RESUMO
Inducibility of NADPH-diaphorase (NADPH-d) or nitric oxide synthase (NOS) has been demonstrated in pyramidal neurones of the hippocampus, but the mechanisms of this induction are not known. The present study aimed to assess the role of anti-inflammatory drugs in injury-induced production of NADPH-d/NOS in CA1 pyramidal neurones. We found that either a steroid, dexamethasone or a non-steroid, indomethacin, prevents induction of these enzymes. We also found that NO is not necessary for the induction. None of the three drugs used had detectable effect on the neurones which contain constitutive NADPH-d/NOS.
Assuntos
Anti-Inflamatórios não Esteroides/farmacologia , Anti-Inflamatórios/farmacologia , Lesões Encefálicas/enzimologia , NADPH Desidrogenase/biossíntese , Células Piramidais/enzimologia , Animais , Arginina/análogos & derivados , Arginina/farmacologia , Dexametasona/farmacologia , Indução Enzimática/efeitos dos fármacos , Hipocampo/citologia , Hipocampo/efeitos dos fármacos , Hipocampo/lesões , Indometacina/farmacologia , NG-Nitroarginina Metil Éster , Óxido Nítrico/antagonistas & inibidores , Células Piramidais/efeitos dos fármacos , Ratos , Ratos Sprague-DawleyRESUMO
Unilateral injury of the cerebral cortex or hippocampus induced a bilateral appearance of NADPH-diaphorase in some pyramidal neuronal and glial cells of both structures. Only in the cerebral cortex, near the needle track, did some V layer pyramidal neurons contain so much of this enzyme that they looked to be stained by the Golgi method. The induction of NADPH-diaphorase in a subset of cortical and hippocampal neurons in both hemispheres after unilateral injections of either cysteamine or artificial cerebro-spinal fluid suggests the existence in the isocortex and the hippocampus of a selective signalling system which may play a role in recovery of function following local brain damage.
