Navegando por Palavras-chave "autoradiography"

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    Distinct effects of sleep deprivation on binding to norepinephrine and serotonin transporters in rat brain
    (Elsevier B.V., 2005-02-01) Hipolide, Debora C. [UNIFESP]; Moreira, Karin M. [UNIFESP]; Barlow, KBL; Wilson, A. A.; Nobrega, J. N.; Tufik, Sergio [UNIFESP]; Ctr Addict & Mental Hlth; Universidade Federal de São Paulo (UNIFESP)
    There is evidence to suggest that the antidepressant activity of sleep deprivation may be due to an enhancement of serotonergic and/or noradrenergic neurotransmission in brain. in the present study we examined the possibility that such changes may occur at the level of the norepinephrine (NET) and serotonin (SERT) and transporters. Rats were deprived of sleep for 96 h using the modified multiple platform method and then sacrificed for autoradiographic assessments of NET and SERT binding throughout the brain. [3 H]Nisoxetine binding to the NE transporter was generally decreased in 44 of 45 areas examined, with significant reductions occurring in the anterior cingulate cortex (- 16%), endopiriform n. (- 18%), anterior olfactory n. (- 19%), glomerular layer of olfactory bulb (- 18%), ventral pallidum (- 14%), medial preoptic area (- 16%), retrochiasmatic/arcuate hypothalamus (- 18%), anteromedial thalamic n. (- 15%), and rostral raphe (- 17%). in contrast, SERT binding measured with [C-11]DASB showed no clear directional trends in 61 brain areas examined, but was significantly reduced in subdivisions of the anterior olfactory nucleus (- 22%) and substantia. nigra (- 18%). Thus, sleep deprivation induced widespread decreases in NET binding, and fewer and well-localized decreases in SERT binding. Significant down-regulation in one brain region, the anterior olfactory nucleus, was observed in the case of both transporters. These results suggest that mechanisms involved in the antidepressant action of sleep deprivation may involve generalized NET down-regulation as well as decreased SERT binding in specific areas. Insofar as these changes may be associated with increased levels of serotonin (5-HT) and norepinephrine (NE) in the synapse, they suggest that sleep deprivation may share some basic mechanisms of action with several current antidepressant medications. (C) 2004 Elsevier Inc. All rights reserved.
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    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.
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    Morphine attenuates the expression of sensitization to ethanol, but opioid antagonists do not
    (Elsevier B.V., 2008-10-28) Abrahao, Karina Possa [UNIFESP]; Quadros, I. M.; Souza-Formigoni, M. L. O. [UNIFESP]; Universidade Federal de São Paulo (UNIFESP); Tufts Univ
    Behavioral sensitization to ethanol is characterized by an increased locomotor activity after repeated exposure. A great variability exists among species and strains in the development of sensitization. There is a growing amount of evidence to indicate that the opioid system is involved in alcoholism; it is possible, therefore, that this system also modulates the sensitization to ethanol. in this study we evaluated the role of the opioid system in determining the variability of the sensitized response to ethanol. Mice received repeated administrations of ethanol (2.2 g/kg) or saline every other day for 10 days. According to their locomotor response on the last day of treatment, ethanol-treated animals were classified into two groups: sensitized or non-sensitized mice. After the treatment, mice were submitted to four challenges 48 h apart. in experiments 1 and 2, mice were challenged, respectively, with i.p. administration of opioid antagonists (naloxone or naltrexone) or an opioid agonist (morphine), followed immediately by 2.2 g/kg ethanol. in experiment 3, animals received morphine by i.c.v., followed by 2.2 g/kg of ethanol (i.p.). Pretreatment with opioid antagonists (naloxone or naltrexone) did not block the expression of ethanol sensitization; however pretreatment with morphine attenuated the increased locomotor activity after ethanol administration in sensitized mice. in experiment 4, after the ethanol or saline treatment, mice brains were processed and brain mu opioid binding was assessed by autoradiography using [3H]D-Ala2,N-mePhe4, Gly-ol5-enkephalin ([3H]DAMGO). No differences were seen between any of the groups of mice, so the agonist effect is not likely to be mediated by differences in binding to mu opioid receptors. (C) 2008 IBRO. Published by Elsevier B.V. All rights reserved.
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    Sleep deprivation does not affect indices of necrosis or apoptosis in rat brain
    (Taylor & Francis Ltd, 2002-02-01) Hipólide, Débora Cristina [UNIFESP]; D'Almeida, Vania [UNIFESP]; Raymond, Roger; Tufik, Sergio [UNIFESP]; Nobrega, J. N.; Ctr Addict & Mental Hlth; Universidade Federal de São Paulo (UNIFESP)
    Recent indications of oxidative stress in hypothalamus of sleep deprived rats prompted us to address the possibility that sleep deprivation may induce pathological cell loss changes in brain. Indices of necrosis and apoptosis were quantified after 96 h of sleep deprivation induced by the classical platform technique in rats. Binding of the peripheral-type benzodiazepine ligand [H-3] PK 11195 to reactive astrocytes, a reliable and sensitive index of necrotic changes, was not altered in any of 14 brain regions examined. Likewise, no changes were found in mRNA levels of the apoptosis-related genes bcl-2 and bax in any of 24 brain regions examined. This was corroborated by quantitative TUNEL analyses in hypothalamus, amygdala, and cortex, which also revealed no effects in sleep deprived animals. These results are consistent with other recent evidence that sleep deprivation does not induce necrotic or apoptotic cell loss in brain. This suggests that recent findings of oxidative stress in sleep deprived brains do not result in cell loss. the possibility that sleep deprivation may result in functional deficits, or that structural changes may emerge after repeated episodes of sleep deprivation, remains to be addressed.