[Receptor agonists as perspective neuroprotective agents].
Selective agonists of adenosine A1, GABAa, GABAb, and alpha 2-receptors (inhibitory neurotransmitter analogs) have a high neuroprotective effects (NPE) on two models of complete cerebral ischemia (CI). These NPEs are specific as they are inhibited by selective antagonists and, in addition, the selective alpha 1- and beta-receptor agonists have no NPE. The natural resistance to CI is also associated with A- and alpha 1-receptors. NPE does not result from improved cerebral blood flow. The receptor agonists protect the brain itself. They use a tolerance strategy and hypothermia is an important component, but not the only mechanism of NPE. Unlike most drugs, receptor neuroprotectors (RNP) guard not only a penumbra zone, but the core of ischemia as they are effective in complete global CI. Moreover, RNP-induced delay of irreversible lesions may increase a therapeutical window for using other drugs. RNPs are promising potential drugs in CI.
Kulinskiĭ
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D000322:Adrenergic Agonists / Q000494:pharmacology*; D058647:Adrenergic alpha-2 Receptor Agonists; D000818:Animals; D002545:Brain Ischemia / Q000188:drug therapy* / Q000378:metabolism; D018755:GABA Agonists / Q000494:pharmacology*; D058785:GABA-A Receptor Agonists; D058786:GABA-B Receptor Agonists; D006801:Humans; D018696:Neuroprotective Agents / Q000494:pharmacology*; D058906:Purinergic P1 Receptor Agonists
D000322:Adrenergic Agonists; D058647:Adrenergic alpha-2 Receptor Agonists; D018755:GABA Agonists; D058785:GABA-A Receptor Agonists; D058786:GABA-B Receptor Agonists; D018696:Neuroprotective Agents; D058906:Purinergic P1 Receptor Agonists