Stress and CRF gate neural activation of BDNF in the mesolimbic reward pathway
Open accessAbstract
Mechanisms controlling release of brain-derived neurotrophic factor (BDNF) in the mesolimbic dopamine reward pathway remain unknown. We report that phasic optogenetic activation of this pathway increases BDNF amounts in the nucleus accumbens (NAc) of socially stressed mice but not of stress-naive mice. This stress gating of BDNF signaling is mediated by corticotrophin-releasing factor (CRF) acting in the NAc. These results unravel a stress context-detecting function of the brain's mesolimbic circuit.
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In mice that exhibit reduced social interaction, ANA-12 infusion into the NAc completely blocks social avoidance.
“Moreover, in mice that exhibit a reduced social interaction, ANA-12 infusion into the NAc has been shown to completely block social avoidance (Walsh et al. 2014).”
From Neurotrophic factors and neuroplasticity pathways in the pathophysiology and treatment of depression (2018) · cites this paper as Walsh et al. 2014
The passage describing the ANA-12 experiment says intra-NAc ANA-12 completely blocked phasic stimulation from inducing social avoidance. It was given before stimulation and testing, so the paper does not show that ANA-12 blocks avoidance in mice already exhibiting reduced social interaction. (LLM, conf=0.84)
Experimental — accuracy not yet measuredPhasic, but not tonic, optogenetic stimulation of ventral tegmental area to nucleus accumbens projecting neurons promotes susceptibility to chronic social defeat stress.
“The effect of chronic stress on VTA DA neuron firing is lasting (37, 65, 66), is driven by activity of intrinsic potassium channels (54), and phasic but not tonic optogenetic stimulation of VTA-NAc projecting neurons promotes susceptibility to CSDS (54, 66–68).”
From Emerging Role for Nucleus Accumbens Medium Spiny Neuron Subtypes in Depression (2017) · cites this paper as [68]
BDNF is responsible for stress susceptibility.
“Rather, BDNF was responsible for stress susceptibility and antagonism of the BDNF receptor TrkB, prevented susceptibility (37, 38, 54, 65, 67, 68).”
From Emerging Role for Nucleus Accumbens Medium Spiny Neuron Subtypes in Depression (2017) · cites this paper as [68]
Antagonism of the BDNF receptor TrkB prevents stress susceptibility.
“Rather, BDNF was responsible for stress susceptibility and antagonism of the BDNF receptor TrkB, prevented susceptibility (37, 38, 54, 65, 67, 68).”
From Emerging Role for Nucleus Accumbens Medium Spiny Neuron Subtypes in Depression (2017) · cites this paper as [68]
Corticotropin releasing factor enhances release of BDNF in the nucleus accumbens.
“Further, another molecule involved in stress signaling, corticotropin releasing factor (CRF), enhances release of BDNF in the NAc and promotes susceptibility to stress caused by the paired induction of phasic firing and social stress (68).”
From Emerging Role for Nucleus Accumbens Medium Spiny Neuron Subtypes in Depression (2017) · cites this paper as [68]
Corticotropin releasing factor promotes susceptibility to stress caused by paired induction of phasic firing and social stress.
“Further, another molecule involved in stress signaling, corticotropin releasing factor (CRF), enhances release of BDNF in the NAc and promotes susceptibility to stress caused by the paired induction of phasic firing and social stress (68).”
From Emerging Role for Nucleus Accumbens Medium Spiny Neuron Subtypes in Depression (2017) · cites this paper as [68]
Phasic firing of dopaminergic neurons from the VTA to the NAc promotes susceptibility, whereas firing from the VTA to the medial PFC promotes resilience.
“In particular, phasic firing of dopaminergic neurons from the VTA to the NAc promotes susceptibility, whereas firing of dopaminergic neurons from the VTA to the medial PFC promotes resilience (4).”
From Neuroanatomic differences associated with stress susceptibility and resilience (2016) · cites this paper as [47]
Receptors for CRF and glucocorticoids are distributed throughout the brain's reward circuitry, and their activation or blockade influences reward-related neurotransmission and behavior.
“receptors for CRF and glucocorticoids are located throughout the reward circuitry of the brain, with their activation or blockade affecting reward-sensitive neurotransmission and behaviors (Bryce and Floresco, 2016; Craenenbroeck et al., 2005; Walsh et al., 2014).”
From The effects of early life stress on reward processing (2018) · cites this paper as Walsh et al., 2014
With a severe stressor such as CSDS, increased release of BDNF from VTA DA inputs to the NAc contributes to social avoidance.
“With a severe stressor such as CSDS, increased release of BDNF from VTA DA inputs to the NAc contributes to social avoidance [149]”
From Neural circuits regulating prosocial behaviors (2023) · cites this paper as [149]
Alterations in VTA DA activity affect activity in multiple downstream targets, including the NAc and mPFC, which appear to be particularly important for mediating social avoidance.
“Alterations in VTA DA activity will affect activity in multiple downstream targets, including the NAc and mPFC, which appear to be particularly important for mediating social avoidance [149, 150, 156-159].”
From Neural circuits regulating prosocial behaviors (2023) · cites this paper as [149]
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- Authors
- Walsh, J. J., Friedman, A. K., Sun, H., Heller, E. A., Ku, S. M., Juarez, B., Burnham, V. L., Mazei-Robison, M. S., Ferguson, D., Golden, S. A., Koo, J. W., Chaudhury, D., Christoffel, D. J., Pomeranz, L., Friedman, J. M., Russo, S. J., Nestler, E. J., & Han, M.-H.
- Affiliations
- Icahn School of Medicine at Mount Sinai (US)
- Howard Hughes Medical Institute (US)
- Corresponding author
- Han, Ming-Hu
- ORCID
- Venue
- Nature Neuroscience
- Published
- 2013-11-24
- Volume
- 17
- Issue
- 1
- Pages
- 27-29
- ISSN
- 1097-6256 (ISSN-L)
- 1546-1726
- PMC
- PMC3984932
- OpenAlex
- W2064784067
- Cited by
- 210
- References
- 21
- Citations by year
- 2026: 6 · 2025: 7 · 2024: 14 · 2023: 11 · 2022: 19 · 2021: 17 · 2020: 13 · 2019: 24 · 2018: 24 · 2017: 26 · 2016: 17 · 2015: 19 · 2014: 13
- FWCI
- 8.01
- Type
- journal article
- Language
- en
- Open access
- green
- www.ncbi.nlm.nih.gov
- Licence
- www.springer.com/tdm (tdm)
- Locations
- Nature Neuroscience (publishedVersion)
- PubMed (publishedVersion)
- Europe PMC (PubMed Central) (acceptedVersion)
- PubMed Central (acceptedVersion)
- Funders
- National Institute on Alcohol Abuse and Alcoholism (R01AA022445)
- National Institute of Mental Health (F31MH108326, P50MH096890, R01MH092306, F31MH095425, T32MH096678, F32MH096464, K99MH094405, R01MH051399, T32MH087004)
- National Institute on Drug Abuse (T32DA007135, R01DA014133)
- 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
- chronic social defeat stress, brain-derived neurotrophic factor, corticotropin-releasing factor, ventral tegmental area, nucleus accumbens, optogenetic stimulation, social stress
- MeSH terms
- Channelrhodopsins, Animals, Azepines, Bacterial Proteins, Benzamides, Corticotropin-Releasing Hormone, Disease Models, Animal, Dopamine, Enzyme Inhibitors, Gene Expression Regulation, Interpersonal Relations, Luminescent Proteins, Male, Mice, Inbred C57BL, Mice, Transgenic, Microinjections, Neurons, Nucleus Accumbens, Peptide Fragments, Photic Stimulation, Stress, Psychological, Time Factors, Tyrosine 3-Monooxygenase, Ventral Tegmental Area, Statistics, Nonparametric, Brain-Derived Neurotrophic Factor, Mice, Optogenetics
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