Abstract
Stress is an important environmental factor influencing human behaviour and causing several mental disorders. Alterations in the structure of polysialic acid (polySia/PSA) due to genetic alterations in ST8SIA2, which encodes a polySia-synthesizing enzyme, are related to certain mental disorders. However, whether stress as an environmental factor leads to changes in polySia structure is unknown. Here we studied the effects of acute stress on polySia expression and found reductions in both the quantity and quality of polySia in the olfactory bulb and prefrontal cortex, even with short-term exposure to acute stress. The use of inhibitors for sialidase, microglia and astrocytes revealed that these declines were due to a transient action of sialidase from microglia and astrocytes in the olfactory bulb and prefrontal cortex, respectively. These data suggest that sialidase dynamically regulates polySia expression in a brain region-specific manner.
Highlights
Mental disorders including schizophrenia (SCZ), bipolar disorder (BD), autism spectrum disorder (ASD), major depression disorder, attention deficit hyperactivity disorder, anxiety disorders and drug and alcohol abuse are becoming global problems[1]
Altered polySia expression was observed in the olfactory bulb (OB), prefrontal cortex (PFC) and suprachiasmatic nucleus (SCN) after exposure to acute stress significantly
We explored the possible involvement of sialidase and/or microglia in the decreased polySia in the OB and PFC induced by acute stress, based on the observation that polySia is degraded by sialidase in exosomes secreted from the microglia[39]
Summary
Mental disorders including schizophrenia (SCZ), bipolar disorder (BD), autism spectrum disorder (ASD), major depression disorder, attention deficit hyperactivity disorder, anxiety disorders and drug and alcohol abuse are becoming global problems[1]. Www.nature.com/scientificreports reduced polySia-NCAM expression was detected in layers IV and V of the dorsolateral PFC in SCZ patients[16] No such difference was observed in the AMG17, implicating region-specific polySia impairment (reduction of polySia-immunostained cells) as a feature of SCZ. PolySia-NCAM was significantly decreased in the lateral amygdala and in the basolateral and basomedial amygdala of patients with depression These data indicate that change in polySia expression in disorder-specific regions of the brain may be a feature of mental disorders, the mechanism is unknown. The rs2168351 SNP present in BD patients was associated with the upregulated expression of polySia[26] All these data are consistent with the reported reduction of the level of polySia-NCAM in the brains of SCZ patients[15,16,17]. These mice display impaired working memory, deficits in prepulse inhibition, anhedonic behaviour and increased sensitivity to amphetamine-induced hyperlocomotion[27]
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