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To authenticate to the full-text of this article, please visit this link: http://dx.doi.org/10.1111/j.1467-9280.2009.02338.x Byline: Gary Bargary (1,2,3), Kylie J. Barnett (1,2,3), Kevin J. Mitchell (2,3), Fiona N. Newell (1,2) Abstract: ABSTRACT Although it is estimated that as many as 4% of people experience some form of enhanced cross talk between (or within) the senses, known as synaesthesia, very little is understood about the level of information processing required to induce a synaesthetic experience. In work presented here, we used a well-known multisensory illusion called the McGurk effect to show that synaesthesia is driven by late, perceptual processing, rather than early, unisensory processing. Specifically, we tested 9 linguistic-color synaesthetes and found that the colors induced by spoken words are related to what is perceived (i.e., the illusory combination of audio and visual inputs) and not to the auditory component alone. Our findings indicate that color-speech synaesthesia is triggered only when a significant amount of information processing has occurred and that early sensory activation is not directly linked to the synaesthetic experience. Author Affiliation: (1)School of Psychology (2)Institute of Neuroscience, and (3)Smurfit Institute of Genetics, Trinity College Dublin Article History: (R eceived 8/8/08; R evision accepted 11/8/08) Article note: Address correspondence to Fiona N. Newell, Institute of Neuroscience, Lloyd Building, Trinity College, Dublin 2, Ireland, e-mail: fiona.newell@tcd.ie.

A reductively mechanistic approach to neuroscience suggests that low-level physical laws determine our actions and that mental states are epiphenomena. In this scheme there seems to be little room for free will or genuine agency. I argue here that physical indeterminacy provides room for the information entailed in patterns of neuronal firing – the mental content of beliefs, goals, and intentions – to have real causal power in decision-making. [ABSTRACT FROM AUTHOR]

The development of different brain regions involves the coordinated control of proliferation and cell fate specification along and across the neuraxis. Here, we identify Plxdc2 as a novel regulator of these processes, using in ovo electroporation and in vitro cultures of mammalian cells. Plxdc2 is a type I transmembrane protein with some homology to nidogen and to plexins. It is expressed in a highly discrete and dynamic pattern in the developing nervous system, with prominent expression in various patterning centres. In the chick neural tube, where Plxdc2 expression parallels that seen in the mouse, misexpression of Plxdc2 increases proliferation and alters patterns of neurogenesis, resulting in neural tube thickening at early stages. Expression of the Plxdc2 extracellular domain alone, which can be cleaved and shed in vivo, is sufficient for this activity, demonstrating a cell non-autonomous function. Induction of proliferation is also observed in cultured embryonic neuroepithelial cells (ENCs) derived from E9.5 mouse neural tube, which express a Plxdc2-binding activity. These experiments uncover a direct molecular activity of Plxdc2 in the control of proliferation, of relevance in understanding the role of this protein in various cancers, where its expression has been shown to be altered. They also implicate Plxdc2 as a novel component of the network of signalling molecules known to coordinate proliferation and differentiation in the developing nervous system. [ABSTRACT FROM AUTHOR]

During their migration, cerebellar granule cells switch from a tangential to a radial mode of migration. We have previously demonstrated that this involves the transmembrane semaphorin Sema6A. We show here that plexin-A2 is the receptor that controls Sema6A function in migrating granule cells. In plexin-A2–deficient (Plxna2−/−) mice, which were generated by homologous recombination, many granule cells remained in the molecular layer, as we saw in Sema6a mutants. A similar phenotype was observed in mutant mice that were generated by mutagenesis with N-ethyl-N-nitrosourea and had a single amino-acid substitution in the semaphorin domain of plexin-A2. We found that this mutation abolished the ability of Sema6A to bind to plexin-A2. Mouse chimera studies further suggested that plexin-A2 acts in a cell-autonomous manner. We also provide genetic evidence for a ligand-receptor relationship between Sema6A and plexin-A2 in this system. Using time-lapse video microscopy, we found that centrosome-nucleus coupling and coordinated motility were strongly perturbed in Sema6a−/− and Plxna2−/− granule cells. This suggests that semaphorin-plexin signaling modulates cell migration by controlling centrosome positioning. [ABSTRACT FROM AUTHOR]