ICT for growth: a targeted approach. Bruegel Policy Contribution 2012/10, June 2012

This Policy Contribution assesses the broad obstacles hampering ICT-led growth in Europe and identifies the main areas in which policy could unlock the greatest value. We review estimates of the value that could be generated through take-up of various technologies and carry out a broad matching with policy areas. According to the literature survey and the collected estimates, the areas in which the right policies could unlock the greatest ICT-led growth are product and labour market regulations and the European Single Market. These areas should be reformed to make European markets more flexible and competitive. This would promote wider adoption of modern data-driven organisational and management practices thereby helping to close the productivity gap between the United States and the European Union. Gains could also be made in the areas of privacy, data security, intellectual property and liability pertaining to the digital economy, especially cloud computing, and next generation network infrastructure investment. Standardisation and spectrum allocation issues are found to be important, though to a lesser degree. Strong complementarities between the analysed technologies suggest, however, that policymakers need to deal with all of the identified obstacles in order to fully realise the potential of ICT to spur long-term growth beyond the partial gains that we report.

Big Decisions and Sparse Data: Adapting Scientific Publishing to the Needs of Practical Conservation

The biggest challenge in conservation biology is breaking down the gap between research and practical management. A major obstacle is the fact that many researchers are unwilling to tackle projects likely to produce sparse or messy data because the results would be difficult to publish in refereed journals. The obvious solution to sparse data is to build up results from multiple studies. Consequently, we suggest that there needs to be greater emphasis in conservation biology on publishing papers that can be built on by subsequent research rather than on papers that produce clear results individually. This building approach requires: (1) a stronger theoretical framework, in which researchers attempt to anticipate models that will be relevant in future studies and incorporate expected differences among studies into those models; (2) use of modern methods for model selection and multi-model inference, and publication of parameter estimates under a range of plausible models; (3) explicit incorporation of prior information into each case study; and (4) planning management treatments in an adaptive framework that considers treatments applied in other studies. We encourage journals to publish papers that promote this building approach rather than expecting papers to conform to traditional standards of rigor as stand-alone papers, and believe that this shift in publishing philosophy would better encourage researchers to tackle the most urgent conservation problems.

G-protein-coupled-receptor-mediated presynaptic inhibition in the cerebellum

Throughout the central nervous system a dominant form of inhibition of neurotransmitter release from presynaptic terminals is mediated by G-protein-coupled receptors (GPCRs). Neurotransmitter release is typically induced by action potentials (APs), but can also occur spontaneously. Presynaptic inhibition by GPCRs has been associated with modulation of voltage-dependent ion channels. However, electrophysiological recordings of spontaneous, AP-independent (so-called ‘miniature’) postsynaptic events reveal an additional, important form of GPCR-mediated presynaptic inhibition, distinct from effects on ionic conductances and consistent with a direct action on the vesicle release machinery. Recent studies suggest that such miniature events might be of physiological relevance not only in signalling but also in development. In the cerebellum, neurotransmitter release onto Purkinje cells occurs by AP-dependent and AP-independent pathways. Here, I focus on inhibitory synapses between interneurons and Purkinje cells, which are subject to strong, identifiable regulation by endogenous GPCR agonists, to consider mechanisms of GPCR-mediated presynaptic inhibition.