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S1→SDH pathway

Candidate: concept label1 source documents5 linked claims
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Aliases

descending neurons projecting directly from the primary somatosensory (S1) cortex to the SDH, S1→SDH neurons

Extracted Explainers

What the tool is doing

This pathway represents descending neurons from primary somatosensory cortex that project directly to the spinal dorsal horn and modulate Aβ fiber-driven allodynia-related signaling.

Source 1DOIPubMed

Resources required

Experimental interrogation in the paper required chemogenetic silencing and readouts of behavior and c-FOS expression.

Source 1DOIPubMed

What problem it solves

It helps explain how innocuous tactile input can be converted into neuropathic pain-related output after peripheral nerve injury.

Source 1DOIPubMed

What it does not solve

The abstract does not establish it as a standalone therapeutic modality or define all molecular components needed for intervention.

Source 1DOIPubMed

Alternatives

The abstract contrasts this descending pathway with local spinal circuit components including NpyP+ neurons and excitatory SDH neurons.

Source 1DOIPubMed

Evidence Snippets

chemogenetic silencing of descending neurons projecting directly from the primary somatosensory (S1) cortex to the SDH (S1→SDH neurons) suppresses both PNI-induced allodynia-like behavior and c-FOS expression
Evidence 1Source 1DOIPubMedprovenance

Supporting Sources

Linked Claims

Claim 1causal mechanismsupports2025Source 1DOIPubMed

Chemogenetic silencing of S1→SDH descending neurons suppresses peripheral nerve injury-induced allodynia-like behavior and superficial spinal dorsal horn c-FOS expression evoked during optogenetic activation of touch-sensing Aβ fibers in male rats.

Quoted textsource-backed
chemogenetic silencing of descending neurons projecting directly from the primary somatosensory (S1) cortex to the SDH (S1→SDH neurons) suppresses both PNI-induced allodynia-like behavior and c-FOS expression in the superficial SDH observed in male rats where touch-sensing Aβ fibers were optogenetically activated
Claim 2causal mechanismsupports2025Source 1DOIPubMed

Loss of inhibition from NpyP+ neurons induces Aβ fiber-derived allodynia, and this effect is attenuated by suppressing descending signaling from S1→SDH neurons to the spinal dorsal horn.

Quoted textsource-backed
loss of inhibition from NpyP+ neurons induced Aβ fiber-derived allodynia, which was attenuated by suppressing descending signaling from S1→SDH neurons to the SDH
Claim 3cellular connectivitysupports2025Source 1DOIPubMed

S1→SDH neurons are excitatory and preferentially target excitatory spinal dorsal horn neurons distributed across laminae I-V.

Quoted textsource-backed
S1→SDH neurons were excitatory and preferentially targeted excitatory SDH neurons (^S1→SDH neurons) broadly distributed across laminae I-V.
Claim 4circuit mechanismsupports2025Source 1DOIPubMed

Superficial lamina S1→SDH target neurons receive excitatory input from Aβ fibers and inhibitory input from NpyP+ spinal dorsal horn neurons.

Quoted textsource-backed
^S1→SDH neurons in the superficial laminae also received excitatory inputs from both Aβ fibers and inhibitory inputs from neuropeptide Y promoter active SDH neurons (NpyP+ neurons).
Claim 5therapeutic relevancesupports2025Source 1DOIPubMed

Silencing S1→SDH target neurons alleviates neuropathic allodynia, supporting the S1→SDH pathway as a potential therapeutic target.

Quoted textsource-backed
silencing ^S1→SDH neurons alleviated neuropathic allodynia. These findings identify a new corticospinal mechanism that contributes to Aβ fiber-mediated neuropathic allodynia and highlight the S1→SDH pathway as a potential therapeutic target.