Calcium domains associated with individual channels can account for anomalous voltage relations of CA-dependent responses.

Computer-assisted modeling of calcium influx through voltage-activated membrane channels predicted that buffer-limited elevation of cytoplasmic free calcium ion concentration occurs within microscopic hemispherical "domains" centered upon the active Ca channels. With increasing depolarization, the number of activated channels, and hence the number of Ca domains, should increase; the single-channel current should, however, decrease, thereby decreasing Ca2+ accumulation in each domain relative to the macroscopic current. Such voltage dependence of the microscopic distribution of Ca2+ may influence relations between total Ca2+ entry and Ca-dependent processes. Ca-mediated inactivation of Ca channels in Aplysia neurons exhibits behavior consistent with the calcium domain hypothesis.     

A clarification of two congeners,Pseudodiaptomus lobipes and P. binghami (Calanoida,Pseudodiaptomidae) from India,with description of P. mixtus sp.n. from Bangladesh

Two closely related and often confused species of Pseudodiaptomus from the Lobus-species group, P. lobipes and P. binghami are redescribed from various locations along the east coast of India. These species predominately occur in freshwater though they can survive temporary periods of increased salinity. The distinctive features of the species are found on: female caudal ramal setae, female and male urosome 1–2 spinulation patterns, and fifth legs. A new species P. mixtus from Bangladesh is described.     

Amphetamine Promotes Neostriatal Ascorbate Release via a Nigro-Thalamo-Cortico-Neostriatal Loop

Abstract: In the neostriatum, amphetamine and other dopamine agonists elevate the extracellular level of ascorbate, which is known to modulate neostriatal function. Although both D₁ and D₂ receptors have been linked to neostriatal ascorbate release, ample evidence suggests it is controlled by areas outside the neostriatum. The present series of experiments used selective lesions and intracerebral drug infusions to probe the involvement of the ventromedial thalamus and substantia nigra pars reticulata. Our results implicate both of these sites in amphetamine-induced increases in the release of neostriatal ascorbate. Thus, whereas unilateral electrolytic lesions of the substantia nigra pars reticulata completely abolished the ability of systemic amphetamine (2.5 mg/kg) to increase extracellular ascorbate in ipsilateral neostriatum, intranigral infusions of this drug (10 and 30 µg/µl) elevated neostriatal ascorbate release. This infusion effect, moreover, was blocked by electrolytic lesions of the ipsilateral ventromedial thalamus, which receives input from the substantia nigra pars reticulata and projects to the cerebral cortex. These results, combined with previous evidence implicating cortical projections to neostriatum as the source of extracellular ascorbate, suggest that neostriatal ascorbate release is regulated, at least in part, by a nigro-thalamo-cortico-neostriatal pathway.     

Dephosphorylation of skeletal muscle phosphorylase,glycogen synthase,and phosphorylase kinase β-subunit by a Mn2+-activated protein phosphatase

An Mn²⁺-activated phosphoprotein phosphatase of M_r = 80,000 from rabbit muscle catalyzes the dephosphorylation of skeletal muscle proteins that are phosphorylated by either phosphorylase kinase or cAMP-dependent protein kinase. Phosphorylase or glycogen synthase labeled by phosphorylase kinase at seryl residues 14 or 7, respectively, are both dephosphorylated by the phosphatase. Phosphorylase a and glycogen synthase compete with one another for the phosphatase. The phosphatase discriminates between different sites labeled by the cAMP-dependent protein kinase: glycogen synthase phosphorylated either to 1.0 or 1.8 mol phosphate/mol, or phosphorylase kinase phosphorylated on its β-subunit serve as substrates for the phosphatase, but the phosphorylase kinase α-subunit, the phosphorylated phosphatase inhibitor 1, or casein do not. Histone fraction IIA, phosphorylated by the catalytic subunit, was a poor substrate even at a concentration of 100 μm. Phosphorylation of the α-subunit of phosphorylase kinase had no influence on the kinetics of dephosphorylation of the β-subunit. Thus, the M_r = 80,000 phosphatase meets the functional definition of a protein phosphatase 1 [Cohen, P. (1978) Curr. Top. Cell. Regul.14, 117–196]. Furthermore, from a comparison of the known phosphorylated sites of these proteins, it appears that the phosphatase discriminates between different sites present in the phosphoproteins tested on the basis of the K_m values for the reactions. It displays a preferential activity toward proteins with a primary structure wherein basic residues are two positions amino-terminal from the phosphoserine, AgrLysX-YSer(P) or LysArgX-YSer(P), rather and one residue away, ArgArgX-Ser(P).     

Ataxin1L Is a Regulator of HSC Function Highlighting the Utility of Cross-Tissue Comparisons for Gene Discovery

Hematopoietic stem cells (HSCs) are rare quiescent cells that continuously replenish the cellular components of the peripheral blood. Observing that the ataxia-associated gene Ataxin-1-like (Atxn1L) was highly expressed in HSCs, we examined its role in HSC function through in vitro and in vivo assays. Mice lacking Atxn1L had greater numbers of HSCs that regenerated the blood more quickly than their wild-type counterparts. Molecular analyses indicated Atxn1L null HSCs had gene expression changes that regulate a program consistent with their higher level of proliferation, suggesting that Atxn1L is a novel regulator of HSC quiescence. To determine if additional brain-associated genes were candidates for hematologic regulation, we examined genes encoding proteins from autism- and ataxia-associated protein–protein interaction networks for their representation in hematopoietic cell populations. The interactomes were found to be highly enriched for proteins encoded by genes specifically expressed in HSCs relative to their differentiated progeny. Our data suggest a heretofore unappreciated similarity between regulatory modules in the brain and HSCs, offering a new strategy for novel gene discovery in both systems.     

Biology and Functional Ecology of Equisetum with Emphasis on the Giant Horsetails

Horsetails are unique survivors of a very ancient group of vascular plants, the Sphenophyta, which has a history reaching back to the Upper Devonian. Despite the striking conservatism of Equisetum architecture and anatomy and the small number of species (15) in the modern flora, their ability to thrive under a wide range of conditions is remarkable. This is due to a diverse suite of adaptations that allow tolerance of disturbance, soil anoxia, high metals, and salinity, along with efficient nutrient uptake and nitrogen fixation. The giant horsetails represent the largest living Sphenophyta and provide insights into how their larger ancestors lived and how this ancient lineage has managed to survive in tropical regions.     

Mapping sea level rise impacts to identify climate change adaptation opportunities in the Chesapeake and Delaware Bays,USA

Wetlands Ecology and Management - Salt marshes are at risk globally if they cannot keep pace with sea level rise. Along the United States Mid-Atlantic coast, high marsh has already declined, and is...     

Stable isotope analysis of vegetation history and land use change at Laguna Santa Elena in southern Pacific Costa Rica

Vegetation History and Archaeobotany - Laguna Santa Elena (8.9290° N, 82.9257° W, 1055 m a.s.l.) is a small lake in the Diquís archaeological sub-region of southern Pacific...