Computations based on statistical distributions are routinely proposed in Bayesian theories of perception (Miyazaki et al., 2006; Yamamoto et al., 2012), while functions similar to averaging over such distributions have been considered in theories of population coding (Roach et al., 2011). Assuming similar mechanisms in principle, we performed a simple simulation, in which we plotted values sampled from two random variables (‘clocks’), after subtracting each from the
average across a population of clocks. We found that this simple renormalisation model could accurately simulate the negative AZD0530 supplier correlation observed (see Supplementary Methods S2 and Supplementary Figure 2 for further details). This serves to demonstrate how the observed negative correlation phenomenon might emerge simply as a consequence of renormalisation, and not due to any explicit antagonism between mechanisms. Neuroscientists and philosophers have long pondered the relationship between subjective
and neural timing (Dennett and Kinsbourne, 1995; Harris et al., 2008; Spence and Squire, 2003; Zeki and Bartels, 1998). Our observations with PH and with neurologically healthy participants confirm that perception is characterised fundamentally by asynchrony and disunity: different aspects of the same pair of multisensory stimuli may be perceived with different asynchronies, and these discrepancies cannot be fully minimised. But an apparent antagonism between complementary measures of subjective timing reveals a superordinate Cobimetinib principle, by which discrepant CH5424802 cell line timings in the brain may nevertheless be renormalised to their average neural timing. By relating subjective timing to average neural timing, temporal renormalisation explains (1) why after a lesion PH experiences auditory leading in one task but
the opposite auditory lead in another, (2) why different timing measures are negatively correlated across normal individuals, and (3) how the brain might tell the time from multiple clocks, with near-veridical accuracy, without needing resynchronising mechanisms. We thank P.H. for participating, and S. Khan, A. Alsius, R. Kanai and T. Schofield for technical assistance; and M. Cappelletti, D. Bueti, S. Gaigg, C. Haenschel, G. Rees, and C. Price, for critical discussions. J.D. was funded by a Royal Society Leverhulme Trust Senior Research Fellowship. Imaging at the Wellcome Trust Centre for Neuroimaging, UCL, and open access publication, were supported by Wellcome Centre grant091593/Z/10/Z. “
“Asymmetries in cognitive maturation throughout the lifespan demonstrate that ageing does not simply reflect development in reverse (Craik & Bialystok, 2006). As we transition through different phases of life external changes to our bodies follow a relatively symmetrical pattern; weakness in infancy is followed by strength in adolescence and middle age and finally frailty again in old age.
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