Genetic analysis revealed that one mutant previously implicated involved in acute ethanol responses, slo-1, as well as two mutants with defects in serotonin synthesis,

tph-1 and bas-1, failed to exhibit ethanol interference with gustatory plasticity. Furthermore, two metabotropic serotonin receptors. SER-4 and SER-7, were found to be involved in ethanol-mediated gustatory plasticity. In addition, the tph-1 and ser-4 loci were also involved in ethanol’s effect on locomotion behavior. These data suggested an essential role of serotonin signaling in modulating acute effects of ethanol. (C) 2011 Elsevier Ireland Ltd and the Japan Neuroscience Society. All rights reserved.”
“This article uses simple models to explore the impact of adaptive movement by consumers on the population dynamics of a consumer-resource metacommunity consisting of two identical patches. Consumer-resource interactions learn more within a patch are described by the Rosenzweig-MacArthur predator-prey model, and these dynamics are assumed to be cyclic in the absence of movement. The per capita movement rate from one patch to the other is an increasing function of the difference between the per capita birth minus death rate

in the destination patch and that in the currently occupied patch. Several variations on this model are considered. Results show that adaptive movement frequently creates anti-phase cycles in the two patches; WH-4-023 cell line these suppress the predator-prey cycle and lead to low temporal variation of the total population sizes of both species. Paradoxically, even when movement is very sensitive

to the fitness difference Selleckchem U0126 between patches, perfect synchrony of patches is often much less likely than in comparable systems with random movement. Under these circumstances adaptive movement of consumers often generates differences in the average properties of the two patches. In addition, mean global densities and responses to global perturbations often differ greatly from similar systems with no movement or random movement. (C) 2011 Elsevier Ltd. All rights reserved.”
“Apoptosis is a significant mechanism of cochlear hair cell loss from noise. Molecules that inhibit apoptotic intracellular signaling reduce cochlear damage and hearing loss from noise. The current study is an extension of a previous study of the protective value of Src-protein tyrosine kinase inhibitors against noise (Harris et al., 2005). The current study tested three Src-inhibitors: the indole-based KX1-141, the biaryl-based KX2-329, and the ATP-competitive KX2-328. Each of the three drugs was delivered into the chinchillas’ cochleae by allowing the solutions to diffuse across the round window membrane thirty minutes prior to exposure to impulse noise. Hearing thresholds were measured using auditory evoked responses from electrodes in the inferior colliculi.