Cocaine reverses the changes in GABAA subunits and in glutamic acid decarboxylase isoenzymes mRNA expression induced by neonatal 6-hydroxydopamine.

Attention-deficit/hyperactivity disorder is related to altered functions in the dopaminergic and GABAergic pathways of cortical and subcortical brain areas The hyperactivity of attention-deficit/hyperactivity disorder is commonly modelled in rats after neonatal lesion with 6-hydroxydopamine (6-OHDA), and amphetamines are effective in reducing hyperactivity in this animal model. Our objectives were to evaluate whether cocaine reverses the motor hyperactivity of 6-OHDA-lesioned rats and to verify cocaine effects in altered mRNA expression of alpha2, alpha4, beta1 and beta2-GABAA subunits and GAD isoenzymes in the prefrontal cortex, hippocampus and striatum of 6-OHDA-lesioned rats. On PND4, 6-OHDA-lesioned or sham rats received 6-OHDA (100 microg intracisternal) or vehicle.