Mechanisms of Disulfiram-induced Cocaine Abstinence: Antabuse and Cocaine Relapse

Abstract

Chemokines are chemoattractant proteins, secreted by a great many cell types, that function particularly to direct the migration of cells of the immune system. Chemokine receptors are G protein–coupled and have been implicated in a number of important disease states, including cancer, inflammatory disorders, and AIDS/HIV. Neuroinflammatory aspects of chronic pain are also chemokine-dependent, and given the many clinical difficulties that often arise in the treatment of chronic pain, novel therapeutics are urgently needed. Chemokine receptors would thus appear to be in ideal target for drug development, and indeed, animal models of neuropathic pain have allowed pharmacologists to identify a number of cell types and signaling pathways that are essential to the initiation and maintenance of chronic pain. In this regard, the chemokine receptor CCR2, activated by a chemokine known as monocyte chemoattractant protein 1, has been attributed to a number of specific regulatory and neural activation processes that contribute to chronic pain. But in order to target chemokine receptors such as CCR2 and thereby develop effective treatment, investigators must identify, from among many cell types and peripheral and central neural pathways, the relevant sites of CCR2 function.