGCs were heterogeneous in morphology. The combined approach of using tracer injection and a single cell injection after immunocytochemistry on a particular protein will provide valuable data to further understand the functional features of the RGCs which constitute the retinotectal pathway.

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“…A more reliable way to distinguish GCs from ACs, however, is retrograde labeling of GCs. [35][36][37] In the retrogradely labeled mouse retina, the specificity of GABA, glycine, ChAT, and nNOS antibodies in labeling retinal ACs has been recently confirmed, 28 but similar investigations have not been done for TH, 38 CR, [32][33][34] and PV. [29][30][31] Of the multiple subtypes of ACs, GABA ACs are the only subtype that have been confirmed to couple with GCs.…”

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confidence: 99%