Corticotropin‐releasing factor increases mouse ventral tegmental area dopamine neuron firing through a protein kinase C‐dependent enhancement of Ih

Wanat, M. J.; Hopf, F. W.; Stuber, G. D.; Phillips, P. E. M.; Bonci, A.

doi:10.1113/jphysiol.2007.150078

Cited by 256Neurotransmitter Receptor Influence on BehaviorNeuropeptides and Animal PhysiologyNeuroscience and Neuropharmacology Research

Corticotropin‐releasing factor increases mouse ventral tegmental area dopamine neuron firing through a protein kinase C‐dependent enhancement of Ih

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Wanat, M. J., Hopf, F. W., Stuber, G. D., Phillips, P. E. M., Bonci, A.·2008·The Journal of Physiology

DOI 10.1113/jphysiol.2007.150078PMC PMC2465205

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Abstract

Stress induces the release of the peptide corticotropin‐releasing factor (CRF) into the ventral tegmental area (VTA), and also increases dopamine levels in brain regions receiving dense VTA input. Therefore, stress may activate the mesolimbic dopamine system in part through the actions of CRF in the VTA. Here, we explored the mechanism by which CRF affects VTA dopamine neuron firing. Using patch‐clamp recordings from brain slices we first determined that the presence of Ih is an excellent predictor of dopamine content in mice. We next showed that CRF dose‐dependently increased VTA dopamine neuron firing, which was prevented by antagonism of the CRF receptor‐1 (CRF‐R1), and was mimicked by CRF‐R1 agonists. Inhibition of the phospholipase C (PLC)–protein kinase C (PKC) signalling pathway, but not the cAMP–protein kinase A (PKA) signalling pathway, prevented the increase in dopamine neuron firing by CRF. Furthermore, the effect of CRF on VTA dopamine neurons was not attenuated by blockade of IA,IK(Ca)or IKir, but was completely eliminated by inhibition of Ih. Although cAMP‐dependent modulation of Ih through changes in the voltage dependence of activation is well established, we surprisingly found that CRF, through a PKC‐dependent mechanism, enhanced Ih independent of changes in the voltage dependence of activation. Thus, our results demonstrated that CRF acted on the CRF‐R1 to stimulate the PLC–PKC signalling pathway, which in turn enhanced Ih to increase VTA dopamine neuron firing. These findings provide a cellular mechanism of the interaction between CRF and dopamine, which can be involved in promoting the avoidance of threatening stimuli, the pursuit of appetitive behaviours, as well as various psychiatric conditions.

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Stress-mediated increases in ventral tegmental area dopamine neuron firing are caused by increased Ih currents.
“The stress-mediated increases in VTA dopamine neuron firing are caused by increased Ih currents [29, 35]”
From The molecular and cellular mechanisms of depression: a focus on reward circuitry (2019) · cites this paper as [35]

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The excitatory actions of corticotropin-releasing factor on ventral tegmental area dopamine neurons
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Increased mesocorticolimbic dopamine during acute and repeated social defeat stress: modulation by corticotropin releasing factor receptors in the ventral tegmental area
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Authors: Wanat, M. J., Hopf, F. W., Stuber, G. D., Phillips, P. E. M., & Bonci, A.
Affiliations: University of California, San Francisco (US)
Ernest Gallo Clinic and Research Center (US)
University of Washington (US)
Corresponding author: Bonci, A.
ORCID: Wanat, M. J.
Hopf, F. W.
Stuber, G. D.
Phillips, P. E. M.
Bonci, A.
Venue: The Journal of Physiology
Publisher: Wiley
Published: 2008-04-14
Volume: 586
Issue: 8
Pages: 2157-2170
ISSN: 0022-3751 (ISSN-L)
1469-7793
DOI: 10.1113/jphysiol.2007.150078
PMC: PMC2465205
OpenAlex: W2146291241
Cited by: 256
References: 74
Citations by year: 2026: 2 · 2025: 8 · 2024: 4 · 2023: 10 · 2022: 18 · 2021: 6 · 2020: 5 · 2019: 16 · 2018: 20 · 2017: 20 · 2016: 18 · 2015: 14 · 2014: 17 · 2013: 24 · 2012: 17
FWCI: 8.22
Type: journal article
Language: en
Open access: bronze
doi.org
Licence: onlinelibrary.wiley.com/termsAndConditions#vor (vor)
Locations: The Journal of Physiology (publishedVersion)
PubMed Central (publishedVersion)
PubMed (publishedVersion)
Funders: National Institutes of Health (7r01da016782-09)
University of California, San Francisco
National Institute on Drug Abuse (F31 DA21464-01, F31DA021464, R01 DA016782-04, R01-DA016782)
USAF Phillips Laboratory
Topics: Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Neurotransmitter Receptor Influence on Behavior
Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Neuropeptides and Animal Physiology
Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Neuroscience and Neuropharmacology Research
Keywords: corticotropin-releasing factor, ventral tegmental area, dopaminergic neurons, protein kinase C, phospholipase C, CRF1 receptor, mesolimbic dopamine system, stress, neuronal firing, voltage dependence of activation
MeSH terms: Action Potentials, Animals, Corticotropin-Releasing Hormone, Dopamine, Dose-Response Relationship, Drug, Membrane Potentials, Mice, Inbred C57BL, Mice, Transgenic, Neurons, Protein Kinase C, Ventral Tegmental Area, Patch-Clamp Techniques, Mice

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Corticotropin‐releasing factor increases mouse ventral tegmental area dopamine neuron firing through a protein kinase C‐dependent enhancement of Ih

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