Abstract
To study cocaine's toxic effects in vitro, we have used primary mesencephalic and striatal cultures from rat embryonic brain. Treatment with cocaine causes a dramatic increase in DNA fragmentation in both primary cultures. The toxicity induced by cocaine was paralleled with a concomitant decrease in the microtubule associated protein 2 (MAP2) and/or neuronal nucleus protein (NeuN) staining. We also observed in both cultures that the cell death caused by cocaine was induced by an apoptotic mechanism, confirmed by TUNEL assay. Therefore, the present paper shows that cocaine causes apoptotic cell death and inhibition of the neurite prolongation in striatal and mesencephalic cell culture. These data suggest that if similar neuronal damage could be produced in the developing human brain, it could account for the qualitative or quantitative defects in neuronal pathways that cause a major handicap in brain function following prenatal exposure to cocaine.
Highlights
Drug abuse can have physiological, psychological, and social consequences [1]
Our results demonstrated that 90% of the neurons present in the culture were GABAergic neurons
We tested for the presence of dopaminergic neurons by antibody staining to identify tyrosine hydroxylase (TH), the rate-limiting enzyme in the dopamine synthetic pathway
Summary
Drug abuse can have physiological, psychological, and social consequences [1]. Cocaine is a drug of abuse with reinforcing proprieties that can lead to the development of dependence. By binding to plasma membrane transporters, cocaine pre vents the uptake of extracellular monoamines, enhancing their extracellular levels, including norepinephrine and dopamine [2,3,4]. The vast majority of developmental studies investigating cocaine effects have focused on the dopaminergic system, presumably as a result of dopamine’s well-studied effects on reward and addiction [5]. The primary mesencephalic culture contains dopaminergic neurons from both the substantia nigra and ventral tegmental area, which expresses tyrosine hydroxylase (TH) [6, 7], the rate-limiting enzyme in dopamine synthesis. Given the reinforcing properties of cocaine such mesencephalic structures have been extensively investigated
Sign-in/Register to view highlights & summary Sign-in/Register to access full text options 
Free) 
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a call
