ArticleJournal of neurochemistry2012
Cocaine decreases expression of neurogranin via alterations in thyroid receptor/retinoid X receptor signaling.
Article in Journal of neurochemistry, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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Who cites it
7 citing papers in PubMed, 10 citations in OpenAlex.
- Citrate shuttling in astrocytes is required for processing cocaine-induced neuron-derived excess peroxidated fatty acids.iScience · 2022Article
- Multi-environment gene interactions linked to the interplay between polysubstance dependence and suicidality.Translational psychiatry · 2021Article
- Cocaine-mediated activation of microglia and microglial MeCP2 and BDNF production.Neurobiology of disease · 2018Article
- Rapid, experience-dependent translation of neurogranin enables memory encoding.Proceedings of the National Academy of Sciences of the United States of America · 2018Article
- Cocaine induces nuclear export and degradation of neuronal retinoid X receptor-γ via a TNF-α/JNK- mediated mechanism.Journal of neuroimmune pharmacology : the official journal of the Society on NeuroImmune Pharmacology · 2015Article
- Neurogranin binds α-synuclein in the human superior temporal cortex and interaction is decreased in Parkinson's disease.Brain research · 2014Article
- Cocaine-induced loss of white matter proteins in the adult mouse nucleus accumbens is attenuated by administration of a β-lactam antibiotic during cocaine withdrawal.The American journal of pathology · 2012Article
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Authors and funding
6 authors at 1 institution in 1 country.
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Abstract
Mounting evidence suggests a potential link between cocaine abuse, disruptions in hypothalamic-pituitary-thyroid axis signaling, and neuroplasticity, but molecular mechanisms remain unknown. Neurogranin (Ng) is a gene containing a thyroid hormone-responsive element within its first intron that is involved in synaptic plasticity. Transcriptional activation requires heterodimerization of thyroid hormone receptor (TR) and retinoid X receptor (RXR) bound by their respective ligands, tri-iodothryonine and 9-cis-retinoic acid (9-cis-RA), and subsequent binding of this complex to the thyroid hormone-responsive element of the Ng gene. In this study, the effects of chronic cocaine abuse on Ng expression in euthyroid and hypothyroid mice were assessed. In cocaine-treated mice, decreased Ng expression was observed in the absence of changes in levels of thyroid hormones or other hypothalamic-pituitary-thyroid signaling factors. Therefore, we hypothesized that cocaine decreases Ng expression via alterations in 9-cis-RA availability and TR/RXR signaling. In support of this hypothesis, RXR-γ was significantly decreased in brains of cocaine-treated mice while CYP26A1, the main enzyme responsible for neuronal RA degradation, was significantly increased. Results from this study provide the first evidence for a direct effect of cocaine abuse on TR/RXR signaling, RA metabolism, and transcriptional regulation of Ng, a gene essential for adult neuroplasticity.
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