ERG changes in albino and pigmented mice after optic nerve transection

Alarcón-Martínez, Luis; Avilés‐Trigueros, Marcelino; Galindo‐Romero, Caridad; Valiente‐Soriano, Francisco J.; Agudo‐Barriuso, Marta; Villa, Pedro de la; Villegas‐Pérez, María Paz; Vidal‐Sanz, Manuel

doi:10.1016/j.visres.2010.08.014

Cited by 53 publications

(45 citation statements)

References 62 publications

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“…Consistent with reports from other groups, 42,49,50 ONC resulted in a significant reduction of pSTR amplitudes in vehicle-treated mice at 7 days after axonal injury. However, this reduction was significantly attenuated by AMG487 treatment ( Figure 5, B and C).…”

Section: Pharmacological Blockade Of Cxcr3 Partially Prevents Rgc Dyssupporting

confidence: 91%

Critical Role of the CXCL10/C-X-C Chemokine Receptor 3 Axis in Promoting Leukocyte Recruitment and Neuronal Injury during Traumatic Optic Neuropathy Induced by Optic Nerve Crush

Liu

Zhu

et al. 2017

The American Journal of Pathology

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Traumatic optic neuropathy (TON) is an acute injury of the optic nerve secondary to trauma. Loss of retinal ganglion cells (RGCs) is a key pathological process in TON, yet mechanisms responsible for RGC death remain unclear. In a mouse model of TON, real-time noninvasive imaging revealed a dramatic increase in leukocyte rolling and adhesion in veins near the optic nerve (ON) head at 9 hours after ON injury. Although RGC dysfunction and loss were not detected at 24 hours after injury, massive leukocyte infiltration was observed in the superficial retina. These cells were identified as T cells, microglia/monocytes, and neutrophils but not B cells. CXCL10 is a chemokine that recruits leukocytes after binding to its receptor C-X-C chemokine receptor (CXCR) 3. The levels of CXCL10 and CXCR3 were markedly elevated in TON, and up-regulation of CXCL10 was mediated by STAT1/3. Deleting CXCR3 in leukocytes significantly reduced leukocyte recruitment, and prevented RGC death at 7 days after ON injury. Treatment with CXCR3 antagonist attenuated TON-induced RGC dysfunction and cell loss. In vitro co-culture of primary RGCs with leukocytes resulted in increased RGC apoptosis, which was exaggerated in the presence of CXCL10. These results indicate that leukocyte recruitment in retinal vessels near the ON head is an early event in TON and the CXCL10/CXCR3 axis has a critical role in recruiting leukocytes and inducing RGC death. (Am J Pathol 2017, 187: 352e365; http://dx

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Section: Pharmacological Blockade Of Cxcr3 Partially Prevents Rgc Dyssupporting

confidence: 91%

Critical Role of the CXCL10/C-X-C Chemokine Receptor 3 Axis in Promoting Leukocyte Recruitment and Neuronal Injury during Traumatic Optic Neuropathy Induced by Optic Nerve Crush

Liu

Zhu

et al. 2017

The American Journal of Pathology

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“…Two weeks after ONT in mice, 82% of RGC (identified via retrograde labelling) were lost and pSTR amplitude had decreased by 60%(Alarcon-Martinez et al, 2010). Interestingly, at 12 weeks post-ONT, the pSTR had increased to only 50% of that of control, despite further loss in RGC.…”

Section: Functional Assessmentsmentioning

confidence: 99%

Evaluating retinal ganglion cell loss and dysfunction

Mead

Tomarev

2016

Experimental Eye Research

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Retinal ganglion cells (RGC) bear the sole responsibility of propagating visual stimuli to the brain. Their axons, which make up the optic nerve, project from the retina to the brain through the lamina cribrosa and in rodents, decussate almost entirely at the optic chiasm before synapsing at the superior colliculus. For many traumatic and degenerative ocular conditions, the dysfunction and/or loss of RGC is the primary determinant of visual loss and are the measurable endpoints in current research into experimental therapies. To actually measure these endpoints in rodent models, techniques must ascertain both the quantity of surviving RGC and their functional capacity. Quantification techniques include phenotypic markers of RGC, retrogradely transported fluorophores and morphological measurements of retinal thickness whereas functional assessments include electroretinography (flash and pattern) and visual evoked potential. The importance of the accuracy and reliability of these techniques cannot be understated, nor can the relationship between RGC death and dysfunction. The existence of up to 30 types of RGC complicates the measuring process, particularly as these may respond differently to disease and treatment. Since the above techniques may selectively identify and ignore particular subpopulations, their appropriateness as measures of RGC survival and function may be further limited. This review discusses the above techniques in the context of their subtype specificity.

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“…Hydroxystilbamidine methanesulfonate (OHSt) (Molecular Probes, Leiden, The Netherlands) diluted at 10% in 0.9% NaCl and 10% dimethylsulfoxide was applied to both superior colliculi (SCi) 1 week before surgery or 10 days before processing (intact animals), as previously described. 21,48,49 In brief, after exposing the midbrain, a small pledge of gel foam (Espongostan Film; Ferrosan A/S, Soeborg, Denmark) soaked in OHSt was applied over the entire surface of both SCi.…”

Section: Surgerymentioning

confidence: 99%