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Leonard A Levin

Publications and source records attributed to Leonard A Levin.

7 recordsLinked to original sources
PubMed2003

Retinal ganglion cells and neuroprotection for glaucoma.

Neuroprotection is a therapeutic strategy directed at keeping retinal ganglion cells (RGCs) alive and functional. This article discusses three commonly asked questions about neuroprotection and attempts to answer them in the context of our current understanding of the pathophysiology of RGC loss in glaucomatous optic neuropathy.

Cytoprotection↗
PubMed2003

Cell-type-specific opening of the retinal ganglion cell mitochondrial permeability transition pore.

PURPOSE: To study the role of the mitochondrial permeability transition pore (PTP) in apoptosis of axotomized retinal ganglion cells (RGCs) in vitro. METHODS: Primary rat retinal cultures containing DiI-labeled RGCs were treated with pharmacological agents that modulate the PTP. Ratiometric imaging of the mitochondrial membrane potential (DeltaPsi(m)) were conducted on similarly treated cultures, with the dual-emission probe JC-1, and the correlation with the results of the viability experiments were determined. RESULTS: The peripheral benzodiazepine receptor agonist PK11195 induced RGC death, but this was not inhibited by cyclosporin A (CsA), which normally maintains the PTP in the closed configuration. Paradoxically, the combination of CsA and PK11195 caused massive RGC death and decreased DeltaPsi(m), suggesting aberrant regulation of the PTP in these cells. Imaging of DeltaPsi(m) revealed morphologic changes in the mitochondria after depolarization, characterized by formation of ringlike bodies, and similar to that with the potassium ionophore valinomycin. There were no such findings with other retinal neurons or neuronally differentiated PC-12 cells. The anomalous RGC death was independent of caspase activation or reactive oxygen species production. CONCLUSIONS: These results suggest an aberrant opening of the RGC PTP and could be the result of structural differences in its components or its interaction with intracellular ligands. Unique RGC PTP behavior could underlie the pathophysiology of those mitochondrial diseases in which RGCs are specifically affected (e.g., Leber hereditary optic neuropathy).

Animals↗
PubMed2002

Current understanding of neuroprotection in glaucoma.

The most common optic neuropathy is glaucomatous optic neuropathy, distinguished by a distinctive and progressive excavation of the optic nerve head without significant pallor of the remaining neuroretinal rim. Neuroprotection is a novel strategy for treating disorders that affect the nervous system by preventing death of neurons. In glaucomatous optic neuropathy, the neurons that die are retinal ganglion cells. This article reviews the recent basic science relevant to neuroprotection, particularly with respect to retinal ganglion cell death in glaucomatous and other optic neuropathies.

Cell Death↗