Cocaine damages or even kills the very brain cells that trigger the “high” felt by users of the drug, scientists said today. This first direct evidence of cocaine-induced damage to key cells in the brain’s “pleasure centre” could help explain many aspects of cocaine addiction. It might also aid the development of new anti-addiction drugs and increase understanding of other disorders involving the same brain cells, such as depression.

The American study was performed at the University of Michigan Health System and the VA Ann Arbor Healthcare System. Leader researcher Karley Little said: “This is the clearest evidence to date that the specific neurons cocaine interacts with don’t like it and are disturbed by the drug’s effects”. The study involved post-mortem brain tissue samples from cocaine abusers and control subjects. The samples were from 36 known cocaine abusers and 35 non-drug users of similar age, sex, race and causes of death. The team looked at the cells of the brain that release a pleasure-signalling chemical called dopamine. They analysed overall dopamine levels as well as the amount of a protein called VMAT2 which interacts with dopamine.

The researchers found levels of dopamine and the VMAT2 protein were significantly lower in cocaine users than control subjects. They also found levels tended to be lowest in cocaine users with depression. The research gives the strongest indication yet that dopamine neurons are harmed by cocaine use. Dopamine triggers the actions required to repeat previous pleasures and helps us work, feel emotions and reproduce. It is also involved in a drug users “high’ as cocaine causes levels to build up and so the pleasure signals are repeated over and over. Long-term effects of cocaine on the dopamine system could contribute to addicts’ cravings and account for their decreased motivation, stunted emotions and uncomfortable withdrawal symptoms. Professor Little said the study highlighted the fragility of dopamine neurons and ‘the vicious cycle that cocaine use can create’.

Source: Author Professor K. Little et al. Published in the American Journal of Psychiatry, Jan 2003