Kynurenate inhibition of cell excitation decreases stroke size and deficits | Zendy

Germano Isabelle M. | Zendy; Pitts Lawrence H. | Zendy; Meldrum Brian S. | Zendy; Bartkowski Henry M. | Zendy; Simon Roger P. | Zendy

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Kynurenate inhibition of cell excitation decreases stroke size and deficits

Author(s) -

Germano Isabelle M.,

Pitts Lawrence H.,

Meldrum Brian S.,

Bartkowski Henry M.,

Simon Roger P.

Publication year - 1987

Publication title -

annals of neurology

Language(s) - English

Resource type - Journals

SCImago Journal Rank - 4.764

H-Index - 296

eISSN - 1531-8249

pISSN - 0364-5134

DOI - 10.1002/ana.410220609

Subject(s) - stroke (engine) , excitation , medicine , physical medicine and rehabilitation , neuroscience , psychology , physics , quantum mechanics , thermodynamics

Pharmacological inhibition of excitatory neurotransmission attenuates cell death in models of global ischemia/reperfusion and hypoglycemia. The current investigations extend these observations to a model of focal ischemia. Kynurenic acid, a broad‐spectrum antagonist at excitatory amino acid receptors, was used as treatment (300 mg/kg; 3 doses at 4‐hour intervals) before and after focal cerebral ischemia in rats (n = 54). Preischemia but not 1 hour postischemia treatment with kynurenate attenuated infarction size ( p < 0.001) and improved neurological outcome ( p < 0.001) studied at 24 hours after injury. These data support the role of excitatory neurotransmission in acute neuronal injury and support pharmacological inhibition of cell excitation as a potential therapy for stroke.

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