Crack cocaine inhalation induces schizophrenia-like symptoms and molecular alterations in mice prefrontal cortex.

摘要: Crack cocaine (crack) addiction represents a major social and health burden, especially seeing as users are more prone to engage in criminal violent acts. show higher prevalence of psychiatric comorbidities - particularly antisocial personality disorders when compared powder users. They also develop cognitive deficits related mainly executive functions, including working memory. It is noteworthy that stimulant drugs can induce psychotic states, which appear mimic some symptoms schizophrenia among Social withdraw function are, respectively, negative mediated by reduced dopamine (DA) tone the prefrontal cortex (PFC) patients. That could be explained an increased expression D2R short isoform (D2S) PFC such patients and/or hypofunctioning NMDA receptors this region. Reduced DA has already been described mice exposed crack smoke. Therefore, it possible behavioral alterations presented result from molecular biochemical neuronal akin schizophrenia. Accordingly, we found upon inhalation have shown decreased interaction memory analogous schizophrenia's symptoms, along with D2S/D2L ratio NR1, NR2A NR2B receptor subunits PFC. Herein propose two mechanisms explain elicited consumption mice, bringing first direct evidence use may schizophrenia-like neurochemical, alterations.