10 research outputs found

    SHELTER AVAILABILITY, OCCUPANCY, AND RESIDENCY IN SIZE-ASYMMETRIC CONTESTS BETWEEN RUSTY CRAYFISH, \u3ci\u3eORCONECTES RUSTICUS\u3c/i\u3e

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    Contest outcomes are usually determined by differences in resource holding potential, the social histories of the combatants, and perceptions of resource value. One understudied aspect of gaining an advantage is the residency effect. Prior occupancy of a particular place can affect the knowledge and motivation of the resident. There could be a tactical advantage in knowing the terrain or an increased willingness to fight to maintain control of a familiar area. In this study we evaluated the importance of shelter residency effects relative to size differences between rusty crayfish (Orconectes rusticus) as potential competitors for access to shelter. The intensity of any residency effects was manipulated by altering the number of shelters in the arena. Our results suggest that any residency effect is very weak in this system, and if present may often be masked by the strong and pervasive influence on contest outcome of the relative body sizes of the contestants. We also found that both shelter number and crayfish size asymmetries had strong, independent effects on levels of aggression. Dominance, but not residency status, was a factor in shelter use

    Norepinephrine transporter variant A457P knock-in mice display key features of human postural orthostatic tachycardia syndrome

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    SUMMARY Postural orthostatic tachycardia syndrome (POTS) is a common autonomic disorder of largely unknown etiology that presents with sustained tachycardia on standing, syncope and elevated norepinephrine spillover. Some individuals with POTS experience anxiety, depression and cognitive dysfunction. Previously, we identified a mutation, A457P, in the norepinephrine (NE; also known as noradrenaline) transporter (NET; encoded by SLC6A2) in POTS patients. NET is expressed at presynaptic sites in NE neurons and plays a crucial role in regulating NE signaling and homeostasis through NE reuptake into noradrenergic nerve terminals. Our in vitro studies demonstrate that A457P reduces both NET surface trafficking and NE transport and exerts a dominant-negative impact on wild-type NET proteins. Here we report the generation and characterization of NET A457P mice, demonstrating the ability of A457P to drive the POTS phenotype and behaviors that are consistent with reported comorbidities. Mice carrying one A457P allele (NET+/P) exhibited reduced brain and sympathetic NE transport levels compared with wild-type (NET+/+) mice, whereas transport activity in mice carrying two A457P alleles (NETP/P) was nearly abolished. NET+/P and NETP/P mice exhibited elevations in plasma and urine NE levels, reduced 3,4-dihydroxyphenylglycol (DHPG), and reduced DHPG:NE ratios, consistent with a decrease in sympathetic nerve terminal NE reuptake. Radiotelemetry in unanesthetized mice revealed tachycardia in NET+/P mice without a change in blood pressure or baroreceptor sensitivity, consistent with studies of human NET A457P carriers. NET+/P mice also demonstrated behavioral changes consistent with CNS NET dysfunction. Our findings support that NET dysfunction is sufficient to produce a POTS phenotype and introduces the first genetic model suitable for more detailed mechanistic studies of the disorder and its comorbidities

    Advances in bioprinted cell-laden hydrogels for skin tissue engineering

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