ArticleCell reports2025
The dorsal column nuclei scale mechanical sensitivity in naive and neuropathic pain states.
Article in Cell reports, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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Who cites it
7 citing papers in PubMed.
- Neural Mechanisms and Brain Alterations in Orofacial Pain: A Narrative Review of Human Neuroimaging.Diagnostics (Basel, Switzerland) · 2026Review
- Spinal signatures of entrenched and treated neuropathic pain in male mice.Nature communications · 2026Article
- Hierarchical Studies in TRAP2 Mice Demonstrate that Neuronal Activation and Mitochondrial Networks Integration Constitute the Key Mechanism Underlying Painful Syncope.Neuroscience bulletin · 2026Article
- Dorsal root ganglion neuromodulation restores accumbal gate to inhibit mechanical allodynia.The journal of headache and pain · 2026Article
- Thalamo-hippocampal pathway determines aggression and self-harm.Science advances · 2025Article
- The dorsal column nuclei encode and transmit the network signatures of mechanical allodynia.Cell reports · 2025Article
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Abstract
During pathological conditions, tactile stimuli can aberrantly engage nociceptive pathways leading to the perception of touch as pain, known as mechanical allodynia. The brain stem dorsal column nuclei integrate tactile inputs, yet their role in mediating tactile sensitivity and allodynia remains understudied. We found that gracile nucleus (Gr) inhibitory interneurons and thalamus-projecting neurons are differentially innervated by primary afferents and spinal inputs. Functional manipulations of these distinct Gr neuronal populations bidirectionally shifted tactile sensitivity but did not affect noxious mechanical or thermal sensitivity. During neuropathic pain, Gr neurons exhibited increased sensory-evoked activity and asynchronous excitatory drive from primary afferents. Silencing Gr projection neurons or activating Gr inhibitory neurons in neuropathic mice reduced tactile hypersensitivity, and enhancing inhibition ameliorated paw-withdrawal signatures of neuropathic pain and induced conditioned place preference. These results suggest that Gr activity contributes to tactile sensitivity and affective, pain-associated phenotypes of mechanical allodynia.
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