Repeated intermittent administration of cocaine to rodents has been shown to result in behavioral sensitization, or enhanced locomotor activity. Because there are similarities between effects of intermittent cocaine use in humans and sensitization in rats, understanding the neural mechanism underlying sensitization may provide insights into mechanisms of psychopathologies in humans.There is abundant evidence that the mesolimbic dopaminergic pathways, originating in the ventral tegmental area (VTA) and terminating in both nucleus accumbens (NAc) and prefrontal cortex (PFC), are critically important for development of sensitization to the motor-stimulating effects of cocaine. Evidence also suggests that changes in glutamate (Glu) transmission in the mesolimbic DA pathways are associated with sensitization to cocaine. In recent collaborative studies, we have shown that cocaine administration transiently decreases the density of nerve terminal glutamate immunolabeling within the NAc shell following withdrawal from continuous or intermittent cocaine administration. Locomotor activity was not assessed in either of these studies.
Oral fluid cocaine and benzoylecgonine concentrations following controlled intravenous cocaine administration
