31 research outputs found

    The Mw = 6.3, November 21, 2004, Les Saintes earthquake (Guadeloupe): Tectonic setting, slip model and static stress changes,

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    International audienceOn November 21, 2004, a magnitude 6.3 earthquake occurred offshore, 10 km south of Les Saintes archipelago in Guadeloupe (French West Indies). There were more than 30000 aftershocks recorded in the following two years, most of them at shallow depth near the islands of the archipelago. The main shock and its main aftershock of February 14, 2005 (Mw = 5.8) ruptured a NE-dipping normal fault (Roseau fault), mapped and identified as active from high-resolution bathymetric data a few years before. This fault belongs to an arc-parallel en echelon fault system that follows the inner edge of the northern part of the Lesser Antilles arc, accommodating the sinistral component of oblique convergence between the North American and Caribbean plates. The distribution of aftershocks and damage (destruction and landslides) are consistent with the main fault plane location and attitude. The slip model of the main shock, obtained by inverting jointly global broadband and local strong motion records, is characterized by two main slip zones located 5 to 10 km to the SE and NW of the hypocenter. The main shock is shown to have increased the Coulomb stress at the tips of the ruptured plane by more than 4 bars where most of the aftershocks occurred, implying that failures on fault system were mainly promoted by static stress changes. The earthquake also had an effect on volcanic activity since the Boiling Lake in Dominica drained twice, probably as a result of the extensional strain induced by the earthquake and its main aftershock

    Serotonin, genetic variability, behaviour, and psychiatric disorders - a review

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    Brain monoamines, and serotonin in particular, have repeatedly been shown to be linked to different psychiatric conditions such as depression, anxiety, antisocial behaviour, and dependence. Many studies have implicated genetic variability in the genes encoding monoamine oxidase A (MAOA) and the serotonin transporter (5HTT) in modulating susceptibility to these conditions. Paradoxically, the risk variants of these genes have been shown, in vitro, to increase levels of serotonin, although many of the conditions are associated with decreased levels of serotonin. Furthermore, in adult humans, and monkeys with orthologous genetic polymorphisms, there is no observable correlation between these functional genetic variants and the amount or activity of the corresponding proteins in the brain. These seemingly contradictory data might be explained if the association between serotonin and these behavioural and psychiatric conditions were mainly a consequence of events taking place during foetal and neonatal brain development. In this review we explore, based on recent research, the hypothesis that the dual role of serotonin as a neurotransmitter and a neurotrophic factor has a significant impact on behaviour and risk for neuropsychiatric disorders through altered development of limbic neurocircuitry involved in emotional processing, and development of the serotonergic neurons, during early brain development

    Epistasis among Presynaptic Serotonergic System Components

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    Epistatic interactions among regulatory components of the serotonin (5-HT) neurotransmitter system may be an important aspect of 5-HT function. Because 5-HT dysregulation is associated with several common psychiatric disorders, the potential for epistasis among genetic variants in the 5-HT transporter (SERT), 5-HT 1B terminal autoreceptor and the 5-HT 1A somatodendritic autoreceptor should be examined. In this study, output from a dynamic minimal model of 5-HT function was compared to empirical results in the literature. Parameters representing extracellular 5-HT clearance rates (SERT), 5-HT release levels (5-HT 1B ) and inhibitory thresholds (the amount of extracellular 5-HT above which cell firing is inhibited, an indication of 5-HT 1A autoreceptor sensitivity) were varied to simulate genetic deletion (i.e. knockout) of each component singly, and in combination. Simulated knockout effects on extracellular 5-HT level and presynaptic neural firing rates were in the same direction and of similar relative magnitude as studies in the literature. Epistasis among presynaptic components appears to be important in the 5-HT system’s regulation of extracellular 5-HT levels, but not of firing rates.Peer Reviewedhttp://deepblue.lib.umich.edu/bitstream/2027.42/44113/1/10519_2004_Article_1019.pd
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