Age-dependent changes in autophosphorylation of alpha calcium/calmodulin dependent kinase II in hippocampus and amygdala after contextual fear conditioning

The hippocampus and amygdala are essential brain regions responsible for contextual fear conditioning (CFC). The autophosphorylation of alpha calciumcalmodulin kinase II (αCaMKII) at threonine-286 (T286) is a critical step 3 implicated in long-term potentiation (LTP), learning and memory. However, the changes in αCaMKII levels with aging and training in associated brain regions are not fully understood. Here, we studied how aging and training affect the levels of phosphorylated (T286) and proportion of phosphorylated:total αCaMKII in the hippocampus and amygdala. Young and aged mice, naïve (untrained) and trained in CFC, were analysed by immunohistochemistry for the levels of total and phosphorylated αCaMKII in the hippocampus and amygdala. We found that two hours after CFC training, young mice exhibited a higher level of phosphorylated and increased ratio of phosphorylated:total αCaMKII in hippocampal CA3 stratum radiatum. Furthermore, aged untrained mice showed a higher ratio of phosphorylated:total αCaMKII in the CA3 region of the hippocampus when compared to the young untrained group. No effect of training or aging were seen in the central, lateral and basolateral amygdala regions, for both phosphorylated and ratio of phosphorylated:total αCaMKII. These results show that aging impairs the training-induced upregulation of autophosphorylated (T286) αCaMKII in the CA3 stratum radiatum of the hippocampus. This indicates that distinct age-related mechanisms underlie CFC that may rely more heavily on NMDA receptor-dependent plasticity in young age

Successful Cognitive Aging in Rats: A Role for mGluR5 Glutamate Receptors, Homer 1 Proteins and Downstream Signaling Pathways

Normal aging is associated with impairments in cognition, especially learning and memory. However, major individual differences are known to exist. Using the classical Morris Water Maze (MWM) task, we discriminated a population of 24-months old Long Evans aged rats in two groups - memory-impaired (AI) and memory-unimpaired (AU) in comparison with 6-months old adult animals. AI rats presented deficits in learning, reverse memory and retention. At the molecular level, an increase in metabotropic glutamate receptors 5 (mGluR5) was observed in post-synaptic densities (PSD) in the hippocampus of AU rats after training. Scaffolding Homer 1b/c proteins binding to group 1 mGluR facilitate coupling with its signaling effectors while Homer 1a reduces it. Both Homer 1a and 1b/c levels were up-regulated in the hippocampus PSD of AU animals following MWM task. Using immunohistochemistry we further demonstrated that mGluR5 as well as Homer 1b/c stainings were enhanced in the CA1 hippocampus sub-field of AU animals. In fact mGluR5 and Homer 1 isoforms were more abundant and co-localized in the hippocampal dendrites in AU rats. However, the ratio of Homer 1a/Homer 1b/c bound to mGluR5 in the PSD was four times lower for AU animals compared to AI rats. Consequently, AU animals presented higher PKCγ, ERK, p70S6K, mTOR and CREB activation. Finally the expression of immediate early gene Arc/Arg3.1 was shown to be higher in AU rats in accordance with its role in spatial memory consolidation. On the basis of these results, a model of successful cognitive aging with a critical role for mGluR5, Homer 1 proteins and downstream signalling pathways is proposed here

Body Size Evolution in Extant Oryzomyini Rodents: Cope's Rule or Miniaturization?

At the macroevolutionary level, one of the first and most important hypotheses that proposes an evolutionary tendency in the evolution of body sizes is “Cope's rule". This rule has considerable empirical support in the fossil record and predicts that the size of species within a lineage increases over evolutionary time. Nevertheless, there is also a large amount of evidence indicating the opposite pattern of miniaturization over evolutionary time. A recent analysis using a single phylogenetic tree approach and a Bayesian based model of evolution found no evidence for Cope's rule in extant mammal species. Here we utilize a likelihood-based phylogenetic method, to test the evolutionary trend in body size, which considers phylogenetic uncertainty, to discern between Cope's rule and miniaturization, using extant Oryzomyini rodents as a study model. We evaluated body size trends using two principal predictions: (a) phylogenetically related species are more similar in their body size, than expected by chance; (b) body size increased (Cope's rule)/decreased (miniaturization) over time. Consequently the distribution of forces and/or constraints that affect the tendency are homogenous and generate this directional process from a small/large sized ancestor. Results showed that body size in the Oryzomyini tribe evolved according to phylogenetic relationships, with a positive trend, from a small sized ancestor. Our results support that the high diversity and specialization currently observed in the Oryzomyini tribe is a consequence of the evolutionary trend of increased body size, following and supporting Cope's rule

The RESET project: constructing a European tephra lattice for refined synchronisation of environmental and archaeological events during the last c. 100 ka

This paper introduces the aims and scope of the RESET project (. RESponse of humans to abrupt Environmental Transitions), a programme of research funded by the Natural Environment Research Council (UK) between 2008 and 2013; it also provides the context and rationale for papers included in a special volume of Quaternary Science Reviews that report some of the project's findings. RESET examined the chronological and correlation methods employed to establish causal links between the timing of abrupt environmental transitions (AETs) on the one hand, and of human dispersal and development on the other, with a focus on the Middle and Upper Palaeolithic periods. The period of interest is the Last Glacial cycle and the early Holocene (c. 100-8 ka), during which time a number of pronounced AETs occurred. A long-running topic of debate is the degree to which human history in Europe and the Mediterranean region during the Palaeolithic was shaped by these AETs, but this has proved difficult to assess because of poor dating control. In an attempt to move the science forward, RESET examined the potential that tephra isochrons, and in particular non-visible ash layers (cryptotephras), might offer for synchronising palaeo-records with a greater degree of finesse. New tephrostratigraphical data generated by the project augment previously-established tephra frameworks for the region, and underpin a more evolved tephra 'lattice' that links palaeo-records between Greenland, the European mainland, sub-marine sequences in the Mediterranean and North Africa. The paper also outlines the significance of other contributions to this special volume: collectively, these illustrate how the lattice was constructed, how it links with cognate tephra research in Europe and elsewhere, and how the evidence of tephra isochrons is beginning to challenge long-held views about the impacts of environmental change on humans during the Palaeolithic. © 2015 Elsevier Ltd.RESET was funded through Consortium Grants awarded by the Natural Environment Research Council, UK, to a collaborating team drawn from four institutions: Royal Holloway University of London (grant reference NE/E015905/1), the Natural History Museum, London (NE/E015913/1), Oxford University (NE/E015670/1) and the University of Southampton, including the National Oceanography Centre (NE/01531X/1). The authors also wish to record their deep gratitude to four members of the scientific community who formed a consultative advisory panel during the lifetime of the RESET project: Professor Barbara Wohlfarth (Stockholm University), Professor Jørgen Peder Steffensen (Niels Bohr Institute, Copenhagen), Dr. Martin Street (Romisch-Germanisches Zentralmuseum, Neuwied) and Professor Clive Oppenheimer (Cambridge University). They provided excellent advice at key stages of the work, which we greatly valued. We also thank Jenny Kynaston (Geography Department, Royal Holloway) for construction of several of the figures in this paper, and Debbie Barrett (Elsevier) and Colin Murray Wallace (Editor-in-Chief, QSR) for their considerable assistance in the production of this special volume.Peer Reviewe

Development and validation of a weather-based model for predicting infection of loquat fruit by Fusicladium eriobotryae

A mechanistic, dynamic model was developed to predict infection of loquat fruit by conidia of Fusicladium eriobotryae, the causal agent of loquat scab. The model simulates scab infection periods and their severity through the sub-processes of spore dispersal, infection, and latency (i.e., the state variables); change from one state to the following one depends on environmental conditions and on processes described by mathematical equations. Equations were developed using published data on F. eriobotryae mycelium growth, conidial germination, infection, and conidial dispersion pattern. The model was then validated by comparing model output with three independent data sets. The model accurately predicts the occurrence and severity of infection periods as well as the progress of loquat scab incidence on fruit (with concordance correlation coefficients .0.95). Model output agreed with expert assessment of the disease severity in seven loquatgrowing seasons. Use of the model for scheduling fungicide applications in loquat orchards may help optimise scab management and reduce fungicide applications.This work was funded by Cooperativa Agricola de Callosa d'En Sarria (Alicante, Spain). Three months' stay of E. Gonzalez-Dominguez at the Universita Cattolica del Sacro Cuore (Piacenza, Italy) was supported by the Programa de Apoyo a la Investigacion y Desarrollo (PAID-00-12) de la Universidad Politecnica de Valencia. The funders had no role in study design, data collection and analysis, decision to publish, or preparation of the manuscript.González Domínguez, E.; Armengol Fortí, J.; Rossi, V. (2014). Development and validation of a weather-based model for predicting infection of loquat fruit by Fusicladium eriobotryae. PLoS ONE. 9(9):1-12. https://doi.org/10.1371/journal.pone.0107547S11299Sánchez-Torres, P., Hinarejos, R., & Tuset, J. J. (2009). 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M. (1994). Discontinuous Wetting and Survival of Conidia ofVenturia inaequalison Apple Leaves. Phytopathology, 84(4), 372. doi:10.1094/phyto-84-372Hartman, J. R., Parisi, L., & Bautrais, P. (1999). Effect of Leaf Wetness Duration, Temperature, and Conidial Inoculum Dose on Apple Scab Infections. Plant Disease, 83(6), 531-534. doi:10.1094/pdis.1999.83.6.531Holb, I. J., Heijne, B., Withagen, J. C. M., & Jeger, M. J. (2004). Dispersal of Venturia inaequalis Ascospores and Disease Gradients from a Defined Inoculum Source. Journal of Phytopathology, 152(11-12), 639-646. doi:10.1111/j.1439-0434.2004.00910.xRossi, V., Giosue, S., & Bugiani, R. (2003). Influence of Air Temperature on the Release of Ascospores of Venturia inaequalis. Journal of Phytopathology, 151(1), 50-58. doi:10.1046/j.1439-0434.2003.00680.xStensvand, A., Gadoury, D. M., Amundsen, T., Semb, L., & Seem, R. C. (1997). Ascospore Release and Infection of Apple Leaves by Conidia and Ascospores ofVenturia inaequalisat Low Temperatures. Phytopathology, 87(10), 1046-1053. doi:10.1094/phyto.1997.87.10.1046Machardy WE (1996) Apple scab. Biology, epidemiology and management. St. Paul: APS Press. 545.James, J. R. (1982). Environmental Factors Influencing Pseudothecial Development and Ascospore Maturation ofVenturia inaequalis. Phytopathology, 72(8), 1073. doi:10.1094/phyto-72-1073Li, B., Zhao, H., Li, B., & Xu, X.-M. (2003). Effects of temperature, relative humidity and duration of wetness period on germination and infection by conidia of the pear scab pathogen (Venturia nashicola). Plant Pathology, 52(5), 546-552. doi:10.1046/j.1365-3059.2003.00887.xLi, B.-H., Xu, X.-M., Li, J.-T., & Li, B.-D. (2005). Effects of temperature and continuous and interrupted wetness on the infection of pear leaves by conidia of Venturia nashicola. Plant Pathology, 54(3), 357-363. doi:10.1111/j.1365-3059.2005.01207.xUMEMOTO, S. 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Phytopathology, 72(10), 1339. doi:10.1094/phyto-72-1339MARZO, L., FRISULLO, S., LOPS, F., & ROSSI, V. (1993). Possible dissemination of Spilocaea oleagina conidia by insects (Ectopsocus briggsi). EPPO Bulletin, 23(3), 389-391. doi:10.1111/j.1365-2338.1993.tb01341.xLOPS, F., FRISULLO, S., & ROSSI, V. (1993). Studies on the spread of the olive scab pathogen, Spilocaea oleagina. EPPO Bulletin, 23(3), 385-387. doi:10.1111/j.1365-2338.1993.tb01340.xObanor, F. O., Walter, M., Jones, E. E., & Jaspers, M. V. (2007). Effect of temperature, relative humidity, leaf wetness and leaf age on Spilocaea oleagina conidium germination on olive leaves. European Journal of Plant Pathology, 120(3), 211-222. doi:10.1007/s10658-007-9209-6Obanor, F. O., Walter, M., Jones, E. E., & Jaspers, M. V. (2010). Effects of temperature, inoculum concentration, leaf age, and continuous and interrupted wetness on infection of olive plants by Spilocaea oleagina. Plant Pathology, 60(2), 190-199. doi:10.1111/j.1365-3059.2010.02370.xViruega, J. R., Moral, J., Roca, L. F., Navarro, N., & Trapero, A. (2013). Spilocaea oleaginain Olive Groves of Southern Spain: Survival, Inoculum Production, and Dispersal. Plant Disease, 97(12), 1549-1556. doi:10.1094/pdis-12-12-1206-reViruega, J. R., Roca, L. F., Moral, J., & Trapero, A. (2011). Factors Affecting Infection and Disease Development on Olive Leaves Inoculated withFusicladium oleagineum. Plant Disease, 95(9), 1139-1146. doi:10.1094/pdis-02-11-0126Eikemo, H., Gadoury, D. M., Spotts, R. A., Villalta, O., Creemers, P., Seem, R. C., & Stensvand, A. (2011). Evaluation of Six Models to Estimate Ascospore Maturation in Venturia pyrina. Plant Disease, 95(3), 279-284. doi:10.1094/pdis-02-10-0125Li, B.-H., Yang, J.-R., Dong, X.-L., Li, B.-D., & Xu, X.-M. (2007). A dynamic model forecasting infection of pear leaves by conidia of Venturia nashicola and its evaluation in unsprayed orchards. 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