Role of serotonin transporter function in rat orbitofrontal cortex in impulsive choice
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Impulsivity is a multi-faceted personality construct that plays a prominent role in drug abuse vulnerability. Dysregulation of 5-hydroxytryptamine (serotonin, 5-HT) systems in subregions of the prefrontal cortex has been implicated in impulsivity. Extracellular 5-HT concentrations are regulated by 5-HT transporters (SERTs), indicating that these transporters may be important molecular targets underlying individual differences in impulsivity and drug abuse vulnerability. The present study evaluated the role of SERT in mediating individual differences in impulsivity. Rats were tested for both impulsive action using the cued go/no-go task and for impulsive choice using a delay discounting task in a counterbalanced design. Following behavioral evaluation, Km and Vmax were obtained from kinetic analysis of [(3)H]5-HT uptake by SERT using synaptosomes prepared from both orbitofrontal cortex (OFC) and medial prefrontal cortex (mPFC) obtained from each individual rat. Vmax for SERT in OFC, but not mPFC, was negatively correlated with mean adjusted delay scores in the delay discounting task. In contrast, Vmax for SERT in OFC and mPFC was not correlated with performance in the cued go/no-go task. To further evaluate the relationship between SERT function and impulsive choice, a selective SERT inhibitor, fluoxetine (0, 15, 50 and 150pmol/side) was microinjected bilaterally into OFC and effects on the delay discounting task determined. Following stabilization of behavior, fluoxetine increased mean adjusted delay scores (decreased impulsivity) in high impulsive rats compared to saline microinjection, but had no effect in low impulsive rats. These ex vivo and in vivo results suggest that enhanced SERT function in OFC underlies high impulsive choice behavior.
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SSRIs within the PFC directly affect animals already exhibiting a deficit but do not enhance response inhibition in normal animals.
“Microinjections of fluoxetine into the OFC increase response inhibition in rats already showing impulsive tendencies, but have no effect in low impulsivity rats. This finding indicates direct effects of SSRIs within the PFC of animals already exhibiting a deficit, but do not enhance response inhibition in normal animals (Darna et al 2015).”
From Prefrontal cortex executive processes affected by stress in health and disease (2018) · cites this paper as Darna et al 2015
Microinjections of fluoxetine into the OFC increase response inhibition in rats already showing impulsive tendencies.
“Microinjections of fluoxetine into the OFC increase response inhibition in rats already showing impulsive tendencies, but have no effect in low impulsivity rats. This finding indicates direct effects of SSRIs within the PFC of animals already exhibiting a deficit, but do not enhance response inhibition in normal animals (Darna et al 2015).”
From Prefrontal cortex executive processes affected by stress in health and disease (2018) · cites this paper as Darna et al 2015
Fluoxetine has no effect on response inhibition in low-impulsivity rats.
“Microinjections of fluoxetine into the OFC increase response inhibition in rats already showing impulsive tendencies, but have no effect in low impulsivity rats. This finding indicates direct effects of SSRIs within the PFC of animals already exhibiting a deficit, but do not enhance response inhibition in normal animals (Darna et al 2015).”
From Prefrontal cortex executive processes affected by stress in health and disease (2018) · cites this paper as Darna et al 2015
VNS may increase 5-HT and norepinephrine levels, leading to increased NMDA-R function in the mPFC and beneficial effects on response inhibition.
“which may increase levels of 5-HT and norepinephrine leading to increased NMDA-R function within the mPFC, and subsequent beneficial effects on response inhibition measures (Carli et al 2011, Carli & Invernizzi 2014, Darna et al 2015, Mirjana et al 2004).”
From Prefrontal cortex executive processes affected by stress in health and disease (2018) · cites this paper as Darna et al 2015
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GENETICS OF THE RESEARCH DOMAIN CRITERIA (RDoC): GENOME-WIDE ASSOCIATION STUDY OF DELAY DISCOUNTING
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Yates, J. R. (2026) · Springer eBooks · doi:10.1007/978-3-032-15602-0_7
Self-citation
- Authors
- Darna, M., Chow, J. J., Yates, J. R., Charnigo, R. J., Beckmann, J. S., Bardo, M. T., & Dwoskin, L. P.
- Affiliations
- University of Kentucky (US)
- Corresponding author
- Dwoskin, Linda P.
- Venue
- Behavioural Brain Research
- Publisher
- Elsevier BV
- Published
- 2015-10
- Volume
- 293
- Pages
- 134-142
- ISSN
- 0166-4328 (ISSN-L)
- PMC
- PMC4808810
- OpenAlex
- W1152482960
- Cited by
- 28
- References
- 66
- Citations by year
- 2026: 1 · 2025: 1 · 2024: 2 · 2023: 1 · 2022: 4 · 2021: 1 · 2020: 1 · 2019: 5 · 2018: 2 · 2017: 5 · 2016: 4 · 2015: 1
- FWCI
- 1.84
- Type
- journal article
- Language
- en
- Open access
- green
- www.ncbi.nlm.nih.gov
- Locations
- Behavioural Brain Research (publishedVersion)
- PubMed (publishedVersion)
- Europe PMC (PubMed Central) (acceptedVersion)
- PubMed Central (acceptedVersion)
- UKnowledge (University of Kentucky) (submittedVersion)
- Funders
- National Institutes of Health (UL1TR000117)
- National Institute on Drug Abuse (T32DA016176, P50DA005312)
- National Center for Advancing Translational Sciences
- Topics
- Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Neurotransmitter Receptor Influence on Behavior
- Life Sciences › Neuroscience › Cognitive Neuroscience › Neural and Behavioral Psychology Studies
- Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Neuroscience and Neuropharmacology Research
- Keywords
- serotonin transporter, impulsivity, impulsive choice, delay discounting, orbitofrontal cortex, medial prefrontal cortex, individual differences, fluoxetine, serotonin, drug abuse vulnerability
- MeSH terms
- Animals, Choice Behavior, Cues, Dose-Response Relationship, Drug, Fluoxetine, Impulsive Behavior, Functional Laterality, Male, Serotonin, Tritium, Rats, Sprague-Dawley, Prefrontal Cortex, Serotonin Plasma Membrane Transport Proteins, Rats
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