Excitatory transmission at thalamo-striatal synapses mediates susceptibility to social stress
Open accessAbstract
Postsynaptic remodeling of glutamatergic synapses on ventral striatum (vSTR) medium spiny neurons (MSNs) is critical for shaping stress responses. However, it is unclear which presynaptic inputs are involved. Susceptible mice exhibited increased synaptic strength at intralaminar thalamus (ILT), but not prefrontal cortex (PFC), inputs to vSTR MSNs following chronic social stress. Modulation of ILT-vSTR versus PFC-vSTR neuronal activity differentially regulated dendritic spine plasticity and social avoidance.
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Each glutamatergic projection to the NAcc from the PFC, thalamus, amygdala, and hippocampus has a distinct contribution to modulating social anhedonia following social stress.
“each of these projections has been shown to have a distinct contribution to modulating social anhedonia following social stress”
From Social functioning in major depressive disorder (2016) · cites this paper as Christoffel et al., 2015
Susceptible mice show increased synaptic strength at thalamic inputs to NAcc.
“susceptible mice show increased synaptic strength at thalamic inputs to NAcc”
From Social functioning in major depressive disorder (2016) · cites this paper as Christoffel et al., 2015
Modulating thalamo-NAcc projections bi-directionally alters social interaction after social stress.
“modulating thalamo-NAcc projections bi-directionally alters social interaction after social stress (Christoffel et al., 2015).”
From Social functioning in major depressive disorder (2016) · cites this paper as Christoffel et al., 2015
Enhancing hippocampal and thalamic input to the nucleus accumbens promotes depressive-like outcomes.
“In contrast to PFC-NAc afferents, enhancing hippocampal and thalamic input to the NAc promotes depressive-like outcomes.”
From Emerging Role for Nucleus Accumbens Medium Spiny Neuron Subtypes in Depression (2017) · cites this paper as [48]
Increased synaptic strength is observed on intralaminar thalamic nucleus accumbens inputs.
“Increased synaptic strength is observed on intralaminar thalamic NAc inputs and driving the thalamic inputs promotes susceptibility to CSDS (48).”
From Emerging Role for Nucleus Accumbens Medium Spiny Neuron Subtypes in Depression (2017) · cites this paper as [48]
Driving thalamic inputs promotes susceptibility to chronic social defeat stress.
“Increased synaptic strength is observed on intralaminar thalamic NAc inputs and driving the thalamic inputs promotes susceptibility to CSDS (48).”
From Emerging Role for Nucleus Accumbens Medium Spiny Neuron Subtypes in Depression (2017) · cites this paper as [48]
CSDS induced enhancement of synaptic transmission at thalamic inputs, but not cortical inputs to the NAc, promoted social avoidance.
“CSDS induced enhancement of synaptic transmission at thalamic inputs, but not cortical inputs to the NAc, promoted social avoidance [160].”
From Neural circuits regulating prosocial behaviors (2023) · cites this paper as [160]
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Self-citation
- Authors
- Christoffel, D. J., Golden, S. A., Walsh, J. J., Guise, K. G., Heshmati, M., Friedman, A. K., Dey, A., Smith, M., Rebusi, N., Pfau, M., Ables, J. L., Aleyasin, H., Khibnik, L. A., Hodes, G. E., Ben-Dor, G. A., Deisseroth, K., Shapiro, M. L., Malenka, R. C., Ibanez-Tallon, I., Han, M.-H., & Russo, S. J.
- Affiliations
- Stanford University (US)
- Icahn School of Medicine at Mount Sinai (US)
- Howard Hughes Medical Institute (US)
- Corresponding author
- Russo, Scott J
- ORCID
- Venue
- Nature Neuroscience
- Published
- 2015-06-01
- Volume
- 18
- Issue
- 7
- Pages
- 962-964
- ISSN
- 1097-6256 (ISSN-L)
- 1546-1726
- PMC
- PMC4482771
- OpenAlex
- W1524070957
- Cited by
- 101
- References
- 24
- Citations by year
- 2026: 3 · 2025: 4 · 2024: 5 · 2023: 1 · 2022: 10 · 2021: 15 · 2020: 7 · 2019: 12 · 2018: 20 · 2017: 10 · 2016: 10 · 2015: 4
- FWCI
- 6.81
- 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)
- PubMed Central (acceptedVersion)
- Funders
- National Institute on Alcohol Abuse and Alcoholism (R01AA022445)
- National Institute of Mental Health (F31MH105217, F30MH100835, R01MH090264, P50MH096890, R01MH092306, R01MH065658, T32MH096678, F32MH096464, P50MH094263, F32MH106206, R01MH073689, R01MH104559, T32MH087004)
- National Institute on Drug Abuse (P01DA008227, T32DA035165)
- National Institute of General Medical Sciences (T32GM089626)
- Topics
- Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Neuroscience and Neuropharmacology Research
- Life Sciences › Neuroscience › Behavioral Neuroscience › Stress Responses and Cortisol
- Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Neurotransmitter Receptor Influence on Behavior
- Keywords
- chronic social stress, intralaminar thalamus, ventral striatum, medium spiny neurons, glutamatergic neurotransmission, synaptic plasticity, dendritic spine plasticity, social avoidance, depression vulnerability, behavioral coping, prefrontal cortex
- MeSH terms
- Animals, Behavior, Animal, Disease Susceptibility, Male, Mice, Inbred C57BL, Neuronal Plasticity, Reward, Social Behavior, Stress, Psychological, Thalamus, Prefrontal Cortex, Excitatory Postsynaptic Potentials, Dendritic Spines, Mice, Ventral Striatum
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