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Alterations in glutathione levels of brain structures caused by acute restraint stress and by nitric oxide synthase inhibition but not by intraspecific agonistic interaction.
Behav Brain Res. 2006 Jan 06; 166(1):71-7.BB

Abstract

Glutathione is the major non-protein thiol to which many different roles in the central nervous system (CNS) are attributed. To further investigate the glutathione response in the CNS, we tested the effect of three stress models on glutathione levels in the brain. We tested the effect of two models of repeated intraspecific agonistic interaction in mice. No influence was observed over the glutathione levels in the mice cerebral cortex, cerebellum, liver, and blood. Acute restraint stress in rats was found to induce an increase in glutathione levels in the cerebellum after 2 and 4 h of immobilization, an effect not observed in the cerebral cortex, striatum, and hippocampus. To investigate the interference of an inhibitor of nitric oxide synthase (NOS), N(omega)Nitro-L-arginine-methyl-ester (L-NAME, 50 mg/kg) was applied i.p. at the beginning of restraint stress. L-NAME alone did not lead to a change in glutathione levels although, in combination with restraint stress, it induced an increase in such levels. This effect was observed in all four structures studied, i.e. cortex, hippocampus, striatum, and cerebellum. The values returned to basal levels after 6h of immobilization. In conclusion, the pattern of dominance, after repeated intraspecific agonistic interaction, was ineffective in producing alterations in brain glutathione, whereas acute restraint stress led to an increase in glutathione levels within a window of 2-4 h, and the inhibition of NOS increased glutathione levels in all studied rat brain structures, suggesting a specificity interference of acute restraint stress with the glutathione system.

Authors+Show Affiliations

Departamento de Ciências Fisiológicas, Centro de Ciências Biológicas, Universidade Federal de Santa Catarina, 88040-900 Florianópolis, SC, Brazil.No affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info available

Pub Type(s)

Comparative Study
Journal Article

Language

eng

PubMed ID

16140401

Citation

Ghizoni, Daniel Mathias, et al. "Alterations in Glutathione Levels of Brain Structures Caused By Acute Restraint Stress and By Nitric Oxide Synthase Inhibition but Not By Intraspecific Agonistic Interaction." Behavioural Brain Research, vol. 166, no. 1, 2006, pp. 71-7.
Ghizoni DM, Pavanati KC, Arent AM, et al. Alterations in glutathione levels of brain structures caused by acute restraint stress and by nitric oxide synthase inhibition but not by intraspecific agonistic interaction. Behav Brain Res. 2006;166(1):71-7.
Ghizoni, D. M., Pavanati, K. C., Arent, A. M., Machado, C., Faria, M. S., Pinto, C. M., Gasparotto, O. C., Gonçalves, S., & Dafre, A. L. (2006). Alterations in glutathione levels of brain structures caused by acute restraint stress and by nitric oxide synthase inhibition but not by intraspecific agonistic interaction. Behavioural Brain Research, 166(1), 71-7.
Ghizoni DM, et al. Alterations in Glutathione Levels of Brain Structures Caused By Acute Restraint Stress and By Nitric Oxide Synthase Inhibition but Not By Intraspecific Agonistic Interaction. Behav Brain Res. 2006 Jan 6;166(1):71-7. PubMed PMID: 16140401.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Alterations in glutathione levels of brain structures caused by acute restraint stress and by nitric oxide synthase inhibition but not by intraspecific agonistic interaction. AU - Ghizoni,Daniel Mathias, AU - Pavanati,Kelly Cristine Alves, AU - Arent,André Mendes, AU - Machado,Claudia, AU - Faria,Moacir Serralvo, AU - Pinto,Cristina Maria Henrique, AU - Gasparotto,Odival Cezar, AU - Gonçalves,Sonia, AU - Dafre,Alcir Luiz, Y1 - 2005/09/02/ PY - 2005/02/02/received PY - 2005/07/15/revised PY - 2005/07/15/accepted PY - 2005/9/6/pubmed PY - 2006/3/15/medline PY - 2005/9/6/entrez SP - 71 EP - 7 JF - Behavioural brain research JO - Behav Brain Res VL - 166 IS - 1 N2 - Glutathione is the major non-protein thiol to which many different roles in the central nervous system (CNS) are attributed. To further investigate the glutathione response in the CNS, we tested the effect of three stress models on glutathione levels in the brain. We tested the effect of two models of repeated intraspecific agonistic interaction in mice. No influence was observed over the glutathione levels in the mice cerebral cortex, cerebellum, liver, and blood. Acute restraint stress in rats was found to induce an increase in glutathione levels in the cerebellum after 2 and 4 h of immobilization, an effect not observed in the cerebral cortex, striatum, and hippocampus. To investigate the interference of an inhibitor of nitric oxide synthase (NOS), N(omega)Nitro-L-arginine-methyl-ester (L-NAME, 50 mg/kg) was applied i.p. at the beginning of restraint stress. L-NAME alone did not lead to a change in glutathione levels although, in combination with restraint stress, it induced an increase in such levels. This effect was observed in all four structures studied, i.e. cortex, hippocampus, striatum, and cerebellum. The values returned to basal levels after 6h of immobilization. In conclusion, the pattern of dominance, after repeated intraspecific agonistic interaction, was ineffective in producing alterations in brain glutathione, whereas acute restraint stress led to an increase in glutathione levels within a window of 2-4 h, and the inhibition of NOS increased glutathione levels in all studied rat brain structures, suggesting a specificity interference of acute restraint stress with the glutathione system. SN - 0166-4328 UR - https://www.unboundmedicine.com/medline/citation/16140401/Alterations_in_glutathione_levels_of_brain_structures_caused_by_acute_restraint_stress_and_by_nitric_oxide_synthase_inhibition_but_not_by_intraspecific_agonistic_interaction_ L2 - https://linkinghub.elsevier.com/retrieve/pii/S0166-4328(05)00284-6 DB - PRIME DP - Unbound Medicine ER -