What neural mechanisms explain the transition from recreational drug to compulsive abuse and relapse? A study published online this week in Nature Neuroscience sheds some light on this process, by finding that the duration of some cocaine-induced changes in neuronal connectivity is gated by a particular type of glutamate receptor.
Addictive drugs, such as cocaine, leave detectable imprints in the brain. In particular, exposure to cocaine can modify connections between neurons so that they transmit signals to other neurons with greater or lesser strength, a process called drug-induced synaptic plasticity.
Christian Luscher and colleagues studied neuronal activity and behavioral changes that mimic drug relapse in mice. They found that the duration of cocaine-induced synaptic plasticity in a mid-brain area called the VTA ― previously linked to reward processing ― is regulated by the glutamate receptor mGluR1. Manipulating the activity of mGluR1 in the VTA of mice affected early and enduring forms of synaptic plasticity in a region known to be important for cocaine-seeking behavior after withdrawal. Blocking changes in the VTA reduced cocaine craving behavior in mice.