ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2015
Amphetamine action at the cocaine- and antidepressant-sensitive serotonin transporter is modulated by αCaMKII.
Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 18 papers.
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Who cites it
18 citing papers in PubMed, 29 citations in OpenAlex.
- α-Synuclein regulates monoamine transporter capacity and amphetamine-induced efflux via modulation of transporter expression.The Journal of pharmacology and experimental therapeutics · 2026Article
- Doxycycline reversal of amphetamine-induced mania-like behavior is related to adjusting brain monoamine abnormalities and antioxidant effects in primary hippocampal neurons.Naunyn-Schmiedeberg's archives of pharmacology · 2024Article
- STAT3 in the dorsal raphe gates behavioural reactivity and regulates gene networks associated with psychopathology.Molecular psychiatry · 2021Article
- Psychoactive Drugs-From Chemical Structure to Oxidative Stress Related to Dopaminergic Neurotransmission. A Review.Antioxidants (Basel, Switzerland) · 2021Review
- Glycogen synthase kinase-3ß supports serotonin transporter function and trafficking in a phosphorylation-dependent manner.Journal of neurochemistry · 2021Article
- Multiscale neurobiological correlates of human neuroticism.Human brain mapping · 2020Article
- The Amino Terminus of LeuT Changes Conformation in an Environment Sensitive Manner.Neurochemical research · 2020Article
- Article
- Functions of p38 MAP Kinases in the Central Nervous System.Frontiers in molecular neuroscience · 2020Review
- The Serotonin Syndrome: From Molecular Mechanisms to Clinical Practice.International journal of molecular sciences · 2019Review
- Flotillin-1 interacts with the serotonin transporter and modulates chronic corticosterone response.Genes, brain, and behavior · 2019Article
- Effect of Electroacupuncture on Reuptake of Serotonin via miRNA-16 Expression in a Rat Model of Depression.Evidence-based complementary and alternative medicine : eCAM · 2019Article
- A kinetic account for amphetamine-induced monoamine release.The Journal of general physiology · 2018Article
- Phosphorylation of the Amino Terminus of the Dopamine Transporter: Regulatory Mechanisms and Implications for Amphetamine Action.Advances in pharmacology (San Diego, Calif.) · 2018Review
- The N Terminus Specifies the Switch between Transport Modes of the Human Serotonin Transporter.The Journal of biological chemistry · 2017Article
- Kinase-dependent Regulation of Monoamine Neurotransmitter Transporters.Pharmacological reviews · 2016Review
- Structural Features and Potent Antidepressant Effects of Total Sterols and β-sitosterol Extracted from Sargassum horneri.Marine drugs · 2016Article
- Amphetamine Withdrawal Differentially Increases the Expression of Organic Cation Transporter 3 and Serotonin Transporter in Limbic Brain Regions.Journal of experimental neuroscience · 2016Article
Corrections and comments
- Erratum issued
Authors and funding
11 authors at 5 institutions in 6 countries.
Funding
Abstract
Serotonergic neurotransmission is terminated by reuptake of extracellular serotonin (5-HT) by the high-affinity serotonin transporter (SERT). Selective 5-HT reuptake inhibitors (SSRIs) such as fluoxetine or escitalopram inhibit SERT and are currently the principal treatment for depression and anxiety disorders. In addition, SERT is a major molecular target for psychostimulants such as cocaine and amphetamines. Amphetamine-induced transport reversal at the closely related dopamine transporter (DAT) has been shown previously to be contingent upon modulation by calmodulin kinase IIα (αCaMKII). Here, we show that not only DAT, but also SERT, is regulated by αCaMKII. Inhibition of αCaMKII activity markedly decreased amphetamine-triggered SERT-mediated substrate efflux in both cells coexpressing SERT and αCaMKII and brain tissue preparations. The interaction between SERT and αCaMKII was verified using biochemical assays and FRET analysis and colocalization of the two molecules was confirmed in primary serotonergic neurons in culture. Moreover, we found that genetic deletion of αCaMKII impaired the locomotor response of mice to 3,4-methylenedioxymethamphetamine (also known as "ecstasy") and blunted d-fenfluramine-induced prolactin release, substantiating the importance of αCaMKII modulation for amphetamine action at SERT in vivo as well. SERT-mediated substrate uptake was neither affected by inhibition of nor genetic deficiency in αCaMKII. This finding supports the concept that uptake and efflux at monoamine transporters are asymmetric processes that can be targeted separately. Ultimately, this may provide a molecular mechanism for putative drug developments to treat amphetamine addiction.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.