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Relationship between cyclooxygenase‐2 and nitric oxide synthase‐2 in rat cortex after stress
Author(s) -
Madrigal José L. M.,
GarcíaBueno Borja,
Moro María A.,
Lizasoain Ignacio,
Lorenzo Pedro,
Leza Juan C.
Publication year - 2003
Publication title -
european journal of neuroscience
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.346
H-Index - 206
eISSN - 1460-9568
pISSN - 0953-816X
DOI - 10.1046/j.1460-9568.2003.02888.x
Subject(s) - cyclooxygenase , nitric oxide synthase , context (archaeology) , oxidative stress , nitric oxide , chemistry , gene isoform , corticosterone , endocrinology , medicine , pharmacology , prostaglandin e2 , prostaglandin , enzyme , biochemistry , biology , paleontology , gene , hormone
Many studies have focused on the relationships between distinct enzymatic sources of oxidative mediators. Recently, we have shown that cyclooxygenase‐2 (COX‐2) and inducible nitric oxide synthase (NOS‐2) isoforms are up‐regulated and account for oxidative damage in brain after stress. To assess the time course of these events, we have used adult male Wistar rats, some of which were immobilized for 6 h. Whereas pretreatment with the specific COX‐2 inhibitor NS‐398 (5 mg/kg i.p.) decreased Ca 2+ ‐independent NOS activity after 6 h of stress, pretreatment with the specific NOS‐2 inhibitor 1400 W (4 mg/kg i.p.) did not decrease prostaglandin E2 (PGE2) accumulation induced by stress after 6 h. The observed effects of NS‐398 and 1400 W were independent of the general response to stress – neither drug modified stress‐induced corticosterone response – which might indicate a possible adaptive role for COX‐2 and NOS‐2 pathways in this situation. These findings are discussed as possible therapeutic targets in the context of neuropsychiatric disorders related to stress.