Navegando por Palavras-chave "N-methyl-D-aspartate"

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    Effect of nitric oxide on excitatory amino acid-evoked discharge of neurons in NTS
    (Amer Physiological Soc, 2003-01-01) Dias, ACR; Colombari, E.; Mifflin, S. W.; Univ Texas; Universidade Federal de São Paulo (UNIFESP)
    N-methyl-D-aspartate (NMDA) and non-NMDA excitatory amino acid (EAA) receptor subtypes are involved in the integration of visceral afferent inputs within the nucleus of the solitary tract (NTS). Microinjection studies indicate interactions between nitric oxide (NO) and EAA receptors within the NTS. To examine these interactions at the single cell level, this study characterized the effects of the NO synthase inhibitor N-G-nitro-L-arginine methyl ester (L-NAME) and the NO donor 3-[2-hydroxy-2-nitroso-1-propylhydrazino]-1-propanamine (PAPA-NONOate) on the excitatory responses of vagus nerve (VN)-evoked NTS neurons to the activation of (RS)-alpha-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid (AMPA) and NMDA receptors in rats. Iontophoresis of L-NAME did not alter spontaneous or VN-evoked discharges, but significantly decreased the number of action potentials (APs) evoked by iontophoretic application of AMPA. the effects of L-NAME on NMDA-evoked discharge were variable; for the population, L-NAME did not change the number of APs evoked by NMDA. PAPA-NONOate enhanced the spontaneous discharge and the number of APs elicited by AMPA but not NMDA. Iontophoresis of the inactive enantiomers N-G-nitro-D-arginine methyl ester and hydroxydiazenesulfonic acid 1-oxide disodium salt had no effect on AMPA-evoked discharge. Our data suggest that NO facilitates AMPA-mediated neuronal transmission within the NTS.
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    Influence of N-methyl-D-aspartate receptors on ouabain activation of nuclear factor-kappa B in the rat hippocampus
    (Wiley-Blackwell, 2012-01-01) Kawamoto, Elisa Mitiko; Lima, Larissa de Sá; Munhoz, Carolina Demarchi; Yshii, Lidia Mitiko; Kinoshita, Paula Fernanda; Amaral, Fernanda Gaspar; Pestana, Rafaela R. Ferrão; Orellana, Ana Maria Marques; Cipolla-Neto, Jose; Britto, Luiz Roberto Giorgetti de; Avellar, Maria Christina Werneck [UNIFESP]; Rossoni, Luciana Venturini; Scavone, Cristoforo; Universidade de São Paulo (USP); Universidade Federal de São Paulo (UNIFESP)
    It has been shown that ouabain (OUA) can activate the Na,K-ATPase complex and mediate intracellular signaling in the central nervous system (CNS). Inflammatory stimulus increases glutamatergic transmission, especially at N-methyl-D-aspartate (NMDA) receptors, which are usually coupled to the activation of nitric oxide synthase (NOS). Nuclear factor-kappa B (NF-kappa B) activation modulates the expression of genes involved in development, plasticity, and inflammation. the present work investigated the effects of OUA on NF-kappa B binding activity in rat hippocampus and the influence of this OUA-Na,K-ATPase signaling cascade in NMDA-mediated NF-kappa B activation. the findings presented here are the first report indicating that intrahippocampal administration of OUA, in a concentration that did not alter Na,K-ATPase or NOS activity, induced an activation of NF-kappa B, leading to increases in brain-derived neurotrophic factor (Bdnf), inducible NOS (iNos), tumor necrosis factor-alpha (Tnf-alpha), and B-cell leukemia/lymphoma 2 (Bcl2) mRNA levels. This response was not linked to any significant signs of neurodegeneration as showed via Fluoro-Jade B and Nissl stain. Intrahippocampal administration of NMDA induced NF alpha B activation and increased NOS and alpha 2/3-Na,K-ATPase activities. NMDA treatment further increased OUA-induced NF-kappa B activation, which was partially blocked by MK-801, an antagonist of NMDA receptor. These results suggest that OUA-induced NF-kappa B activation is at least in part dependent on Na,K-ATPase modulatory action of NMDA receptor in hippocampus. the interaction of these signaling pathways could be associated with biological mechanisms that may underlie the basal homeostatic state linked to the inflammatory signaling cascade in the brain. (c) 2011 Wiley Periodicals, Inc.
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    MK-801 and 7-Ni attenuate the activation of brain NF-kappa B induced by LPS
    (Elsevier B.V., 2003-12-01) Glezer, Isaias; Munhoz, Carolina Demarchi; Kawamoto, Elisa Mitiko; Marcourakis, Tania; Avellar, Maria Christina Werneck [UNIFESP]; Scavone, Cristoforo; Universidade de São Paulo (USP); Universidade Federal de São Paulo (UNIFESP)
    The activation of nuclear factor-kappaB (NF-kappaB) leads to an increase in the expression of genes involved in important events in the central nervous system (CNS), such as development, plasticity and inflammation. It has been shown that inflammatory stimulus in the brain increases excitatory glutamatergic transmission, especially at N-methyl-D-aspartate (NMDA) receptor. These receptors have an important role in glutamate neurotoxicity and are in general coupled with the generation of nitric oxide (NO) through the activation of neuronal nitric oxide synthase (NOS). We have investigated the involvement of NMDA-NO pathway in LPS induction of NF-kappaB in CNS. Our results demonstrate that systemic LPS activates NF-kappaB in several regions of the CNS, which was partially reduced by the NMDA receptor antagonist dizolcipine (MK-801) and by the selective brain NOS inhibitor 7-Nitroindazol (7-Ni). 7-Ni effects were not synergic to MK-801 effects, suggesting that these compounds act through the same pathway. Dexamethasone caused a stronger reduction in LPS induction of NF-kappaB in CNS, demonstrating that MK-801 and 7-Ni act on a pathway that is responsible only by a fraction of the overall NF-kappaB activation. These results suggest that a considerable part of NF-kappaB activation by LIPS is linked to the NMDA/NO pathway in CNS. (C) 2003 Elsevier B.V. All rights reserved.
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    MK-801 blocks the development of behavioral sensitization to ethanol
    (Lippincott Williams & Wilkins, 2000-03-01) Camarini, R.; Frussa, R.; Monteiro, M. G.; Calil, H. M.; Universidade Federal de São Paulo (UNIFESP)
    Background: Studies have indicated that MK-801 (a noncompetitive N-methyl-D-aspartate receptor antagonist) participates in the long-term neural changes responsible for sensitization to stimulant drugs. It is known that repeated administration of low doses of ethanol sensitizes animals to its stimulant effect. in this work we investigated whether MK-801 alters the development of behavioral sensitization to ethanol.Methods: Groups of male Swiss mice were treated with saline or ethanol (2.0 g/kg) plus saline or MK-801 (0.25 mg/kg) for 21 days. On day 25, all animals received an ethanol challenge injection (2.0 g/kg). We measured locomotor activity on days 1, 7, 14, 21 and 25. in addition, we assessed the effects of different doses of MK-801 on the response to a low dose of ethanol (2.0 g/kg).Results: Ethanol-treated mice developed sensitization to the locomotor-stimulating effect of the drug, whereas those concomitantly receiving ethanol and MK-801 did nut. All doses of MK-801 that were used stimulated the locomotor activity of both ethanol and saline-treated animals.Conclusions: the findings support the hypothesis that N-methyl-D-aspartate receptors have an important role in the development of sensitization to drugs of abuse.