Comparative Study on Calretinin Immunoreactivity in Gerbil and Rat Retina

Hwang, In Koo; Yoo, Ki‐Yeon; Kim, D. S.; Jung, Jongwan; Shin, Min Cheol; Seo, Kangmoon; Kim, K.-S.; Kang, Tae‐Cheon; Won, Moo‐Ho

doi:10.1111/j.1439-0264.2004.00583.x

Cited by 24 publications

(17 citation statements)

References 28 publications

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“…multiple types of retinal neurons in other species. 33,34 With GCs being retrogradely identified, our results demonstrate that neither GCs nor ACs can be safely identified by PV-IR or CR-IR in the mouse retina. Some CR-IR ACs were found to couple to GCs.…”

Section: Several Immunological Subtypes Of Acs Can Couple To Gcs Butmentioning

confidence: 71%

“…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.…”

mentioning

confidence: 98%

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Survey on Amacrine Cells Coupling to Retrograde-Identified Ganglion Cells in the Mouse Retina

Pang

Paul

2013

Invest. Ophthalmol. Vis. Sci.

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Section: Several Immunological Subtypes Of Acs Can Couple To Gcs Butmentioning

confidence: 71%

mentioning

confidence: 98%

Survey on Amacrine Cells Coupling to Retrograde-Identified Ganglion Cells in the Mouse Retina

Pang

Paul

2013

Invest. Ophthalmol. Vis. Sci.

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“…These cells are usually positive to CaB, but negative to CaR and PV (Hamano et al, 1990;Haverkamp and Wä ssle, 2000;Bytyqi and Layer, 2005;Hwang et al, 2005;Curto et al, 2007). Nonetheless, discrepancies exist between members of a given subfamily (Sanna et al, 1993), likely in relation with their environmental adaptation.…”

Section: Retinal Anatomymentioning

confidence: 93%

Retinal anatomy and visual performance in a diurnal cone‐rich laboratory rodent, the Nile grass rat (Arvicanthis niloticus)

Gaillard

Bonfield

Gilmour

et al. 2008

J of Comparative Neurology

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Unlike laboratory rats and mice, muridae of the Arvicanthis family (A. ansorgei and A. niloticus) are adapted to functioning best in daylight. To date, they have been used as experimental models mainly in studies of circadian rhythms. However, recent work aimed at optimizing photoreceptor-directed gene delivery vectors (Khani et al. [2007] Invest Ophthalmol Vis Sci 48:3954-3961) suggests their potential usefulness for studying retinal pathologies and therapies. In the present study we analyzed the retinal anatomy and visual performance of the Nile grass rat (A. niloticus) using immunohistofluorescence and the optokinetic response (OKR). We found that approximately 35-40% of photoreceptors are cones; that many neural features of the inner retina are similar to those in other diurnal mammals; and that spatial acuity, measured by the OKR, is more than two times that of the usual laboratory rodents. These observations are consistent with the known diurnal habits of this animal, and further support its pertinence as a complementary model for studies of structure, function, and pathology in cone-rich mammalian retinae.

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“…Mouse anticalretinin (1:1,000 dilution; BD Transduction) was employed as a reference marker of inner retina cells. The characteristics of the anti-CRT antibody have been fully described by Acosta et al (5), and the calretinin antibody has been fully characterized in the mouse (1) and rat (48) retina. The immunocytochemical protocol includes 1 h of blocking in 6% normal goat serum, 1% (vol/vol) bovine serum albumin, and 0.5% (vol/vol) Triton X-100, followed by incubation overnight in antibodies diluted in 3% (vol/vol) normal goat serum, 1% (vol/vol) bovine serum albumin, and 0.5% (vol/vol) Triton X-100.…”

Section: Methodsmentioning

confidence: 99%

Retinal metabolic state of the proline-23-histidine rat model of retinitis pigmentosa

Acosta¹,

Shin²,

Ready³

et al. 2010

American Journal of Physiology-Cell Physiology

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-We determined the metabolic changes that precede cell death in the dystrophic proline-23-histidine (P23H) line 3 (P23H-3) rat retina compared with the normal SpragueDawley (SD) rat retina. Metabolite levels and metabolic enzymes were analyzed early in development and during the early stages of degeneration in the P23H-3 retina. Control and degenerating retinas showed an age-dependent change in metabolite levels and enzymatic activity, particularly around the time when phototransduction was activated. However, lactate dehydrogenase (LDH) activity was significantly higher in P23H-3 than SD retina before the onset of photoreceptor death. The creatine/phosphocreatine system did not contribute to the increase in ATP, because phosphocreatine levels, creatine kinase, and expression of the creatine transporter remained constant. However, Na ϩ -K ϩ -ATPase and Mg 2ϩ -Ca 2ϩ -ATPase activities were increased in the developing P23H-3 retina. Therefore, photoreceptor apoptosis in the P23H-3 retina occurs in an environment of increased LDH, ATPase activity, and higher-than-normal ATP levels. We tested the effect of metabolic challenge to the retina by inhibiting monocarboxylate transport with ␣-cyano-4-hydroxycinnamic acid or systemically administering the phosphodiesterase inhibitor sildenafil. Secondary to monocarboxylate transport inhibition, the P23H-3 retina did not demonstrate alterations in metabolic activity. However, administration of sildenafil significantly reduced LDH activity in the P23H-3 retina and increased the number of terminal deoxynucleotidyl transferase biotin-dUPT nick end-labeled photoreceptor cells. Photoreceptor cells with a rhodopsin mutation display an increase in apoptotic markers secondary to inhibition of a phototransduction enzyme (phosphodiesterase), suggesting increased susceptibility to altered cation entry.phosphocreatine; ATP; ␣-cyano-4-hydroxycinnamic acid; sildenafil; lactate dehydrogenase; ATPase RETINITIS PIGMENTOSA is the term given to a family of retinal disorders that cause blindness due to gradual loss of photoreceptors. Although photoreceptor cell death in retinitis pigmentosa has a number of underlying causes that include rhodopsin mutations (94), altered photoreceptor oxygen environment (36,103,104), disk morphogenesis, retinal pigment epithelium dysfunction, and chronic activation of photoreceptor transduction cascade (80), the understanding of the cell death pathways is still evolving. It is generally accepted that cell death in inherited forms of retinal degeneration occurs via the process of apoptosis (16,66,82,92), an active cellular process requiring energy (25). The concept of apoptosis as the major pathway of cell death in inherited forms of retinal degeneration has recently been questioned with a proposal that nonapoptotic pathways also contribute to photoreceptor death (7,23,42,63,86,107).Increased metabolic activity is a potential cause of photoreceptor death in some models of retinal dystrophy, such as the rd/rd (rd1) model, where cyclic nucleotide channels are malfu...

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Comparative Study on Calretinin Immunoreactivity in Gerbil and Rat Retina

Cited by 24 publications

References 28 publications

Survey on Amacrine Cells Coupling to Retrograde-Identified Ganglion Cells in the Mouse Retina

Survey on Amacrine Cells Coupling to Retrograde-Identified Ganglion Cells in the Mouse Retina

Retinal anatomy and visual performance in a diurnal cone‐rich laboratory rodent, the Nile grass rat (Arvicanthis niloticus)

Retinal metabolic state of the proline-23-histidine rat model of retinitis pigmentosa

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