Optic nerve degeneration and potential neuroprotection: implications for glaucoma.
In order to study the course of optic nerve degeneration and devise possible ways to achieve neuroprotection, a well-controlled, animal model of partial crush injury of the optic nerve was used. Following the controlled partial crush injury of the rat optic nerve, quantitative morphological and electrophysiological measurements were made of primary and secondary neuronal losses. The neuroprotective effects of NMDA-receptor antagonists and alpha 2-adrenoreceptor agonists were also studied. The results suggested that the ongoing progression of the optic nerve degeneration in glaucoma might be a consequence of the toxic extracellular environment produced by neurons that degenerate as a result of the primary cause of the disease (such as increased IOP).
Schwartz
M
M
Department of Neurobiology, Weizmann Institute of Science, Rehovot, Israel.
Yoles
E
E
D000200:Action Potentials / Q000502:physiology; D000316:Adrenergic alpha-Agonists / Q000494:pharmacology; D000818:Animals; D004195:Disease Models, Animal; D016291:Dizocilpine Maleate / Q000494:pharmacology; D013759:Dronabinol / Q000031:analogs & derivatives / Q000494:pharmacology; D005074:Evoked Potentials, Visual / Q000502:physiology; D005901:Glaucoma / Q000188:drug therapy*; D006801:Humans; D009410:Nerve Degeneration / Q000517:prevention & control*; D018696:Neuroprotective Agents / Q000494:pharmacology*; D009900:Optic Nerve / Q000187:drug effects*; D009901:Optic Nerve Diseases / Q000517:prevention & control*; D051381:Rats; D016194:Receptors, N-Methyl-D-Aspartate / Q000037:antagonists & inhibitors
D000316:Adrenergic alpha-Agonists; D018696:Neuroprotective Agents; D016194:Receptors, N-Methyl-D-Aspartate; D016291:Dizocilpine Maleate; D013759:Dronabinol; C062018:HU 211