ArticleJournal of molecular neuroscience : MN2021
Potentiated Response of ERK/MAPK Signaling is Associated with Prolonged Withdrawal from Cocaine Behavioral Sensitization.
Article in Journal of molecular neuroscience : MN, 2021. 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, 9 citations in OpenAlex.
- Transcriptional characterization of cocaine withdrawal versus extinction within nucleus accumbens in male rats.Nature communications · 2025Article
- Activation of RMTg projections to the VTA reverse cocaine-induced molecular adaptation in the reward system.Translational psychiatry · 2024Article
- Activation of nucleus accumbens projections to the ventral tegmental area alters molecular signaling and neurotransmission in the reward system.Frontiers in molecular neuroscience · 2024Article
- Synaptic Structure and Transcriptomic Profiling of Reward and Sensory Brain Areas in Male Mice of Fentanyl Addiction.Substance abuse and rehabilitation · 2024Article
- Identification of key genes and therapeutic drugs for cocaine addiction using integrated bioinformatics analysis.Frontiers in neuroscience · 2023Article
- A novel microRNA, novel-m009C, regulates methamphetamine rewarding effects.Molecular psychiatry · 2022Article
- Peri-adolescent exposure to (meth)amphetamine in animal models.International review of neurobiology · 2022Review
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Among the neuroadaptations underlying the expression of cocaine-induced behaviors are modifications in glutamate-mediated signaling and synaptic plasticity via activation of mitogen-activated protein kinases (MAPKs) within the nucleus accumbens (NAc). We hypothesized that exposure to cocaine leads to alterations in MAPK signaling in NAc neurons, which facilitates changes in the glutamatergic system and thus behavioral changes. We have previously shown that following withdrawal from cocaine-induced behavioral sensitization (BS), an increase in glutamate receptor expression and elevated MAPK signaling was evident. Here, we set out to determine the time course and behavioral consequences of inhibition of extracellular signal-regulated kinase (ERK) or NMDA receptors following withdrawal from BS. We found that inhibiting ERK by microinjection of U0126 into the NAc at 1 or 6 days following withdrawal from BS did not affect the expression of BS when challenged with cocaine at 14 days. However, inhibition of ERK 1 day before the cocaine challenge abolished the expression of BS. We also inhibited NR2B-containing NMDA receptors in the NAc by microinjection of ifenprodil into the NAc following withdrawal from BS, which had no effect on the expression of BS. However, microinjection of ifenprodil to the NAc 1 day before challenge attenuated the expression of BS similar to ERK inhibition. These results suggest that following a prolonged period of withdrawal, NR2B-containing NMDA receptors and ERK activity play a critical role in the expression of cocaine behavioral sensitization.
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