ArticleCNS neuroscience & therapeutics2025
Upregulation of NR2B Subunits of NMDA Receptors in the Lateral Parabrachial Nucleus Contributes to Chronic Pancreatitis Pain.
Article in CNS neuroscience & therapeutics, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
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Who cites it
5 citing papers in PubMed.
- From Inflammation to Neuroplasticity: Molecular Mechanisms of Pain in Acute, Recurrent and Chronic Pancreatitis.International journal of molecular sciences · 2026Review
- Targeting N-methyl-D-aspartate 2B receptor in painful diabetic neuropathy - mechanisms, challenges, and emerging therapeutics.World journal of diabetes · 2026Review
- Lidocaine for Depressive Symptoms and Comorbid Pain: A Narrative Review of Mechanisms, Evidence, and Safety.Drug design, development and therapy · 2026Review
- Endothelin A receptor in nociceptors is essential for persistent mechanical pain in a chronic pancreatitis of mouse model.World journal of gastroenterology · 2025Article
- Navigating chronic pancreatitis pain: a pathophysiological and therapeutic overview.Frontiers in physiology · 2025Review
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Authors and funding
8 authors.
Funding
Abstract
aimsChronic pancreatitis (CP) is a localized or diffuse chronic progressive inflammation of the pancreas that can be caused by a variety of factors and is characterized by abdominal pain. However, the underlying mechanisms are poorly understood. Increasing evidence suggests that central sensitization plays a crucial role in the development of visceral pain, but the precise mechanisms of central neural processing remain unclear.
methodsCP was induced using repeated intraperitoneal injections of caerulein in mice. Neurospecific anterograde tracing was achieved using herpes simplex virus type 1 (HSV-1). Fiber photometry was used to assess neuronal activity. Optogenetic, chemogenetic, or pharmacological approaches were applied to manipulate the lateral parabrachial nucleus (LPB) glutamatergic neurons. The abdominal withdrawal threshold (AWT) was measured to evaluate the CP pain. A glutamate sensor was used to detect glutamate release in the LPB.
resultsIn the present study, we demonstrated that glutamatergic neurons in the LPB are activated in CP mice, leading to the development of CP pain. Notably, glutamatergic release is increased in the LPB, and the increased release primarily mediates CP pain by binding to the N-methyl-D-aspartate (NMDA) receptor rather than α-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid (AMPA) receptors. Specifically, this process involves the binding of the N-Methyl-D-Aspartate Receptor Subunit 2B (NR2B) in the LPB, leading to the development of CP pain.
conclusionsThis study identified the NR2B subunits of NMDA receptors in the LPB as playing a critical role in the regulation of CP pain.
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