Plankton composition,biomass, phylogeny and toxin genes in Lake Big Momela,Tanzania

Lake Big Momela, one of the East African soda lakes in Northern Tanzania characterised by highly saline-alkaline conditions, making them inhospitable to a range of organisms, although supporting massive growths of some adapted planktonic microorganisms that serve as food for birds, such as Lesser Flamingo. The temporal dynamics of plankton, with an emphasis on cyanobacteria, were examined in 2007 using morphological traits and ribosomal genetic markers (16S and 18S rRNA). Cyanobacterial genes encoding for hepatotoxins (mcyE and ndaF) were also screened. Rotifers and copepods dominated the zooplankton, whereas cyanobacteria, such as Anabaenopsis elenkinii and Arthrospira fusiformis dominated the phytoplankton community, and these being related to representatives in other East African soda lakes. The cyanobacteria community also showed distinct seasonal patterns influenced by environmental parameters, mainly salinity, pH and nitrate. Significant positive correlations were found between phytoplankton abundance and nitrate concentrations (r = 0.617, p = 0.033). No signals of the hepatotoxin synthetase genes mcyE and ndaF were retrieved from cyanobacteria during the whole year. In general, our data illustrate the presence of rich planktonic communities, including some unique and potentially endemic cyanobacteria.     

The Role of Cell Volume in the Dynamics of Seizure,Spreading Depression,and Anoxic Depolarization

Cell volume changes are ubiquitous in normal and pathological activity of the brain. Nevertheless, we know little of how cell volume affects neuronal dynamics. We here performed the first detailed study of the effects of cell volume on neuronal dynamics. By incorporating cell swelling together with dynamic ion concentrations and oxygen supply into Hodgkin-Huxley type spiking dynamics, we demonstrate the spontaneous transition between epileptic seizure and spreading depression states as the cell swells and contracts in response to changes in osmotic pressure. Our use of volume as an order parameter further revealed a dynamical definition for the experimentally described physiological ceiling that separates seizure from spreading depression, as well as predicted a second ceiling that demarcates spreading depression from anoxic depolarization. Our model highlights the neuroprotective role of glial K buffering against seizures and spreading depression, and provides novel insights into anoxic depolarization and the relevant cell swelling during ischemia. We argue that the dynamics of seizures, spreading depression, and anoxic depolarization lie along a continuum of the repertoire of the neuron membrane that can be understood only when the dynamic ion concentrations, oxygen homeostasis,and cell swelling in response to osmotic pressure are taken into consideration. Our results demonstrate the feasibility of a unified framework for a wide range of neuronal behaviors that may be of substantial importance in the understanding of and potentially developing universal intervention strategies for these pathological states.