Navegando por Palavras-chave "Medial amygdala"

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    CRF type 1 receptors of the medial amygdala modulate inhibitory avoidance responses in the elevated T-maze
    (Elsevier B.V., 2014-03-01) Vicentini, Jéssica Elias [UNIFESP]; Céspedes, Isabel Cristina [UNIFESP]; Nascimento, Juliana Olivetti Guzman [UNIFESP]; Bittencourt, Jackson C.; Viana, Milena de Barros [UNIFESP]; Universidade Federal de São Paulo (UNIFESP); Universidade de São Paulo (USP)
    Corticotropin-releasing factor (CRF) plays a critical role in the mediation of physiological and behavioral responses to stressors. in the present study, we investigated the role played by the CRF system within the medial amygdala (MeA) in the modulation of anxiety and fear-related responses. Male Wistar rats were bilaterally administered into the MeA with CRF (125 and 250 ng/0.2 mu l, experiment 1) or with the CRFR1 antagonist antalarmin (25 ng/0.2 mu l, experiment 2) and 10 min later tested in the elevated T-maze (ETM) for inhibitory avoidance and escape measurements. in clinical terms, these responses have been respectively related to generalized anxiety and panic disorder. To further verify if the anxiogenic effects of CRF were mediated by CRFR1 activation, we also investigated the effects of the combined treatment with CRF (250 ng/0.2 mu l) and antalarmin (25 ng/0.2 mu l) (experiment 3). All animals were tested in an open field, immediately after the ETM, for locomotor activity assessment. Results showed that CRF, in the two doses administered, facilitated ETM avoidance, an anxiogenic response. Antalarmin significantly decreased avoidance latencies, an anxiolytic effect, and was able to counteract the anxiogenic effects of CRF. None of the compounds administered altered escape responses or locomotor activity measurements. These results suggest that CRF in the MeA exerts anxiogenic effects by activating type 1 receptors, which might be of relevance to the physiopathology of generalized anxiety disorder. (C) 2014 Elsevier Inc. All rights reserved.
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    Effects of medial amygdala inactivation on a panic-related behavior
    (Elsevier B.V., 2006-09-25) Herdade, Karina Costa Paes; Strauss, Christiana Villela de Andrade; Zangrossi Junior, Helio; Viana, Milena de Barros [UNIFESP]; Universidade Federal de São Paulo (UNIFESP); Universidade de São Paulo (USP); Pontificia Univ Catolica
    In the last years, the role played by the medial nucleus of the amygdala (MeA) in the modulation of fear- and anxiety-related behaviors has been increasingly investigated. This nucleus plays an important role in the processing of predator odor-induced defensive reactions, i.e. freezing and risk-assessment behaviors. Immunohistochemical evidence also indicates that the MeA may be involved in the regulation of escape, a defensive behavior related to panic attacks. in this study, we further addressed this question by investigating the effects of the reversible inactivation of the nucleus on escape behavior generated in male Wistar rats by two different aversive stimuli, electrical stimulation of the dorsal periaqueductal gray matter (dPAG) and exposure to one of the open arms of the elevated T-maze. Results showed that intra-MeA administration of either the reversible sodium channel blocker lidocaine (34 nmol/0.2 mu l) or the GABA(A) receptor agonist muscimol (0.22 nmol/0.2 mu l) raised the threshold of aversive electrical stimulation, increasing the amount of current that applied to the dPAG evokes escape, an antiaversive effect. Local microinjection of muscimol (0.22 nmol/0.2 mu l) inhibited escape behavior in the elevated T-maze, also suggesting an antiaversive effect. in this latter test, muscimol did not affect inhibitory avoidance, a behavior associated with generalized anxiety disorder. Muscimol effect in the elevated T-maze was independent of changes in general exploratory activity as measured in an open-field. Taken together, our data corroborate previous evidences suggesting that the MeA is involved in the modulation of escape. Dysfunction of this regulatory mechanism may be of relevance in the genesis/maintenance of panic disorder. (c) 2006 Elsevier B.V. All rights reserved.