期刊
EUROPEAN JOURNAL OF PHARMACOLOGY
卷 667, 期 1-3, 页码 182-187出版社
ELSEVIER SCIENCE BV
DOI: 10.1016/j.ejphar.2011.05.069
关键词
Ischemic brain damage; Neuroprotection; 4VO model; Kynurenine
资金
- OTKA [K 75628]
- TAMOP-4 [2.2-08/1/2008-0002]
- Err [02-64]
- Teller Ede Foundation [NAP-BIO-06-BAYBIOSZ]
Global forebrain ischemia results in damage to the pyramids in the CA1 hippocampal subfield, which is particularly vulnerable to excitotoxic processes. Morphological and functional disintegration of this area leads to a cognitive dysfunction and neuropsychiatric disorders. Treatment with N-methyl-D-aspartate receptor antagonists is a widely accepted method with which to stop the advance of excitotoxic processes and concomitant neuronal death. From a clinical aspect, competitive glycine- and polyamine-site antagonists with relatively low affinity and moderate side-effects are taken into account. Endogenous kynurenic acid acts as an antagonist on the obligatory co-agonist glycine site, and has long been at the focus of neuroprotective trials. In the present study, we estimated the neuroprotective capability of a novel kynurenic acid analog in transient global forebrain ischemia, measuring the rate of hippocampal CA1 pyramidal cell loss and the preservation of long-term potentiation at Schaffer collateral-CA1 synapses. The neuroprotective potential was reflected by a significantly diminished hippocampal CA1 cell loss and preserved long-term potentiation expression. The neuroprotective effect was robust in the event of pretreatment, and also when the drug was administered at the time of reperfusion. This result is beneficial since a putative neuroprotectant proven to be effective as post-treatment is of much greater benefit. (C) 2011 Elsevier B.V. All rights reserved.
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