Schizophrenia 3.0: Salience dysregulation.

This post is prompted by an article published in this February’s Trends in Neurosciences under the title “Dopaminergic Basis of Salience Dysregulation inPsychosis” by Winton-Brown, Fusar-Poli, Ungless, & Howes (2014) and an earlier paper in the Schizophrenia bulletin entitled “The dopamine hypothesisof schizophrenia: version II – the final common pathway” (Howes & Kapur, 2009). As stated in the first title, Winton-Brown et al.’s work reviews extensively what they consider to be evidence of the dopaminergic basis of salience dysregulation and more briefly consider the argument for salience dysregulation as a causal force in the etiology of schizophrenia. Their work was building on an argument made by Howes & Kapur who suggested that a panoply of genetic and environmental risk factors all converge on increased striatal dopaminergic function, producing aberrant salience and thereby psychosis.

Pain, Rejection, and the Optimal Calibration Hypothesis

A paper by Chester et al. was published in the July 2012 issue of Frontiers in Evolutionary Neuroscience under the title:

"The optimal calibration hypothesis: how life history modulates the brain's social pain network."

This work presents a novel way of looking at adaptations in the sensitivity of the "social pain network" throughout the human lifespan.

The authors start out by reviewing the evidence of overlap between the brain networks involved in pain perception, and the neural substrates of the affective response to social threats, such as rejection. Reviewed are the two neocortical structures which appear to be involved in both. The anterior cingulate cortex (ACC) is thought to support the affective features of pain, but activation in this region is also observed in response to perceived social rejection. Similarly, the anterior insula appears to be involved in affective responses to both physical pain and social rejection.