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- ItemAcesso aberto (Open Access)The brain decade in debate: II. Panic or anxiety? From animal models to a neurobiological basis(Associação Brasileira de Divulgação Científica, 2001-02-01) Andreatini, R.; Blanchard, C.; Blanchard, R.; Brandão, M.l.; Carobrez, A.p.; Griebel, G.; Guimarães, F.s.; Handley, S.l.; Jenck, F.; Leite, Jose Roberto [UNIFESP]; Rodgers, J.; Schenberg, L.c.; Da Cunha, C.; Graeff, F.g.; Universidade Federal do Paraná Departamento de Farmacologia Laboratório de Fisiologia e Farmacologia do Sistema Nervoso Central; University of Hawaii Department of Neurobiology; University of Hawaii Department of Psychology; Universidade de São Paulo (USP); Universidade Federal de Santa Catarina Departamento de Farmacologia; Central Nervous System Research Department Sanofi Synthelabo; Aston University Institute of Pharmaceutical Sciences; Hoffmann-La Roche Ltd.; Universidade Federal de São Paulo (UNIFESP); University of Leeds Department of Psychology Ethopharmacology Laboratory; Universidade Federal do Espírito Santo Centro de Biomedicina Departamento de Ciências FisiológicasThis article is a transcription of an electronic symposium sponsored by the Brazilian Society of Neuroscience and Behavior (SBNeC). Invited researchers from the European Union, North America and Brazil discussed two issues on anxiety, namely whether panic is a very intense anxiety or something else, and what aspects of clinical anxiety are reproduced by animal models. Concerning the first issue, most participants agreed that generalized anxiety and panic disorder are different on the basis of clinical manifestations, drug response and animal models. Also, underlying brain structures, neurotransmitter modulation and hormonal changes seem to involve important differences. It is also common knowledge that existing animal models generate different types of fear/anxiety. A challenge for future research is to establish a good correlation between animal models and nosological classification.
- ItemSomente MetadadadosBrain prolactin is involved in stress-induced REM sleep rebound(Academic Press Inc Elsevier Science, 2017) Machado, Ricardo Borges; Rocha, Murilo Ramos [UNIFESP]; Suchecki, Deborah [UNIFESP]REM sleep rebound is a common behavioural response to some stressors and represents an adaptive coping strategy. Animals submitted to multiple, intermittent, footshock stress (FS) sessions during 96 h of REM sleep deprivation (REMSD) display increased REM sleep rebound (when compared to the only REMSD ones, without FS), which is correlated to high plasma prolactin levels. To investigate whether brain prolactin plays a role in stress-induced REM sleep rebound two experiments were carried out. In experiment 1, rats were either not sleep-deprived (NSD) or submitted to 96 h of REMSD associated or not to FS and brains were evaluated for PRL immunoreactivity (PRL-ir) and determination of PRL concentrations in the lateral hypothalamus and dorsal raphe nucleus. In experiment 2, rats were implanted with cannulas in the dorsal raphe nucleus for prolactin infusion and were sleep-recorded. REMSD associated with FS increased PRL-ir and content in the lateral hypothalamus and all manipulations increased prolactin content in the dorsal raphe nucleus compared to the NSD group. Prolactin infusion in the dorsal raphe nucleus increased the time and length of REM sleep episodes 3 h after the infusion until the end of the light phase of the day cycle. Based on these results we concluded that brain prolactin is a major mediator of stress-induced REMS. The effect of PRL infusion in the dorsal raphe nucleus is discussed in light of the existence of a bidirectional relationship between this hormone and serotonin as regulators of stress induced REM sleep rebound. (C) 2016 Elsevier Inc. All rights reserved.