Conceptos Básicos
Endogenous κ-opioid signaling pathway involving cerebrospinal fluid-contacting neurons and prodynorphin-expressing cells regulates ependymal cell proliferation and scar formation after spinal cord injury.
Resumen
The article explores the mechanisms underlying the regulation of ependymal cell proliferation and scar formation in the spinal cord following injury. It uncovers an endogenous κ-opioid signaling pathway that controls ependymal cell proliferation.
Key highlights:
- Ependymal cells undergo massive proliferation and differentiation into astroglia after certain spinal cord injuries, becoming a core component of the scar tissue.
- The authors detected the expression of the κ-opioid receptor OPRK1 in a cell type called cerebrospinal fluid-contacting neurons (CSF-cNs).
- They also discovered a neighboring cell population that expresses the cognate ligand prodynorphin (PDYN).
- Whereas κ-opioids are typically considered inhibitory, they excite CSF-cNs to inhibit ependymal proliferation.
- Systemic administration of a κ-antagonist enhances ependymal proliferation in uninjured spinal cords in a CSF-cN-dependent manner.
- A κ-agonist impairs ependymal proliferation, scar formation, and motor function following injury.
- The findings suggest a paracrine signaling pathway in which PDYN+ cells tonically release κ-opioids to stimulate CSF-cNs and suppress ependymal proliferation, revealing an endogenous mechanism and potential pharmacological strategy for modulating scarring after spinal cord injury.
Estadísticas
After certain spinal cord injuries, ependymal cells undergo massive proliferation and differentiation into astroglia, becoming a core component of the scar tissue.
Systemic administration of a κ-antagonist enhances ependymal proliferation in uninjured spinal cords in a CSF-cN-dependent manner.
A κ-agonist impairs ependymal proliferation, scar formation, and motor function following injury.
Citas
"Whereas κ-opioids are typically considered inhibitory, they excite CSF-cNs to inhibit ependymal proliferation."
"The findings suggest a paracrine signaling pathway in which PDYN+ cells tonically release κ-opioids to stimulate CSF-cNs and suppress ependymal proliferation, revealing an endogenous mechanism and potential pharmacological strategy for modulating scarring after spinal cord injury."