998 resultados para Hippocampus erectus complex


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Bycatch studies have largely ignored population level effects on fish species of little commercial interest. Here we analyze bycatch of the lined seahorse (Hippocampus erectus) in the bait-shrimp trawl fishery in Hernando Beach, Florida, providing the first fisheries data for this species. Based on catch per unit of effort (CPUE), size, sex, and reproductive status of trawled H. erectus, 1) approximately 72,000 seahorses were caught annually by this fleet, from a population of unknown size, 2) trawling affected population cohorts differentially because of temporal and spatial variation in CPUE and population size, and 3) a greater proportion of females than males was removed in trawling. Our findings suggest that trawling may affect seahorse populations through direct mortality, social disruption, and habitat damage. However, the lack of specific abundance or catchability estimates for H. erectus means that the precise impact of trawling on this fish remains uncertain. This paper focuses attention on the need for research and monitoring of small fishes that are caught incidentally in nonselective gear.

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Dissertação de mest., Ciências, Faculdade de Ciências do Mar e do Ambiente, Univ. do Algarve, 2009

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Coordenação de Aperfeiçoamento de Pessoal de Nível Superior (CAPES)

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Hippocampus and amygdala changes have been implicated in the pathophysiology and symptomatology of both schizophrenia (SCZ) and bipolar disorder (BD). However relationships between illness course, neuropathological changes and variations in symptomatology remain unclear. This investigation examined the associations between hippocampus and amygdala volumes and symptom dimensions in schizophrenia and bipolar disorder patients after their first episode of psychosis. Symptom severity was associated with decreases in hippocampus/amygdala complex volume across groups. In keeping with previous work bilateral hippocampus and amygdala volume reductions were also identified in the SCZ patients while in BD patients only evidence of amygdala inflation reached significance. The study concludes that there appear to be important relationships between volume changes in the hippocampus and amygdala and dimensions and severity of symptomatology in psychosis. Structural alterations are apparent in both SCZ and BD after first episode of psychosis but present differently in each illness and are more severe in SCZ.

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Os cavalos-marinhos têm cativado a imaginação e a curiosidade dos seres humanos por centenas de anos. No entanto, nos dias de hoje, esses animais correm um sério risco de extinção por fatores como a pesca desordenada para suprir os mercados de peixes ornamentais e da medicina tradicional chinesa e principalmente, a destruição do seu habitat. Nesse contexto, é crescente o número de estudos sobre a ecologia, a biologia (reprodutiva, especialmente) e o cultivo de várias espécies do gênero Hippocampus, inclusive para fins conservacionistas e de recomposição de estoques. Duas espécies de cavalos-marinhos são encontradas no Brasil: Hippocampus reidi Ginsburg 1933 e Hippocampus erectus Perry. No entanto, as informações sobre essas espécies estão basicamente restritas ao seu grau de ocorrência ou a sua área de ocupação. No presente estudo, foi avaliado o desempenho reprodutivo de Hippocampus reidi do estuário do rio Potengi (05° 47' 42'' S; 35° 12' 34'' W), em Natal, Rio Grande do Norte. Para tanto, cavalos-marinhos grávidos (n = 38) foram coletados no referido estuário nos meses de setembro, outubro e novembro de 2008 e julho, agosto, setembro e outubro de 2009 e mantidos em laboratório até que liberassem os filhotes. O comprimento padrão (CPA), altura (ATA), volume da bolsa (VB) e peso úmido (PuA) dos adultos, bem como o comprimento padrão (CPF), altura (ATF), peso úmido (PuF) e peso seco (PsF) dos filhotes foram determinados. Os resultados obtidos mostraram que houve correlações significativas entre o CPA e a ATA (r²=0,171), CPA e PuA (r²=0,624), CPA e VB (r²=0,256), ATA e PuA (r²=0,788), PuA e VB (r²=0,211), CPF e ATF (r²=0,903) e CPF e PsF (r²=0,163). A análise de correspondência (AC) que associou as classes do comprimento padrão dos adultos (CPA) e o volume da bolsa de H. reidi ao número de filhotes mostrou que animais entre 19 cm e 21 cm e com volume de bolsa entre 3 mL e 4 mL foram os que liberaram o maior número de filhotes. Os resultados do presente estudo também indicam que o tamanho mínimo de captura recomendado pela CITES (10 cm de altura) para H. reidi deve ser revisto, uma vez que não foram encontrados animais menores que 13,5 cm que estivessem grávidos. Finalmente, o número médio de filhotes por desova obtido no presente estudo (n = 775 ± 398 filhotes) realçou o potencial reprodutivo de H. reidi e a necessidade de estudos adicionais com esta espécie

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Conselho Nacional de Desenvolvimento Científico e Tecnológico (CNPq)

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At the core of our uniquely human cognitive abilities is the capacity to see things from different perspectives, or to place them in a new context. We propose that this was made possible by two cognitive transitions. First, the large brain of Homo erectus facilitated the onset of recursive recall: the ability to string thoughts together into a stream of potentially abstract or imaginative thought. This hypothesis is sup-ported by a set of computational models where an artificial society of agents evolved to generate more diverse and valuable cultural outputs under conditions of recursive recall. We propose that the capacity to see things in context arose much later, following the appearance of anatomically modern humans. This second transition was brought on by the onset of contextual focus: the capacity to shift between a minimally contextual analytic mode of thought, and a highly contextual associative mode of thought, conducive to combining concepts in new ways and ‘breaking out of a rut’. When contextual focus is implemented in an art-generating computer program, the resulting artworks are seen as more creative and appealing. We summarize how both transitions can be modeled using a theory of concepts which high-lights the manner in which different contexts can lead to modern humans attributing very different meanings to the interpretation of one concept.

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To investigate the neural systems that contribute to the formation of complex, self-relevant emotional memories, dedicated fans of rival college basketball teams watched a competitive game while undergoing functional magnetic resonance imaging (fMRI). During a subsequent recognition memory task, participants were shown video clips depicting plays of the game, stemming either from previously-viewed game segments (targets) or from non-viewed portions of the same game (foils). After an old-new judgment, participants provided emotional valence and intensity ratings of the clips. A data driven approach was first used to decompose the fMRI signal acquired during free viewing of the game into spatially independent components. Correlations were then calculated between the identified components and post-scanning emotion ratings for successfully encoded targets. Two components were correlated with intensity ratings, including temporal lobe regions implicated in memory and emotional functions, such as the hippocampus and amygdala, as well as a midline fronto-cingulo-parietal network implicated in social cognition and self-relevant processing. These data were supported by a general linear model analysis, which revealed additional valence effects in fronto-striatal-insular regions when plays were divided into positive and negative events according to the fan's perspective. Overall, these findings contribute to our understanding of how emotional factors impact distributed neural systems to successfully encode dynamic, personally-relevant event sequences.

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Serotonin (5-HT) can either increase or decrease anxiety-like behaviour in animals, actions that depend upon neuroanatomical site of action and 5-HT receptor subtype. Although systemic studies with 5-HT(2) receptor agonists and antagonists suggest a facilitatory role for this receptor subtype in anxiety, somewhat inconsistent results have been obtained when such compounds have been directly applied to limbic targets such as the hippocampus and amygdala. The present study investigated the effects of the 5-HT(2B/2C) receptor agonist mCPP bilaterally microinjected into the dorsal hippocampus (DH: 0, 0.3 1.0 or 3.0 nmol/0.2 mu l), the ventral hippocampus (VH: 0, 0.3, 1.0 or 3.0 nmol/0.2 mu l) or the amygdaloid complex (0, 0.15, 0.5, 1.0 or 3.0 nmol/0.1 mu l) in mice exposed to the elevated plus-maze (EPM). Test sessions were videotaped and subsequently scored for conventional indices of anxiety (percentage of open arm entries and percentage of open arm time) and locomotor activity (closed arm entries). Results showed that mCPP microinfusions into the DH or VH failed to affect any behavioural measure in the EPM. However, when injected into the amygdaloid complex, the dose of 1.0 nmol of this 5HT(2B/2C) receptor agonist increased behavioural indices of anxiety without significantly altering general activity levels. This anxiogenic-like effect of mCPP was selectively and completely blocked by local injection of a behaviourally-inactive dose of SDZ SER-082 (10 nmol/0.1 mu l), a preferential 5-HT(2C) receptor antagonist. These data suggest that 5HT(2C) receptors located within the amygdaloid complex (but not the dorsal or ventral hippocampus) play a facilitatory role in plus-maze anxiety in mice. (c) 2007 Elsevier B.V. All rights reserved.

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It has been shown that ouabain (OUA) can activate the Na,K-ATPase complex and mediate intracellular signaling in the central nervous system (CNS). Inflammatory stimulus increases glutamatergic transmission, especially at N-methyl-D-aspartate (NMDA) receptors, which are usually coupled to the activation of nitric oxide synthase (NOS). Nuclear factor-kappa B (NF-kappa B) activation modulates the expression of genes involved in development, plasticity, and inflammation. The present work investigated the effects of OUA on NF-kappa B binding activity in rat hippocampus and the influence of this OUA-Na,K-ATPase signaling cascade in NMDA-mediated NF-kappa B activation. The findings presented here are the first report indicating that intrahippocampal administration of OUA, in a concentration that did not alter Na,K-ATPase or NOS activity, induced an activation of NF-kappa B, leading to increases in brain-derived neurotrophic factor (Bdnf), inducible NOS (iNos), tumor necrosis factor-alpha (Tnf-alpha), and B-cell leukemia/lymphoma 2 (Bcl2) mRNA levels. This response was not linked to any significant signs of neurodegeneration as showed via Fluoro-Jade B and Nissl stain. Intrahippocampal administration of NMDA induced NF alpha B activation and increased NOS and alpha 2/3-Na,K-ATPase activities. NMDA treatment further increased OUA-induced NF-kappa B activation, which was partially blocked by MK-801, an antagonist of NMDA receptor. These results suggest that OUA-induced NF-kappa B activation is at least in part dependent on Na,K-ATPase modulatory action of NMDA receptor in hippocampus. The interaction of these signaling pathways could be associated with biological mechanisms that may underlie the basal homeostatic state linked to the inflammatory signaling cascade in the brain. (c) 2011 Wiley Periodicals, Inc.

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Tuberous sclerosis complex (TSC) is a multisystem, autosomal dominant disorder affecting approximately 1 in 6000 births. Developmental brain abnormalities cause substantial morbidity and mortality and often lead to neurological disease including epilepsy, cognitive disabilities, and autism. TSC is caused by inactivating mutations in either TSC1 or TSC2, whose protein products are known inhibitors of mTORC1, an important kinase regulating translation and cell growth. Nonetheless, neither the pathophysiology of the neurological manifestations of TSC nor the extent of mTORC1 involvement in the development of these lesions is known. Murine models would greatly advance the study of this debilitating disorder. This thesis will describe the generation and characterization of a novel brain-specific mouse model of TSC, Tsc2flox/ko;hGFAP-Cre. In this model, the Tsc2 gene has been removed from most neurons and glia of the cortex and hippocampus by targeted Cre-mediated deletion in radial glial neuroprogenitor cells. The Tsc2flox/ko;hGFAP-Cre mice fail to thrive beginning postnatal day 8 and die from seizures around 23 days. Further characterization of these mice demonstrated megalencephaly, enlarged neurons, abnormal neuronal migration, altered progenitor pools, hypomyelination, and an astrogliosis. The similarity of these defects to those of TSC patients establishes this mouse as an excellent model for the study of the neuropathology of TSC and testing novel therapies. We further describe the use of this mouse model to assess the therapeutic potential of the macrolide rapamycin, an inhibitor of mTORC1. We demonstrate that rapamycin administered from postnatal day 10 can extend the life of the mutant animals 5 fold. Since TSC is a neurodevelopmental disorder, we also assessed in utero and/or immediate postnatal treatment of the animals with rapamycin. Amazingly, combined in utero and postnatal rapamycin effected a histologic rescue that was almost indistinguishable from control animals, indicating that dysregulation of mTORC1 plays a large role in TSC neuropathology. In spite of the almost complete histologic rescue, behavioral studies demonstrated that combined treatment resulted in poorer learning and memory than postnatal treatment alone. Postnatally-treated animals behaved similarly to treated controls, suggesting that immediate human treatment in the newborn period might provide the most opportune developmental timepoint for rapamycin administration.

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While many tend to think of memory systems in the brain as a single process, in reality several experiments have supported multiple dissociations of different forms of learning, such as spatial learning and response learning. In both humans and rats, the hippocampus has long been shown to be specialized in the storage of spatial and contextual memory whereas the striatum is associated with motor responses and habitual behaviors. Previous studies have examined how damage to hippocampus or striatum has affected the acquisition of either a spatial or response navigation task. However even in a very familiar environment organisms must continuously switch between place and response strategies depending upon circumstances. The current research investigates how these two brain systems interact under normal conditions to produce navigational behavior. Rats were tested using a task developed by Jacobson and colleagues (2006) in which the two types of navigation could be controlled and studied simultaneously. Rats were trained to solve a plus maze using both a spatial and a response strategy. A cue (flashing light) was employed to indicate the correct strategy on a given trial. When no light was present, the animals were rewarded for making a 90º right turn (motor response). When the light was on, the animals were rewarded for going to a specific goal location (place strategy). After learning the task, animals had a sham surgery or dorsal striatum or hippocampus damaged. In order to investigate the individual role of each brain system and evaluate whether these brain regions compete or cooperate for control over strategy, we utilized a within-animal comparisons. The configuration of the maze allowed for the comparison of behavior in individual animals before and after specific brain areas were damaged. Animals with hippocampal lesions showed selective deficits on place trials after surgery and learned the reversal of the motor response more rapidly than striatal lesioned or sham rats. Unlike previous findings regarding maze learning, animals with striatal lesions showed deficits in both place and response trials and had difficulty learning the reversal of motor response. Therefore, the effects of lesions on the ability to switch back and forth between strategies were more complex than previously suggested. This work may reveal important new insight on the integration of hippocampal and striatal learning systems, and facilitate a better understanding of the brain dynamics underlying similar navigational processes in humans.

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Chronic exposure to cocaine induces modifications to neurons in the brain regions involved in addiction. Hence, we evaluated cocaine-induced changes in the hippocampal CA1 field in Fischer 344 (F344) and Lewis (LEW) rats, 2 strains that have been widely used to study genetic predisposition to drug addiction, by combining intracellular Lucifer yellow injection with confocal microscopy reconstruction of labeled neurons. Specifically, we examined the effects of cocaine self-administration on the structure, size, and branching complexity of the apical dendrites of CA1 pyramidal neurons. In addition, we quantified spine density in the collaterals of the apical dendritic arbors of these neurons. We found differences between these strains in several morphological parameters. For example, CA1 apical dendrites were more branched and complex in LEW than in F344 rats, while the spine density in the collateral dendrites of the apical dendritic arbors was greater in F344 rats. Interestingly, cocaine self-administration in LEW rats augmented the spine density, an effect that was not observed in the F344 strain. These results reveal significant structural differences in CA1 pyramidal cells between these strains and indicate that cocaine self-administration has a distinct effect on neuron morphology in the hippocampus of rats with different genetic backgrounds.

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The invasion of sodium spikes from the soma into dendrites was studied in hippocampal pyramidal cells by simultaneous extracellular and intracellular recordings in anesthetized rats and by simultaneous extracellular recordings of the somatic and dendritic potentials in freely behaving animals. During complex-spike patterns, recorded in the immobile or sleeping animal, dendritic invasion of successive spikes was substantially attenuated. Complex-spike bursts occurred in association with population discharge of CA3-CA1 pyramidal cells (sharp wave field events). Synaptic inhibition reduced the amplitude of sodium spikes in the dendrites and prevented the occurrence of calcium spikes. These findings indicate that (i) the voltage-dependent calcium influx into the dendrites is under the control of inhibitory neurons and (ii) the temporal coincidence of synaptic depolarization and activation of voltage-dependent calcium conductances by the backpropagating spikes during sharp wave bursts may be critical for synaptic plasticity in the intact hippocampus.