ArticleMolecular brain2024
Spared nerve injury leads to reduced activity of neurons projecting from the ventrolateral periaqueductal gray to the locus coeruleus.
Article in Molecular brain, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
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Who cites it
3 citing papers in PubMed.
- Glutamatergic Periaqueductal Gray Projections to the Locus Coeruleus Orchestrate Adaptive Arousal States in Threatening Contexts.Neuroscience bulletin · 2026Article
- Ginger Moxibustion Activates TRPV1 to Modulate the Locus Coeruleus-Spinal Cord-Uterus Pathway and Alleviates Primary Dysmenorrhea in Rats.Journal of pain research · 2025Article
- Physiological actions of a humanized P2X4 scFv on peripheral and central neurons in male mice with neuropathic pain.Neurobiology of pain (Cambridge, Mass.)Article
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Authors and funding
3 authors.
Funding
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Abstract
The ventrolateral periaqueductal gray (vlPAG) serves as a central hub for descending pain modulation. It receives upstream projections from the medial prefrontal cortex (mPFC) and the ventrolateral orbitofrontal cortex (vlOFC), and projects downstream to the locus coeruleus (LC) and the rostroventral medulla (RVM). While much research has focused on upstream circuits and the LC-RVM connection, less is known about the PAG-LC circuit and its involvement in neuropathic pain. Here we examined the intrinsic electrophysiological properties of vlPAG-LC projecting neurons in Sham and spared nerve injury (SNI) operated mice. Injection of the retrotracer Cholera Toxin Subunit B (CTB-488) into the LC allowed the identification of LC-projecting neurons in the vlPAG. Electrophysiological recordings from CTB-488 positive cells revealed that both GABAergic and glutamatergic cells that project to the LC exhibited reduced intrinsic excitability after peripheral nerve injury. By contrast, CTB-488 negative cells did not exhibit alterations in firing properties after SNI surgery. An SNI-induced reduction of LC projecting cells was confirmed with c-fos labeling. Hence, SNI induces plasticity changes in the vlPAG that are consistent with a reduction in the descending modulation of pain signals.
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