GABA gene expression is differentially expressed across the prefrontal cortex following sensitisation to methamphetamine

Aim: Psychotic disorders, such as schizophrenia, are characterized by prev- alent and persistent executive deficits that are believed to be the result of dysfunctional inhibitory gamma-aminobutyric acid (GABA) processing of the prefrontal cortex (PFC). Methamphetamine (METH) is a commonly used psychostimulant that can induce psychotic and cognitive symptoms that are indistinguishable to schizophrenia, suggesting that METH-induced psychosis may have a similar GABAergic profile of the PFC. As the PFC consists of multiple subregions, the aim of the current study was to investi- gate changes to GABA genetic expression in the prelimbic (PRL) and orbi- tofrontal (OFC) cortices of the PFC following METH sensitization