ArticleFrontiers in psychiatry2013
Dopaminergic dysregulation in prefrontal cortex of rhesus monkeys following cocaine self-administration.
Article in Frontiers in psychiatry, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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Who cites it
10 citing papers in PubMed, 16 citations in OpenAlex.
- Intersectin1/cdc42 signaling regulates methamphetamine-induced neuronal remodeling in the hippocampus.Cellular and molecular life sciences : CMLS · 2025Article
- Article
- Changes in synaptic markers after administration of ketamine or psychedelics: a systematic scoping review.Frontiers in psychiatry · 2023Article
- Interplay between Cocaine, Drug Removal, and Methylphenidate Reversal on Phospholipid Alterations inACS chemical neuroscience · 2020Article
- Neuronal scaffolding protein spinophilin is integral for cocaine-induced behavioral sensitization and ERK1/2 activation.Molecular brain · 2019Article
- Contributions of prolonged contingent and non-contingent cocaine exposure to escalation of cocaine intake and glutamatergic gene expression.Psychopharmacology · 2018Article
- Incubation of cocaine-craving relates to glutamate over-flow within ventromedial prefrontal cortex.Neuropharmacology · 2016Article
- Chronic cocaine disrupts mesocortical learning mechanisms.Brain research · 2015Review
- Synaptic Cytoskeletal Plasticity in the Prefrontal Cortex Following Psychostimulant Exposure.Traffic (Copenhagen, Denmark) · 2015Review
- Clinical potential of methylphenidate in the treatment of cocaine addiction: a review of the current evidence.Substance abuse and rehabilitation · 2015Review
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Authors and funding
3 authors at 2 institutions in 1 country.
Funding
Abstract
Chronic cocaine administration regulates the expression of several proteins related to dopaminergic signaling and synaptic function in the mesocorticolimbic pathway, including the prefrontal cortex. Functional abnormalities in the prefrontal cortex are hypothesized to be due in part to the expression of proteins involved in dopamine signaling and plasticity. Adult male rhesus monkeys self-administered cocaine (i.v.) under limited (n = 4) and extended access conditions (n = 6). The abundance of surrogate markers of dopamine signaling and plasticity in the dorsolateral prefrontal cortex (DLPFC), orbitofrontal cortex (OFC), and anterior cingulate cortex (ACC) were examined: glycosylated and non-glycosylated forms of the dopamine transporter (efficiency of dopamine transport), tyrosine hydroxylase (TH; marker of dopamine synthesis) and phosphorylated TH at Serine 30 and 40 (markers of enzyme activity), extracellular signal-regulated kinase 1 and 2 (ERK1 and ERK 2), and phosphorylated ERK1 and ERK2 (phosphorylates TH Serine 31; markers of synaptic plasticity), and markers of synaptic integrity, spinophilin and post-synaptic density protein 95 (roles in dopamine signaling and response to cocaine). Extended cocaine access increased non-glycosylated and glycosylated DAT in DLPFC and OFC. While no differences in TH expression were observed between groups for any of the regions, extended access induced significant elevations in pTH(Ser31) in all regions. In addition, a slight but significant reduction in phosphorylated pTH(Ser40) was found in the DLPFC. Phosphorylated ERK2 was increased in all regions; however, pERK1 was decreased in ACC and OFC but increased in DLPFC. PSD-95 was increased in the OFC but not in DLPFC or ACC. Furthermore, extended cocaine self-administration elicited significant increases in spinophilin protein expression in all regions. Results from the study provide insight into the biochemical alterations occurring in primate prefrontal cortex.
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