Aberrant beta-gamma (20-80 Hz) frequency oscillations and impaired cognitive function are reported in schizophrenia patients. Impaired oscillations could be caused by changes in interneuron populations and increased neuroinflammation, as reported in post-mortem studies. Cognitive and network dysfunction can be modelled in rodents using the N-methyl-D-aspartate acid (NMDA) receptor antagonist phencyclidine (PCP). In vivo studies suggest sigma-1 receptor (σ1R) activation may reverse these deficits. We investigated the effect of acute PCP application and σ1R activation on glia and interneurons in a rat brain slice model of NMDA receptor hypofunction. Rat anterior cingulate cortex (ACC) slices were incubated in artificial cerebral spinal fluid for 4 hours in an interface chamber, with kainate or kainate and PCP, to evoke network oscillations. To activate σ1Rs, slices were pre-incubated with the σ1R agonist PRE-084 for 30 minutes before kainate and PCP incubation. Slices were fixed, re-sectioned and immunostained for microglia (Iba1) and reactive-astrocytes (GFAP), parvalbumin-positive (PV+) and somatostatin-positive (SST+) interneurons, and perineuronal nets. Preliminary data suggests that exposing ACC slices to kainate and PCP increases Iba1 expression across the ACC, and GFAP expression in the superficial layers only, compared to kainate alone. Prior activation of σ1Rs reduced these neuroinflammatory changes. Future work will assess the effects of acute PCP application on PV+ and SST+ interneurons and perineuronal net expression.Our data suggests that PCP increases neuroinflammation in vitro, whilst the σ1R agonist PRE-084 reduces PCP’s neuroinflammatory effect. Further investigation is required to better understand the interplay between NMDA receptors and σ1Rs.