title: Activin A is increased in the nucleus accumbens following a cocaine binge.
abstract: Drug addiction is a long-lasting disease characterized by compulsive drug intake mediated in part by neuronal and biological adaptations in key brain areas, such as the nucleus accumbens (NAc). While we previously demonstrated involvement of the activin 2a receptor in drug taking, the role of its ligand, activin A, in cocaine relapse is unknown. Activin A levels in the NAc were assessed via ELISA and immunohistochemistry (in neurons, astrocytes, and microglia) following a cocaine binge paradigm. Cocaine exposure significantly increased the levels of activin A in the NAc of animals that had self-administered cocaine prior to the 14-day withdrawal compared with levels in saline controls. This was accompanied by an increase in the proportion of IBA1+microglia in the NAc that were immunopositive for activin A. In contrast, the proportions of NeuN+neurons and GFAP+astrocytes that were immunopositive for activin A remained unaltered. In conclusion, these data suggest that increased secretion of activin A, particularly from microglia, in the NAc represents a novel potential target for the treatment of cocaine relapse.
authors.affiliation: Department of Pharmacology and Toxicology, Research Institute on Addictions, Program in Neuroscience, State University of New York at Buffalo, Buffalo, NY, USA.|Department of Psychology, State University of New York at Buffalo, Buffalo, NY, USA.
authors.forename: Zi-Jun
authors.initials: ZJ
authors.lastname: Wang
authors.affiliation: Department of Pharmacology and Toxicology, Research Institute on Addictions, Program in Neuroscience, State University of New York at Buffalo, Buffalo, NY, USA.|Department of Psychology, State University of New York at Buffalo, Buffalo, NY, USA.
authors.forename: Jennifer A
authors.initials: JA
authors.lastname: Martin
authors.affiliation: Department of Pharmacology and Toxicology, Research Institute on Addictions, Program in Neuroscience, State University of New York at Buffalo, Buffalo, NY, USA.|Department of Psychology, State University of New York at Buffalo, Buffalo, NY, USA.|Department of Psychology, California State University Bakersfield, Bakersfield, CA, USA.
authors.forename: Amy M
authors.initials: AM
authors.lastname: Gancarz
authors.affiliation: Department of Pharmacology and Toxicology, Research Institute on Addictions, Program in Neuroscience, State University of New York at Buffalo, Buffalo, NY, USA.
authors.forename: Danielle N
authors.initials: DN
authors.lastname: Adank
authors.affiliation: Department of Pharmacology and Toxicology, Research Institute on Addictions, Program in Neuroscience, State University of New York at Buffalo, Buffalo, NY, USA.
authors.forename: Fraser J
authors.initials: FJ
authors.lastname: Sim
authors.affiliation: Department of Pharmacology and Toxicology, Research Institute on Addictions, Program in Neuroscience, State University of New York at Buffalo, Buffalo, NY, USA.|Department of Psychology, State University of New York at Buffalo, Buffalo, NY, USA.
authors.forename: David M
authors.initials: DM
authors.lastname: Dietz
mesh_terms: D028341:Activins / Q000378:metabolism*; D000818:Animals; D001253:Astrocytes / Q000378:metabolism; D015415:Biomarkers; D019970:Cocaine-Related Disorders / Q000378:metabolism*; D004797:Enzyme-Linked Immunosorbent Assay; D005455:Fluorescent Antibody Technique; D008297:Male; D017628:Microglia / Q000378:metabolism; D009474:Neurons / Q000378:metabolism; D009714:Nucleus Accumbens / Q000378:metabolism*; D051381:Rats
chemical_list: D015415:Biomarkers; C422405:activin A; D028341:Activins