Search

Psychophysical studies have frequently found that adults with normal hearing exhibit systematic errors (biases) in their auditory localisation judgments. Here we tested (i) whether systematic localisation errors could reflect reliance on prior knowledge, as has been proposed for other systematic perceptual biases, and (ii) whether auditory localisation biases can be reduced following training with accurate visual feedback. Twenty-four normal hearing participants were asked to localise the position of a noise burst along the azimuth before, during, and after training with visual feedback. Consistent with reliance on prior knowledge to reduce sensory uncertainty, we found that auditory localisation biases increased when auditory localisation uncertainty increased. Specifically, participants mis-localised auditory stimuli as being more eccentric than they were, and did so more when auditory uncertainty was greater. However, biases also increased with eccentricity, despite no corresponding increase in uncertainty, which is not readily explained by use of a simple prior favouring peripheral locations. Localisation biases decreased (improved) following training with visual feedback, but the reliability of the visual feedback stimulus did not change the effects of training. We suggest that further research is needed to identify alternative mechanisms, besides use of prior knowledge, that could account for increased perceptual biases under sensory uncertainty.

Sickness behaviors and metabolic responses to invading pathogens are common to nearly all types of infection. These responses evolved to provide short-term benefit to the host to ward off infection, but impact on quality of life and when prolonged lead to neurodegeneration, depression and cachexia. Among the major infectious agents, viruses most frequently enter the brain, resulting in profound neuroinflammation. We sought to define the unique features of the inflammatory response in the brain to these infections. We demonstrate that the molecular pathway defining the central response to dsRNA is distinct from that found in the periphery. The behavioral and physical response to the dsRNA mimetic poly I:C is dependent on signaling via MyD88 when it is delivered centrally, whereas this response is mediated via the TRIF pathway when delivered peripherally. We also define the likely cellular candidates for this MyD88-dependent step. These findings suggest that symptom management is possible without ameliorating protective antiviral immune responses.