ArticleBrain and behavior2025
A Neural Circuit From Paraventricular Nucleus of the Thalamus to the Nucleus Accumbens Mediates Inflammatory Pain in Mice.
Article in Brain and behavior, 2025. 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.
- Excitatory paraventricular thalamus-posterior insular cortex circuit mediates pain-anxiety comorbidity in diabetic neuropathy.Translational psychiatry · 2026Article
- Dorsal root ganglion neuromodulation restores accumbal gate to inhibit mechanical allodynia.The journal of headache and pain · 2026Article
- Anatomical mapping of whole-brain monosynaptic inputs to the orbitofrontal cortex.Frontiers in neural circuits · 2025Article
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14 authors.
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Abstract
backgroundPain is a prevalent comorbidity in numerous clinical conditions and causes suffering; however, the mechanism of pain is intricate, and the neural circuitry underlying pain in the brain remains incompletely elucidated. More research into the perception and modulation of pain within the central nervous system is essential. The nucleus accumbens (NAc) plays a pivotal role in the regulation of animal behavior, and extensive research has unequivocally demonstrated its significant involvement in the occurrence and development of pain. NAc receives projections from various other neural nuclei within the brain, including the paraventricular nucleus of the thalamus (PVT). In this experiment, we demonstrate that the specific glutamatergic neural circuit projection from PVT to NAc (PVT
methodsWe compared the difference in pain thresholds between complete Freund's adjuvant (CFA)-induced inflammatory pain models and controls. Then in a well-established mouse model of CFA-induced inflammatory pain, immunofluorescence staining was utilized to evaluate changes in c-Fos protein expression within PVT neurons. To investigate the role of PVT
resultsIn the mice with the inflammatory pain group, both the paw withdrawal latencies (PWLs) and paw withdrawal thresholds (PWTs) of the right hind paw were decreased compared to the control group. In addition, compared to the control group, CFA-induced inflammatory pain led to increased c-Fos protein expression in PVT, which means that some of the neurons in this area of the brain region have been activated. Following the injection of retrograde transport fluorescent-labeled virus into NAc, glutamatergic neurons projecting from the PVT to NAc were observed, confirming the projection relationship between PVT and NAc. In the experiments in optogenetic regulation, normal mice exhibited pain behavior when the PVT
conclusionsThe findings unveil a pivotal role of the PVT
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