ArticleFrontiers in pharmacology2025
ER stress in D1-MSNs mediates cocaine-induced behavioral plasticity
Article in Frontiers in pharmacology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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23 authors.
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Abstract
Background: Cocaine-induced endoplasmic reticulum (ER) stress has been increasingly recognized, but its neuronal specificity and functional significance remain unclear. Because the ER is also a major site for lipid and sphingolipid biosynthesis, cocaine-triggered ER stress may influence metabolic pathways linked to cellular stress signaling. Here, we sought to define the cell-type specificity and downstream consequences of cocaine-induced ER stress in the nucleus accumbens (NAc). Methods: We combined cocaine administration with ultrastructural analysis of ER morphology, immunohistochemical and molecular profiling of ER stress pathways, and assays of sphingolipid biosynthesis in the NAc. We also evaluated the effects of pharmacological inhibition of ER stress and sphingolipid synthesis, and performed D1-MSN-specific knockdown of Results: Cocaine selectively activated ER stress in dopamine receptor 1 (D1)-expressing medium spiny neurons (MSNs), marked by induction of activating transcription factor 4 (ATF4). Cocaine also upregulated serine palmitoyltransferase long-chain base subunit 1 (SPTLC1), and promoter analysis with functional validation identified Discussion: These findings identify a D1-MSN ER stress response that promotes cocaine-induced neuroadaptations via the ATF4-SPTLC1 signaling axis and suggest a potential therapeutic target for cocaine addiction.
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