One year after a fluid-percussion traumatic brain injury, male rats showed persistent sensorimotor, learning, memory, and affective deficits; reduced serotonin 2A receptor binding; and microglial changes in the medial prefrontal cortex, including decreased process branching and enlarged soma size. A single dose of psilocybin (1 mg/kg) improved sensorimotor function, restored serotonin 2A receptor binding, and reduced microglial cell counts. These results suggest psilocybin has therapeutic potential for chronic traumatic brain injury and support further investigation of psychedelic treatments.
Sub-chronic exposure to the NMDA receptor antagonist phencyclidine (PCP) in rats produced localized reductions in grey matter density in the hippocampus, anterior cingulate cortex, ventral striatum, and amygdala, along with reduced cortical thickness in the insular cortex. PCP-treated rats also showed impaired sustained visual attention on a 5-choice serial reaction time task, especially under higher attentional load, but no significant effect on attentional filtering in an acoustic startle paradigm. These findings indicate that NMDA receptor antagonism can cause brain structural abnormalities in regions implicated in schizophrenia and dissociable attentional deficits.