Briefly yes, but we want to you show what causes it?
Researchers at Indiana University identify a key brain protein involved in cocaine addiction. In addition, their work suggests that an antibiotic might help control this dependency in the future.
Cocaine addiction, or any other type of drug, is a serious problem for affected individuals, and society as a whole. Experts understand drugs as any natural or synthetic substance that causes the imperative need to re-consume them in order to experience the reward they produce, whether it is a sensation associated with pleasure, euphoria or tension relief.
According to a UN report, 180 million people were using illegal drugs, mostly cannabis and to a lesser extent amphetamines. This study also reported that 14 million people worldwide were addicted to cocaine, 13.5 to opiates and 9 to heroin. What are the neuroscientific bases of a craving for this type of substance? And in particular, what causes cocaine addiction, and how can we fight this dependence?
Acute And Chronic Drug Use
Although drugs have a great diversity in their chemical composition, the fact is that scientists have managed to unravel the common neurophysiological mechanisms that occur in the brain. After the first contact with a particular drug, what is known as acute consumption is occurred, at which point we experience the initial pleasant effects and learning about the sensations caused by these substances.
In other words, drugs produce the activation of certain nerve centers in our brain.
In fact, animal models have shown that the administration of active drugs, not only of psychostimulants but also of opiates, nicotine or cannabinoids, is directly related to the increase of dopamine or serotonin. All drugs, whatever they are, activate in one way or another the one known as the dopaminergic mesolimbic pathway.
This route is known by researchers as responsible for creating certain behavioral habits after certain stimuli, such as food, drink, or sex. Dependence on such substances would, therefore, lead to the alteration of a natural neurophysiological pathway, which leads, among other things, to cocaine addiction.
But how do we go from acute consumption to dependence on a particular substance? The existence of addiction, mediated by our need to take a drug, is what is known as chronic consumption. And at this stage, there is a neuroadaptation, that is, there are very important cellular changes, which in the long run are the ones that cause the processes of dependence and the appearance of the famous withdrawal syndrome. It also produces what scientists call behavioral awareness, which acts directly on two areas of the brain, the so-called tegmental-ventral area or ATV and the Nucleus accumbens.
Chemical Messengers And Neuron Communication
In both regions, there is a common molecule responsible for changes at the nervous level, which give rise to awareness: glutamate. This is an amino acid produced by the brain at the time the blood-brain barrier closes and is no longer able to be captured through the blood.
Inside our brain, there is a complex system of communication between different neurons, mediated through chemical messengers. Among these carriers of nerve, synapses is glutamate, but also other neurotransmitters that are important in relation to psychoactive substances, such as those mentioned above dopamine and serotonin, noradrenaline, gamma-aminobutyric acid or endogenous opioids.
Today, we are looking at glutamate because of the important relationship it has with cocaine addiction, and above all, because of research carried out at the University of Indiana, which could in future make it possible to cure dependence on this drug.
In particular, the team led by George Rebec has studied the relationship of a brain protein and an antibiotic as blockers of cocaine addiction. In his work, published in The Journal of Neuroscience, he has managed to identify the GLT1 protein, responsible for removing part of the concentration of glutamate in our brain, as fundamental to the production step of consumption acute to chronic administration of cocaine in rats.
When these rodents consumed a significant amount of cocaine in the initial experiments, the concentration of the GLT1 protein in the Nucleus accumbens decreased. However, the administration of the antibiotic ceftriaxone was able to balance the levels of GLT1 in the brain, reducing the possibility that the rats become addicted to cocaine.
According to Rebec, the craving observed in cocaine-dependent rats was directly related to the concentration of glutamate in their brain. The presence or absence of GLT1 could help eliminate more or less of this chemical messenger, which in turn could increase or reduce the cocaine addiction of these rodents.
The use of this antibiotic (ceftriaxone) is not accidental, as previous studies had indicated that it could be used to control the activity of GLT1 in patients suffering from Huntington’s disease.
These results represent an important step in the study of the neurobiological bases of cocaine addiction and could be important in the future to treat this type of dependence. Although there is still a long time before this work can be applied clinically, because it has only been shown in rodents, the truth is that from now on the GLT1 protein is positioned as an important molecular target in the study of drug addiction.