mGluRs Protect OPCs

Valuable for Remyelination of Damaged Neurons

We add a new publication to our mGluR Markers Category: Arthur M. Butt, Ilaria Vanzulli, Maria Papanikolaou, Irene Chacon De La Rocha, Virginia E. Hawkins. Metabotropic Glutamate Receptors Protect Oligodendrocytes from Acute Ischemia in the Mouse Optic Nerve. Neurochem Res (2017). doi:10.1007/s11064-017-2220-1. Its focus is the protective characteristics of mGluRs.

Images: Expression of mGluR in optic nerve oligodendrocytes. a RT-qPCR of mGluR subtypes in the postnatal (P8–12) and young adult (P30–35) optic nerve, compared to cortex at the same ages (inset); data are expressed as mean ± SEM ΔΔCT relative to GAPDH, ***p < 0.001 determined by ANOVA and post hoc Bonferroni’s test. b, c Oligodendrocytes in optic nerve explant cultures from P8 PLP-DsRed reporter mice after 10 DIV were immunolabelled for mGluR2/3 (d) and mGluR5 (e), illustrating single channels (Di, Dii, Ei, Eii) and the merged channel in which mGluR colocalization with PLP appears white (Diii, Eiii); scale bars 10 µm

Diabetic retinopathy blindness-root causes

Diabetic retinopathy is a leading cause of acquired blindness. This publication from our friends at University of Buenos Aires touches on potential root causes: Diego C. Fernandez, Laura A. Pasquini, Damián Dorfman, Hernán J. Aldana Marcos, Ruth E. Rosenstein. Early Distal Axonopathy of the Visual Pathway in Experimental Diabetes. doi:10.1016/j.ajpath.2011.09.018
" In animals that had been diabetic for 6 weeks, a large increase in astrocyte reactivity occurred in the distal (but not the intraorbital) portion, which coincided with significant axon loss. Moreover, profound myelin alterations and altered morphologic features of oligodendrocyte lineage were observed at the distal (but not the proximal) optic nerve portion. The present results suggest that axoglial alterations at the distal portion of the optic nerve could be the first structural change in the diabetic visual pathway."
The authors used our PDGFR Alpha/CD140A Marker to Study the change in Oligodendrocyte Lineage precursor cells. Expression of the protein was increased in these cells with the presence of disorganized and hypertrophic cells. This could disrupt formation of myelin resulting the pathological alteration at the distal portion.