Plasticity in astrocyte subpopulations regulates heroin relapse. Sci Adv 2022 Aug 12;8(32):eabo7044
Date
08/11/2022Pubmed ID
35947652Pubmed Central ID
PMC9365285DOI
10.1126/sciadv.abo7044Scopus ID
2-s2.0-85135951017 (requires institutional sign-in at Scopus site) 8 CitationsAbstract
Opioid use disorder (OUD) produces detrimental personal and societal consequences. Astrocytes are a major cell group in the brain that receives little attention in mediating OUD. We determined how astrocytes and the astroglial glutamate transporter, GLT-1, in the nucleus accumbens core adapt and contribute to heroin seeking in rats. Seeking heroin, but not sucrose, produced two transient forms of plasticity in different astroglial subpopulations. Increased morphological proximity to synapses occurred in one subpopulation and increased extrasynaptic GLT-1 expression in another. Augmented synapse proximity by astroglia occurred selectively at D2-dopamine receptor-expressing dendrites, while changes in GLT-1 were not neuron subtype specific. mRNA-targeted antisense inhibition of either morphological or GLT-1 plasticity promoted cue-induced heroin seeking. Thus, we show that heroin cues induce two distinct forms of transient plasticity in separate astroglial subpopulations that dampen heroin relapse.
