Researchers at the Salk Institute for Biological Studies have discovered that a single of injection of recreational drugs, such as cocaine or methamphetamine (crystal meth), in mice caused their brains to stop the action of dopaminergic neurons (neurons that create the sensation of pleasure). The changes in the brain lasted for at least a week in most cases.
Dopamine is a neurotransmitter found in the brain known for it’s ability to generate pleasure. It’s function can be described as “reward based learning” – when you do something positive, your brain rewards you with dopamine. However, doing something positive is solely based on which compounds bind to which receptors. For instance, drinking alcohol would not be positive yet it initiates dopamine release. Other activities that release dopamine; eating nice tasting food, sex, drugs and gambling.
The research was published in the journal Neuron and suggests that the brains reaction to drugs is a defensive one to prevent addiction. The hope is that the response can be replicated in order to help people who are currently addicted to highly addictive substances and possibly other addictions (such as gambling). The research is important because drug use and drug-related fatalities are at an all time high.
Previous research showed that giving mice drugs such as methamphetamine and cocaine increased the number of excitatory connections to dopaminergic neurons. The research then focused on those excitatory neurons and ways to prevent synaptic formation. This is the first study, providing extremely useful information, to focus solely on the dopaminergic neurons.
The research found that the neurons became unable to control their action and as a result released vast amounts of a dopamine inhibitor – GABA (Gamma AminoButyric Acid). It is the release of GABA that is the backbone of the defense mechanism; it causes a behavioural change in a protein known as phosphatase known for controlling potassium channels (as well as a receptor for GABA) in these particular neurons. It affected the electrical activity of the neurons causing a weakening of the signals.
This study had a large drawback though, the inhibition of the neurons were only examined at two time intervals, 24 hours after drug administration and 7 days later. The research needs to be repeated on a larger scale using more time intervals. The researchers will also be investigating why chronic drug use causes addiction.