Traditional approaches to human information processing tend to deal with perception and action planning in isolation, so that an adequate account of the perception-action interface is still missing. On the perceptual side, the dominant cognitive view largely underestimates, and thus fails to account for, the impact of action-related processes on both the processing of perceptual information and on perceptual learning. On the action side, most approaches conceive of action planning as a mere continuation of stimulus processing, thus failing to account (...) for the goal-directedness of even the simplest reaction in an experimental task. We propose a new framework for a more adequate theoretical treatment of perception and action planning, in which perceptual contents and action plans are coded in a common representational medium by feature codes with distal reference. Perceived events (perceptions) and to-be-produced events (actions) are equally represented by integrated, task-tuned networks of feature codes – cognitive structures we call event codes. We give an overview of evidence from a wide variety of empirical domains, such as spatial stimulus-response compatibility, sensorimotor synchronization, and ideomotor action, showing that our main assumptions are well supported by the data. Key Words: action planning; binding; common coding; event coding; feature integration; perception; perception-action interface. (shrink)

In recent years, neurophysiological evidence has accumulated in favor of a common coding between perception and execution of action. We review findings from recent neuroimaging experiments in the action domain with three complementary perspectives: perception of action, covert action triggered by perception, and reproduction of perceived action (imitation). All studies point to the parietal cortex as a key region for body movement representation, both observed and performed.

Circadian rhythm abnormalities in bipolar disorder have led to a search for genetic abnormalities in circadian "clock genes" associated with BD. However, no significant clock gene findings have emerged from genome-wide association studies. At least three factors could account for this discrepancy: complex traits are polygenic, the organization of the clock is more complex than previously recognized, and/or genetic risk for BD may be shared across multiple illnesses. To investigate these issues, we considered the clock gene network at three levels: (...) essential "core" clock genes, upstream circadian clock modulators, and downstream clock controlled genes. Using relaxed thresholds for GWAS statistical significance, we determined the rates of clock vs. control genetic associations with BD, and four additional illnesses that share clinical features and/or genetic risk with BD. Then we compared the results to a set of lithium-responsive genes. Associations with BD-spectrum illnesses and lithium-responsiveness were both enriched among core clock genes but not among upstream clock modulators. Associations with BD-spectrum illnesses and lithium-responsiveness were also enriched among pervasively rhythmic clock-controlled genes but not among genes that were less pervasively rhythmic or non-rhythmic. Our analysis reveals previously unrecognized associations between clock genes and BD-spectrum illnesses, partly reconciling previously discordant results from past GWAS and candidate gene studies. (shrink)