Pharmacological approaches to the treatment of ischaemic neuronal damage.
Retina is particularly susceptible to ischaemic damage following exposure to anoxia or hypoglycaemia. In animal models the neuronal damage following ischaemia resembles that caused by exposure to glutamate or other excitotoxic agents which act on excitatory amino acid receptors. There are a number of pharmacological approaches designed to limit neuronal damage following ischaemia. These include free radical scavenging agents, calcium channel blockers, kappa opiate agonists and excitatory amino acid antagonists. Recent studies with antagonists acting at both NMDA and non-NMDA receptors for glutamate show that such compounds can protect against ischaemic damage, and are effective even when administered several hours after the ischaemic insult.
Iversen
L L
LL
Merck Sharp & Dohme Research Laboratories, Neuroscience Research Centre, Harlow, Essex, UK.
D000818:Animals; D007511:Ischemia / Q000188:drug therapy*; D051379:Mice; D009498:Neurotoxins / Q000037:antagonists & inhibitors; D016194:Receptors, N-Methyl-D-Aspartate / Q000187:drug effects; D012164:Retinal Diseases / Q000188:drug therapy* / Q000473:pathology; D012171:Retinal Vessels / Q000473:pathology*
D009498:Neurotoxins; D016194:Receptors, N-Methyl-D-Aspartate