ncreased risk of neuropsychiatric disorders. The underlying molecular and cellular mechanisms of the neuro-toxic effects of long-term use of SCs have not been well investigated in the literature. Herein, we evaluated the invivo effects of chronic administration of AB-FUBINACA on the hippocampus in mice. Our results revealed thatthe administration of AB-FUBINACA induced a significant impairment in recognition memory associated withhistopathological changes in the hippocampus. These findings were found to be correlated with increased level ofoxidative stress, neuroinflammation, and apoptosis markers, and reduced expression of brain-derived neuro-trophic factor (BDNF), which plays an essential role in modulating synaptic plasticity integral for promotinglearning and memory in the hippocampus. Additionally, we showed that AB-FUBINACA significantly decreasedthe expression of NR1, an important functional subunit of glutamate/NMDA receptors and closely implicated inthe development of toxic ps