ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2013
Hypofunction of glutamatergic neurotransmission in the periaqueductal gray contributes to nerve-injury-induced neuropathic pain.
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 31 papers.
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31 citing papers in PubMed, 61 citations in OpenAlex.
- Distinct lateral hypothalamus GABAergic projections regulate sensory and affective dimensions of pain.Zoological research · 2026Article
- Somatosensory cortical progesterone receptor signaling regulates the episodic to chronic migraine transformation.Neurobiology of disease · 2026Article
- Enhancing peripheral nerve regeneration with rehabilitation and biomaterial-driven drug delivery strategies.Progress in biomedical engineering (Bristol, England) · 2025Review
- Chronic unpredictable stress produces hyperalgesia and promotes inhibitory drive in medial prefrontal cortex.The journal of pain · 2025Article
- Impaired Ventrolateral Periaqueductal Gray-Ventral Tegmental area Pathway Contributes to Chronic Pain-Induced Depression-Like Behavior in Mice.Molecular neurobiology · 2023Article
- Cell type-specific dissection of sensory pathways involved in descending modulation.Trends in neurosciences · 2023Review
- Persistent inflammation selectively activates opioid-sensitive phasic-firing neurons within the vlPAG.Journal of neurophysiology · 2023Article
- Bulbospinal nociceptive ON and OFF cells related neural circuits and transmitters.Frontiers in pharmacology · 2023Review
- Exercise facilitates regeneration after severe nerve transection and further modulates neural plasticity.Brain, behavior, & immunity - health · 2022Article
- Rapid antidepressant-like effects of muscarinic receptor antagonists require BDNF-dependent signaling in the ventrolateral periaqueductal gray.Psychopharmacology · 2022Article
- Neurobiology of Depression: Chronic Stress Alters the Glutamatergic System in the Brain-Focusing on AMPA Receptor.Biomedicines · 2022Review
- Cellular and circuit diversity determines the impact of endogenous opioids in the descending pain modulatory pathway.Frontiers in systems neuroscience · 2022Review
- The σ1 Receptor and the HINT1 Protein Control α2δ1 Binding to Glutamate NMDA Receptors: Implications in Neuropathic Pain.Biomolecules · 2021Article
- Neural Plasticity in the Brain during Neuropathic Pain.Biomedicines · 2021Review
- Activation of CamKIIα expressing neurons on ventrolateral periaqueductal gray improves behavioral hypersensitivity and thalamic discharge in a trigeminal neuralgia rat model.The journal of headache and pain · 2021Article
- Brainstem Pain-Modulation Circuitry and Its Plasticity in Neuropathic Pain: Insights From Human Brain Imaging Investigations.Frontiers in pain research (Lausanne, Switzerland) · 2021Review
- Article
- The Ventrolateral Periaqueductal Gray Contributes to Depressive-Like Behaviors in Recovery of Inflammatory Bowel Disease Rat Model.Frontiers in neuroscience · 2020Article
- Inhibition of GABAergic Neurons and Excitation of Glutamatergic Neurons in the Ventrolateral Periaqueductal Gray Participate in Electroacupuncture Analgesia Mediated by Cannabinoid Receptor.Frontiers in neuroscience · 2019Article
- Responsivity of Periaqueductal Gray Connectivity Is Related to Headache Frequency in Episodic Migraine.Frontiers in neurology · 2018Article
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Authors and funding
3 authors at 2 institutions in 3 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Neuropathic pain, a chronic pain due to neuronal lesion, remains unaltered even after the injury-induced spinal afferent discharges have declined, suggesting an involvement of supraspinal dysfunction. The midbrain ventrolateral periaqueductal gray (vlPAG) is known to be a crucial supraspinal region for initiating descending pain inhibition, but its role in neuropathic pain remains unclear. Therefore, here we examined neuroplastic changes in the vlPAG of midbrain slices isolated from neuropathic rats induced by L5/L6 spinal nerve ligation (SNL) via electrophysiological and neurochemical approaches. Significant mechanical hypersensitivity was induced in rats 2 d after SNL and lasted for >14 d. Compared with the sham-operated group, vlPAG slices from neuropathic rats 3 and 10 days after SNL displayed smaller EPSCs with prolonged latency, less frequent and smaller miniature EPSCs, higher paired-pulse ratio of EPSCs, smaller AMPAR-mediated EPSCs, smaller AMPA currents, greater NMDAR-mediated EPSCs, greater NMDA currents, lower AMPAR-mediated/NMDAR-mediated ratios, and upregulation of the NR1 and NR2B subunits, but not the NR2A, GluR1, or GluR2 subunits, of glutamate receptors. There were no significant differences between day 3 and day 10 neuropathic groups. These results suggest that SNL leads to hypoglutamatergic neurotransmission in the vlPAG resulting from both presynaptic and postsynaptic mechanisms. Upregulation of NMDARs might contribute to hypofunction of AMPARs via subcellular redistribution. Long-term hypoglutamatergic function in the vlPAG may lead to persistent reduction of descending pain inhibition, resulting in chronic neuropathic 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.