ArticleNeuropharmacology2014
Dopamine D2 receptor desensitization by dopamine or corticotropin releasing factor in ventral tegmental area neurons is associated with increased glutamate release.
Article in Neuropharmacology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
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Who cites it
11 citing papers in PubMed, 20 citations in OpenAlex.
- Synaptic Effects Induced by Alcohol.Current topics in behavioral neurosciences · 2025Review
- Neuroendocrine Assessment of Dopaminergic Function during Antidepressant Treatment in Major Depressed Patients.Brain sciences · 2021Article
- Translating striatal activity from brain slice to whole animal neurophysiology: A guide for neuroscience research integrating diverse levels of analysis.Journal of neuroscience research · 2019Review
- An Assessment between D1 Receptor Agonist and D2 receptor Antagonist into the Ventral Tegmental Area on Conditioned Place Preference and Locomotor Activity.Advanced biomedical research · 2019Article
- Ethanol actions on the ventral tegmental area: novel potential targets on reward pathway neurons.Psychopharmacology · 2018Review
- A role for corticotropin-releasing factor signaling in the lateral habenula and its modulation by early-life stress.Science signaling · 2018Article
- Corticotropin-Releasing Factor (CRF) and Addictive Behaviors.International review of neurobiology · 2017Review
- Diversity of Dopaminergic Neural Circuits in Response to Drug Exposure.Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology · 2016Review
- Diacylglycerol lipase disinhibits VTA dopamine neurons during chronic nicotine exposure.Proceedings of the National Academy of Sciences of the United States of America · 2016Article
- Prefrontal and Striatal Glutamate Differently Relate to Striatal Dopamine: Potential Regulatory Mechanisms of Striatal Presynaptic Dopamine Function?The Journal of neuroscience : the official journal of the Society for Neuroscience · 2015Article
- GIRK3 gates activation of the mesolimbic dopaminergic pathway by ethanol.Proceedings of the National Academy of Sciences of the United States of America · 2015Article
Corrections and comments
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Authors and funding
7 authors at 2 institutions in 1 country.
Funding
Abstract
Neurons of the ventral tegmental area (VTA) are the source of dopaminergic (DAergic) input to important brain regions related to addiction. Prolonged exposure of these VTA neurons to moderate concentrations of dopamine (DA) causes a time-dependent decrease in DA-induced inhibition, a complex desensitization called DA inhibition reversal (DIR). DIR is mediated by conventional protein kinase C (cPKC) through concurrent stimulation of D2 and D1-like DA receptors, or by D2 stimulation concurrent with activation of some Gq-linked receptors. Corticotropin releasing factor (CRF) acts via Gq, and can modulate glutamater neurotransmission in the VTA. In the present study, we used brain slice electrophysiology to characterize the interaction of DA, glutamate antagonists, and CRF agonists in the induction and maintenance of DIR in the VTA. Glutamate receptor antagonists blocked induction but not maintenance of DIR. Putative blockers of neurotransmitter release and store-operated calcium channels blocked and reversed DIR. CRF and the CRF agonist urocortin reversed inhibition produced by the D2 agonist quinpirole, consistent with our earlier work indicating that Gq activation reverses quinpirole-mediated inhibition. In whole cell recordings, the combination of urocortin and quinpirole, but not either agent alone, increased spontaneous excitatory postsynaptic currents (sEPSCs) in VTA neurons. Likewise, the combination of a D1-like receptor agonist and quinpirole, but not either agent alone, increased sEPSCs in VTA neurons. In summary, desensitization of D2 receptors induced by dopamine or CRF on DAergic VTA neurons is associated with increased glutamatergic signaling in the VTA.
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Registered trials
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.