Navegando por Palavras-chave "GABA(A) receptor"

Agora exibindo 1 - 2 de 2
  • Nenhuma Miniatura disponível
    Item
    Somente Metadadados
    Effects of microinjections of neurotoxin AvTx8, isolated from the social wasp Agelaia vicina (Hymenoptera, Vespidae) venom, on GABAergic nigrotectal pathways
    (Elsevier B.V., 2005-01-07) Oliveira, L. de; Cunha, AOS; Mortari, M. R.; Pizzo, A. B.; Miranda, A.; Coimbra, N. C.; Santos, W. F. dos; Universidade de São Paulo (USP); Universidade Federal de São Paulo (UNIFESP)
    Several investigations have provided information that defensive behaviors evoked by stimulation of deep layers of the superior colliculus (dISC) are subjected to inhibitory nigral modulation. This inhibition is made mainly through GABAergic neurons from substantia, nigra, pars reticulata (SNpr), that sends outputs toward neural networks of the deep layers of the superior colliculus and dorsal periaqueductal gray matter involved with the organization of fear-like responses. in this work, we compared the effects of two GABAergic agonists, muscimol and baclofen, with the effect of neurotoxin AvTx8 (1567 Da), isolated from the venom of the social wasp Agelaia vicina, microinjected into SNpr of Rattus norvegicus (Wistar rats) prior to dISC saline or bicuculline microinjections, considering that wasp venom has some influence on the uptake of GABA and/or glutamate neurotransmitters. GABA(A) receptor blockade in the dISC evoked a vigorous escape behavior, expressed by rapid running, jumps and turns, as compared to control. These defensive reactions were maximized after the intranigral GABA(A) agonism with muscimol, but not after in situ GABA(B) agonism. Nigral microinjection of AvTx8 induced similar effects to those of baclofen, decreasing the intensity of behavioral defensive reactions caused by GABA(A) receptor blockade in the dorsal mesencephalon. These findings suggest that AvTx8 has some effects on GABAergic neurotransmission, increasing the activity of the inhibitory nigrocollicular pathways, causing an anti-panic (antiaversive) effect. Therefore, our work suggests AvTx8 as a novel pharmacological tool to study differences between the two types of GABAergic receptors and excitatory amino acid-mediated mechanisms in the brain and brainstem networks. (C) 2004 Elsevier B.V. All rights reserved.
  • Nenhuma Miniatura disponível
    Item
    Somente Metadadados
    Heightened aggression after chronic flunitrazepam in male rats: potential links to cortical and caudate-putamen-binding sites
    (Springer, 2008-04-01) Almeida, Rosa Maria M. de; Benini, Quelin; Betat, Juliana S.; Hipolide, Debora C. [UNIFESP]; Miczek, Klaus A.; Svensson, Anders I.; Univ Vale Rio dos Sinos; Universidade Federal de São Paulo (UNIFESP); Tufts Univ; Univ Gothenburg
    Rationale Higher doses of benzodiazepines induce sedation. However, in low to moderate doses, benzodiazepines can increase aggressive behavior both after acute and chronic administration. the determinants for increasing aggression after chronic intake of flunitrazepam, a so-called date rape drug, in violence-prone individuals are incompletely understood.Objectives the aim of this study is to assess the effects of acute and chronic treatment with flunitrazepam on male aggression in resident rats. We also examined possible changes in binding to benzodiazepine receptors throughout the brain of rats that display aggressive behavior after repeated flunitrazepam treatment using quantitative receptor autoradiography.Materials and methods the behaviors of the male Wistar resident rats (n=35) toward a male intruder were recorded for 10 min twice a week. the salient aggressive and non-aggressive elements in the resident rat's behavior were analyzed. Initially, the dose-dependent effects of flunitrazepam (0.01, 0.03, 0.1, 0.18, and 0.3 mg/kg) or vehicle were determined in all rats; subsequently, 0.3 mg/kg per day flunitrazepam was administered for 42 days (n=15), and a parallel group was treated with vehicle (n=20). After the chronic treatment, the flunitrazepam (0, 0.01, 0.03, 0.1, 0.18, and 0.3 mg/kg) effects were again assessed.Results the most significant finding is the escalation of aggression after chronic treatment with flunitrazepam. A previously sedative 0.3 mg/kg dose of flunitrazepam engendered very high levels of attack bites, sideways threats, and aggressive postures (total aggression) after 6 weeks of daily administration. Individual differences emerged, and these were associated with decreased binding to benzodiazepine receptors, mainly in the limbic structures such as the cingulate cortex (cingulate areas 1 and 2) and caudate-putamen (posterior part) of aggressive animals, suggesting that these areas are pivotal in the control of emotional and aggressive behavior.Conclusions Chronic flunitrazepam produces changes in receptor binding in discrete areas of the cingulate cortex and caudate-putamen that are proposed to be part of the mechanisms for increased expression of aggressive behavior.