UC Santa Cruz

Psychological stress has been implicated as a major risk factor in the nation's leading psychiatric disorders. Although much is known about how stress impacts brain regions such as the prefrontal cortex, amygdala, and hippocampus, little is known about its effects on the primary sensory cortex, such as the somatosensory cortex. Interestingly, previous work in the Zuo laboratory found that stress induces synaptic loss and dysregulated excitatory-inhibitory (E-I) balance in mouse primary somatosensory barrel field (S1BF). The collection of cells referred to as neuroglia work together with neurons to support and regulate central nervous system functioning.Amongst these cells, microglia are of particular interest due to their ability to make experience-dependent changes upon neuronal circuits. However, it remains unclear if glial-neuronal interaction may partake in such stress-induced synaptic and E-I balance defects. Due to the known role of microglia participating in synaptic stripping, the current study aimed to determine how microglia mediates stress induced defects in S1BF. To address this question, we examined the density and morphological changes in S1BF microglia in response to restraint stress, and how a known microglial suppressor, minocycline, affects stress-induced changes. The findings revealed that stress impacts S1BF microglia by increasing somatic size and decreasing process complexity, consistent with the morphological changes in microglial phagocytosis in inflammatory states. Minocycline administration in stressed animals blocked stress induced morphological changes in S1BF microglia. Our results suggest that microglia may be involved in stress-related defects, and manipulation of its states, such as prevention of microglial over-activation, may makes the brain more resistant to psychological stressors.