ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2013
Calcium-permeable AMPA receptors in the nucleus accumbens regulate depression-like behaviors in the chronic neuropathic pain state.
Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 80 papers.
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Who cites it
80 citing papers in PubMed, 136 citations in OpenAlex.
- Plasma inflammatory cytokines and treatment-resistant depression with comorbid pain: improvement by ketamine.Journal of neuroinflammation · 2021Trial
- AMPA receptor, neuroimaging, and chronic pain.Journal of anesthesia · 2026Review
- Chronic pain in a modern virally suppressed HIV cohort is associated with disability and poorer mental health.Scientific reports · 2026Observational
- Nonlinear threshold and association of depressive symptoms with pain in middle-aged and older Chinese adults: a cross-sectional and cohort study.Scientific reports · 2026Article
- A top-down neural circuit for affective-motivational responses of pain relief induced by electroacupuncture.Chinese medicine · 2026Article
- Synaptic plasticity in affective comorbidities of neuropathic pain: a bibliometric analysis based on WoSCC and PubMed (2003-2025).Frontiers in neurology · 2026Article
- Gestational stress disrupts the neuroimmune environment in the nucleus accumbens of maternal rats.Brain, behavior, & immunity - health · 2025Article
- Xenon gas as a potential treatment for opioid use disorder, alcohol use disorder, and related disorders.Medical gas research · 2025Review
- A systematic review of the pain-related emotional and cognitive impairments in chronic inflammatory pain induced by CFA injection and its mechanism.IBRO neuroscience reports · 2025Review
- A glutamatergic innervation from medial area of secondary visual cortex to lateral posterior thalamic nucleus facilitates nociceptive and neuropathic pain.Communications biology · 2025Article
- Chronic Pain and Comorbid Emotional Disorders: Neural Circuitry and Neuroimmunity Pathways.International journal of molecular sciences · 2025Review
- A Neural Circuit From Paraventricular Nucleus of the Thalamus to the Nucleus Accumbens Mediates Inflammatory Pain in Mice.Brain and behavior · 2025Article
- Fear-learning is altered in a mouse neuropathic pain model.Frontiers in pain research (Lausanne, Switzerland) · 2025Article
- An ACC-VTA-ACC positive-feedback loop mediates the persistence of neuropathic pain and emotional consequences.Nature neuroscience · 2024Article
- Tianeptine promotes lasting antiallodynic effects in a mouse model of neuropathic pain.Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology · 2023Article
- Pain-related cortico-limbic plasticity and opioid signaling.Neuropharmacology · 2023Review
- Oxytocin promotes prefrontal population activity via the PVN-PFC pathway to regulate pain.Neuron · 2023Article
- Enhanced functional detection of synaptic calcium-permeable AMPA receptors using intracellular NASPM.eLife · 2023Article
- Pramipexole treatment attenuates mechanical hypersensitivity in male rats experiencing chronic inflammatory pain.Neuropharmacology · 2022Article
- Persistent inflammatory pain is linked with anxiety-like behaviors, increased blood corticosterone, and reduced global DNA methylation in the rat amygdala.Molecular pain · 2022Article
20 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
9 authors at 3 institutions in 2 countries.
Funding
Abstract
Depression is a salient emotional feature of chronic pain. Depression alters the pain threshold and impairs functional recovery. To date, however, there has been limited understanding of synaptic or circuit mechanisms that regulate depression in the pain state. Here, we demonstrate that depression-like behaviors are induced in a rat model of chronic neuropathic pain. Using this model, we show that chronic pain selectively increases the level of GluA1 subunits of AMPA-type glutamate receptors at the synapses of the nucleus accumbens (NAc), a key component of the brain reward system. We find, in addition, that this increase in GluA1 levels leads to the formation of calcium-permeable AMPA receptors (CPARs). Surprisingly, pharmacologic blockade of these CPARs in the NAc increases depression-like behaviors associated with pain. Consistent with these findings, an AMPA receptor potentiator delivered into the NAc decreases pain-induced depression. These results show that transmission through CPARs in the NAc represents a novel molecular mechanism modulating the depressive symptoms of pain, and thus CPARs may be a promising therapeutic target for the treatment of pain-induced depression. More generally, these findings highlight the role of central glutamate signaling in pain states and define the brain reward system as an important region for the regulation of depressive symptoms of pain.
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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.