Cocaine addiction is a chronically relapsing disorder characterized by compulsive drug seeking, loss of control in limiting intake, and emergence of negative emotional states. Although the neural and molecular mechanisms underlying cocaine addiction are not yet completely understood, there is now much evidence that cocaine addiction and natural reward-related memory may share similar neural circuits and molecular mechanisms. Recent studies demonstrate that cocaine elicits or modifies synaptic plasticity of glutamatergic transmission in the mesocorticolimbic dopamine system, which is the central component of the brain's reward processing. Despite the promising research on the brain dopaminergic pathways, recent research also highlights the involvement of serotonin (5-hydroxytryptamine, 5-HT) neurotransmission and particularly 5-HT1B receptors in the behavioral effects of cocaine. Here, we summarize experimental characterization of the role of 5-HT1B receptors in mediating the neurobiological effects of cocaine and discuss how cocaine impairs the induction of 5-HT1B receptor-induced long-term depression in the nucleus accumbens.
|Title of host publication||The Neuroscience of Cocaine|
|Subtitle of host publication||Mechanisms and Treatment|
|Number of pages||9|
|Publication status||Published - 2017 May 16|
All Science Journal Classification (ASJC) codes