Social defeat stress-induced sensitization and escalated cocaine self-administration: the role of ERK signaling in the rat ventral tegmental area

Yap, Jasmine J.; Chartoff, Elena H.; Holly, Elizabeth N.; Potter, David N.; Carlezon, William A.; Miczek, Klaus A.

doi:10.1007/s00213-014-3796-7

Cited by 55Neurotransmitter Receptor Influence on BehaviorStress Responses and CortisolNeuroscience and Neuropharmacology Research

Social defeat stress-induced sensitization and escalated cocaine self-administration: the role of ERK signaling in the rat ventral tegmental area

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Yap, Jasmine J., Chartoff, Elena H., Holly, Elizabeth N., Potter, David N., Carlezon, William A., Miczek, Klaus A.·2015·Psychopharmacology

DOI 10.1007/s00213-014-3796-7PMC PMC4397167

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Abstract

Rationale Intermittent social defeat stress can induce neuroadaptations that promote compulsive drug taking. Within the mesocorticolimbic circuit, repeated cocaine administration activates extracellular signal-regulated kinase (ERK).Objective The present experiments examine whether changes in ERK phosphorylation are necessary for the behavioral and neural adaptations that occur as a consequence of intermittent defeat stress.Materials and methods Rats were exposed to four brief intermittent defeats over the course of 10 days. Ten days after the last defeat, rats were challenged with cocaine (10 mg/kg, i.p.) or saline, and ERK activity was examined in mesocorticolimbic regions. To determine the role of ERK in defeat stress-induced behavioral sensitization, we bilaterally microinjected the MAPK/ERK kinase inhibitor U0126 (1 μg/side) or vehicle (20 % DMSO) into the ventral tegmental area (VTA) prior to each of four defeats. Ten days following the last defeat, locomotor activity was assessed for the expression of behavioral cross-sensitization to cocaine (10 mg/kg, i.p.). Thereafter, rats self-administered cocaine under fixed and progressive ratio schedules of reinforcement, including a 24-h continuous access "binge" (0.3 mg/kg/infusion).Results We found that repeated defeat stress increased ERK phosphorylation in the VTA. Inhibition of VTA ERK prior to each social defeat attenuated the development of stress-induced sensitization and prevented stress-induced enhancement of cocaine self-administration during a continuous access binge.Conclusions These results suggest that enhanced activation of ERK in the VTA due to brief defeats is critical in the induction of sensitization and escalated cocaine taking.

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Stress, similar to drugs of abuse, may induce neurological changes that enhance dopaminergic activity and the attribution of incentive value to rewards and their cues.
“Stress, similar to drugs of abuse, may also induce neurological changes that enhance dopaminergic activity and the attribution of incentive value to rewards and their cues (Berridge, 2012; T. E. Robinson, Angus, & Becker, 1985; Yap et al., 2015).”
From Cued for Risk: Evidence for an Incentive Sensitization Framework to Explain the Interplay between Stress and Anxiety, Substance Abuse, and Reward Uncertainty in Disordered Gambling Behavior (2019) · cites this paper as Yap et al., 2015

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Prevention of social stress-escalated cocaine self-administration by CRF-R1 antagonist in the rat VTA
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Episodic Social Stress-Escalated Cocaine Self-Administration: Role of Phasic and Tonic Corticotropin Releasing Factor in the Anterior and Posterior Ventral Tegmental Area
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NMDA receptors in the rat VTA: a critical site for social stress to intensify cocaine taking
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Authors: Yap, J. J., Chartoff, E. H., Holly, E. N., Potter, D. N., Carlezon, W. A., & Miczek, K. A.
Affiliations: Tufts University (US)
Harvard University (US)
Corresponding author: Yap, Jasmine J.
ORCID: Chartoff, Elena H.
Holly, Elizabeth N.
Carlezon, William A.
Miczek, Klaus A.
Venue: Psychopharmacology
Publisher: Springer Science and Business Media LLC
Published: 2014-11-06
Volume: 232
Issue: 9
Pages: 1555-1569
ISSN: 0033-3158 (ISSN-L)
1432-2072
DOI: 10.1007/s00213-014-3796-7
PMC: PMC4397167
OpenAlex: W1982917824
Cited by: 55
References: 80
Citations by year: 2026: 1 · 2025: 4 · 2024: 1 · 2023: 1 · 2022: 2 · 2021: 8 · 2020: 5 · 2019: 3 · 2018: 13 · 2017: 4 · 2016: 10 · 2015: 3
FWCI: 2.59
Type: journal article
Language: en
Open access: green
www.ncbi.nlm.nih.gov
Licence: www.springer.com/tdm (tdm)
Locations: Psychopharmacology (publishedVersion)
PubMed (publishedVersion)
Europe PMC (PubMed Central) (acceptedVersion)
PubMed Central (acceptedVersion)
Funders: National Institutes of Health (5r01mh063266-25)
University of Colorado Denver
National Institute of Mental Health (MH063266, R01-MH063266)
National Institute on Drug Abuse (DA-02632, DA18478, T32DA017637, R01DA002632, F31DA018478, R01DA031734)
National Institute of Neurological Disorders and Stroke (P30NS047243)
Topics: Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Neurotransmitter Receptor Influence on Behavior
Life Sciences › Neuroscience › Behavioral Neuroscience › Stress Responses and Cortisol
Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Neuroscience and Neuropharmacology Research
Keywords: social defeat stress, cocaine self-administration, behavioral sensitization, ERK signaling, ventral tegmental area, U0126, cross-sensitization, compulsive drug taking, mesocorticolimbic circuit, neural adaptation
MeSH terms: Animals, Cocaine, Hierarchy, Social, Male, Reinforcement, Psychology, Self Administration, Stress, Psychological, Signal Transduction, Ventral Tegmental Area, Dopamine Uptake Inhibitors, Rats, Long-Evans, Mitogen-Activated Protein Kinases, Extracellular Signal-Regulated MAP Kinases, Rats

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Social defeat stress-induced sensitization and escalated cocaine self-administration: the role of ERK signaling in the rat ventral tegmental area

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