Chronic psychosocial stressors are associated with alterations in salience processing and corticostriatal connectivity

Abstract

Psychosocial stressors including childhood adversity, migration, and living in an urban environment, have been associated with several psychiatric disorders, including psychotic disorders. The neural and psychological mechanisms mediating this relationship remain unclear. In parallel, alterations in corticostriatal connectivity and abnormalities in the processing of salience, are seen in psychotic disorders. Aberrant functioning of these mechanisms secondary to chronic stress exposure, could help explain how common environmental exposures are associated with a diverse range of symptoms. In the current study, we recruited two groups of adults, one with a high degree of exposure to chronic psychosocial stressors (the exposed group, n = 20), and one with minimal exposure (the unexposed group, n = 22). All participants underwent a resting state MRI scan, completed the Aberrant Salience Inventory, and performed a behavioural task - the Salience Attribution Test (SAT). The exposed group showed reduced explicit adaptive salience scores (cohen's d = 0.69, p = 0.03) and increased aberrant salience inventory scores (d = 0.65, p = 0.04). The exposed group also showed increased corticostriatal connectivity between the ventral striatum and brain regions previously implicated in salience processing. Corticostriatal connectivity in these regions negatively correlated with SAT explicit adaptive salience (r = -0.48, p = 0.001), and positively correlated with aberrant salience inventory scores (r = 0.42, p = 0.006). Furthermore, in a mediation analysis there was tentative evidence that differences in striato-cortical connectivity mediated the group differences in salience scores.

Keywords: Corticostriatal; Functional connectivity; Psychosis; Schizophrenia; Stress; Striatum.

Fig. 1

Proposed pathway in which exposure to chronic psychosocial stressors leads to alterations in corticostriatal connectivity and subsequent alterations in salience processing.

Fig. 2

Salience attribution test, and aberrant salience inventory scores in exposed and unexposed individuals. Error bars (±1SE) ASI – Aberrant Salience Inventory.

Fig. 3

Areas of increased corticostriatal connectivity in the exposed compared to unexposed group. Red clusters relate to the seed in the inferior ventral striatum, and yellow represents the dorsocaudal putamen seed. (For interpretation of the references to colour in this figure legend, the reader is referred to the web version of this article.)

Fig. 4

Relationship between salience scores and inferior ventral striatum connectivity. (A) Inferior ventral striatum connectivity correlates with explicit adaptive SAT scores in both the whole sample (r_p = −0.48, p = 0.001) and exposed individuals (rp = −0.52, p = 0.001). (B) Inferior ventral striatum connectivity correlates with explicit aberrant SAT scores in exposed individuals (r_p = 0.523, p = 0.016). (C) Inferior ventral striatum connectivity correlates with Aberrant Salience Inventory Scores in the whole sample (r_p = 0.42, p = 0.0056). (D) Mediation analysis – the relationship between risk factor exposure (i.e. whether participants in the exposed or unexposed group) and reduced SAT adaptive salience appears to be mediated by altered inferior ventral striatum connectivity.