ArticleMolecular brain2014
Postsynaptic insertion of AMPA receptor onto cortical pyramidal neurons in the anterior cingulate cortex after peripheral nerve injury.
Article in Molecular brain, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 52 papers.
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Who cites it
52 citing papers in PubMed, 80 citations in OpenAlex.
- AMPA receptor, neuroimaging, and chronic pain.Journal of anesthesia · 2026Review
- Cornichon Homolog-3 (Cnih3) deletion impairs spatial memory, operant learning, and fentanyl self-administration behavior.Translational psychiatry · 2026Article
- Can Nutrition Modulate the Progression of Alzheimer's Disease? A Narrative Review.Current nutrition reports · 2026Review
- TMEM251 loss-induced autophagy dysfunction in the anterior cingulate cortex contributes to chronic postoperative pain.EMBO reports · 2026Article
- Decoding chronic pain: the glutamate-GABA tug of war in the cerebral cortex.Frontiers in molecular neuroscience · 2025Review
- Pregnancy ameliorates neuropathic pain through suppression of microglia and upregulation of the δ-opioid receptor in the anterior cingulate cortex in late-pregnant mice.Journal of anesthesia · 2024Article
- Increased GluK1 Subunit Receptors in Corticostriatal Projection from the Anterior Cingulate Cortex Contributed to Seizure-Like Activities.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2024Article
- Article
- Using FASS-LTP in postmortem mice brain tissues to assess pathological synaptic function.Journal of neuroscience methods · 2024Article
- Enhanced long-term potentiation in the anterior cingulate cortex of tree shrew.Philosophical transactions of the Royal Society of London. Series B, Biological sciences · 2024Article
- Synaptic sensitization in the anterior cingulate cortex sustains the consciousness of pain via synchronized oscillating electromagnetic waves.Frontiers in human neuroscience · 2024Article
- Activation of the glutamatergic cingulate cortical-cortical connection facilitates pain in adult mice.Communications biology · 2023Article
- Article
- Synaptic Plasticity in the Pain-Related Cingulate and Insular Cortex.Biomedicines · 2022Review
- Cerebellar glutamatergic system impacts spontaneous motor recovery by regulating Gria1 expression.NPJ Regenerative medicine · 2022Article
- Long-Lasting, Pathway-Specific Impairment of a Novel Form of Spike-Timing-Dependent Long-Term Depression by Neuropathic Pain in the Anterior Cingulate Cortex.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2022Article
- A transcriptomic analysis of neuropathic pain in the anterior cingulate cortex after nerve injury.Bioengineered · 2022Article
- The increased in vivo firing of pyramidal cells but not interneurons in the anterior cingulate cortex after neuropathic pain.Molecular brain · 2022Article
- Different Synaptic Plasticity After Physiological and Psychological Stress in the Anterior Insular Cortex in an Observational Fear Mouse Model.Frontiers in synaptic neuroscience · 2022Article
- Brain-derived neurotrophic factor produced long-term synaptic enhancement in the anterior cingulate cortex of adult mice.Molecular brain · 2021Article
Corrections and comments
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Authors and funding
14 authors at 6 institutions in 4 countries.
Funding
Abstract
Long-term potentiation (LTP) is the key cellular mechanism for physiological learning and pathological chronic pain. Postsynaptic accumulation of AMPA receptor (AMPAR) GluA1 plays an important role for injury-related cortical LTP. However, there is no direct evidence for postsynaptic GluA1 insertion or accumulation after peripheral injury. Here we report nerve injury increased the postsynaptic expression of AMPAR GluA1 in pyramidal neurons in the layer V of the anterior cingulate cortex (ACC), including the corticospinal projecting neurons. Electrophysiological recordings show that potentiation of postsynaptic responses was reversed by Ca2+ permeable AMPAR antagonist NASPM. Finally, behavioral studies show that microinjection of NASPM into the ACC inhibited behavioral sensitization caused by nerve injury. Our findings provide direct evidence that peripheral nerve injury induces postsynaptic GluA1 accumulation in cingulate cortical neurons, and inhibits postsynaptic GluA1 accumulation which may serve as a novel target for treating neuropathic pain.
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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.