We investigated meta- and paracontrast masking using tasks requiring observers to judge the surface brightness or else the contours of target stimuli. The contour task revealed strongest metacontrast at SOAs shorter than those obtained for the brightness task. Paracontrast revealed related temporal differences between the tasks. Additionally, the paracontrast results support the existence not only of prolonged inhibitory effects but also of facilitatory effects. The combined results comport with the existence of cortical mechanisms for: (i) fast contour processing, (ii) slow surface-brightness processing, (iii) prolonged inhibition, and (iv) facilitation.

Recently, E. Freeman and J. Driver (2008) reported a cross-modal temporal interaction in which brief sounds drive the perceived direction of visual apparent-motion, an effect they attributed to “temporal capture” of the visual stimuli by the sounds (S. Morein-Zamir, S. Soto-Faraco, & A. Kingstone, 2003). Freeman and Driver used “long-range” visual motion stimuli, which travel over long spatial and temporal intervals and engage high-order cortical areas (K. G. Claeys, D. T. Lindsey, E. De Schutter, & G. A. Orban, 2003; Y. Zhuo et al., 2003). We asked whether Freeman and Driver’s temporal effects extended to the short-range apparent-motion stimuli that engage cortical area MT, a lower-order area with well-established spatiotemporal selectivity for visual motion (e.g. A. Mikami, 1991, 1992; A. Mikami, W. T. Newsome, & R. H. Wurtz, 1986a, 1986b; W. T. Newsome, A. Mikami, & R. H. Wurtz, 1986). Consistent with a temporal-capture account, we found that static sounds bias the perception of both the direction (Experiment 1) and the speed (Experiment 2) of short-range motion. Our results suggest that auditory timing may interact with visual spatiotemporal processing as early as cortical area MT. Examination of the neuronal responses of this well-studied area to the stimuli used in this study would provide a test and might provide insight into the neuronal representation of time.

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Intermittent fasting (IF) and its mimetic, rapamycin extend lifespan and healthspan through mechanisms that are not fully understood. We investigated different short-term durations of IF and rapamycin on cellular and molecular changes in the brains of young (6-10 months) and old (26-31 months) zebrafish. Interestingly, our results showed that IF significantly lowered glucose levels while increasing DCAMKL1 in both young and old animals. This proliferative effect of IF was supported by the upregulation of foxm1 transcript in old animals. Rapamycin did not change glucose levels in young and old animals but had differential effects depending on age. In young zebrafish, proliferating cell nuclear antigen and the LC3-II/LC3-I ratio was decreased, whereas glial fibrillary acidic protein and gephyrin were decreased in old animals. The changes in proliferative markers and a marker of autophagic flux suggest an age-dependent interplay between autophagy and cell proliferation. Additionally, changes in glia and inhibitory tone suggest a suppressive effect on neuroinflammation but may push the brain toward a more excitable state. Mammalian target of rapamycin (mTOR) activity in the brain following the IF and rapamycin treatment was differentially regulated by age. Interestingly, rapamycin inhibited mTOR more potently in young animals than IF. Principal component analysis supported our conclusion that the regulatory effects of IF and rapamycin were agespecific, since we observed different patterns in the expression levels and clustering of young and old animals. Taken together, our results suggest that even a short-term duration of IF and rapamycin have significant effects in the brain at young and old ages, and that these are age and treatment dependent.