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Related Concept Videos

Nociception01:44

Nociception

Nociception—the ability to feel pain—is essential for an organism’s survival and overall well-being. Noxious stimuli such as piercing pain from a sharp object, heat from an open flame, or contact with corrosive chemicals are first detected by sensory receptors, called nociceptors, located on nerve endings. Nociceptors express ion channels that convert noxious stimuli into electrical signals. When these signals reach the brain via sensory neurons, they are perceived as pain. Thus, pain helps the...
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Postsynaptic Potential (PSP)01:32

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Related Experiment Video

Updated: Jun 30, 2026

A Pipeline to Investigate the Structures and Signaling Pathways of Sphingosine 1-Phosphate Receptors
12:27

A Pipeline to Investigate the Structures and Signaling Pathways of Sphingosine 1-Phosphate Receptors

Published on: June 8, 2022

Sphingosine 1-phosphate modulates spinal nociceptive processing.

Ovidiu Coste1, Christian Brenneis, Bona Linke

  • 1Pharmazentrum Frankfurt, ZAFES, Institute for Clinical Pharmacology, Klinikum der Johann Wolfgang Goethe-Universität Frankfurt, Theodor-Stern-Kai 7, 60590 Frankfurt, Germany.

The Journal of Biological Chemistry
|September 23, 2008
PubMed
Summary
This summary is machine-generated.

Sphingosine 1-Phosphate (S1P) levels decrease during pain. This study shows S1P modulates pain by inhibiting neuronal cyclic AMP (cAMP) synthesis in the spinal cord.

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Area of Science:

  • Neuroscience
  • Pain Research
  • Cellular Signaling

Background:

  • Sphingosine 1-Phosphate (S1P) is abundant in the central nervous system, but its role in neuronal function is largely unknown.
  • S1P influences various cellular processes, including apoptosis, differentiation, and migration.

Purpose of the Study:

  • To investigate the role of S1P in modulating pain perception and spinal nociceptive processing.
  • To determine the mechanism by which S1P affects neuronal activity related to pain.

Main Methods:

  • Measured S1P concentrations in cerebrospinal fluid of rats in pain models.
  • Utilized pharmacological inhibition of sphingosine kinases (SPHK) and SphK2 knockout mice.
  • Administered S1P and dihydro-S1P intrathecally and assessed nociceptive behavior.
  • Quantified cyclic AMP (cAMP) synthesis in spinal cord neurons using FRET and MELC techniques.

Main Results:

  • S1P concentrations were reduced in cerebrospinal fluid during acute and inflammatory pain.
  • Sphingosine kinase 2 (SphK2) knockout mice exhibited decreased pain sensitivity.
  • Intrathecal S1P and dihydro-S1P reduced nociceptive behavior and inhibited neuronal cAMP synthesis.
  • S1P specifically decreased cAMP synthesis in excitatory dorsal horn neurons, affecting NMDA receptor phosphorylation.

Conclusions:

  • S1P plays a significant role in modulating spinal nociceptive processing.
  • The mechanism involves the inhibition of neuronal cAMP synthesis by S1P.
  • Targeting the S1P pathway may offer new therapeutic strategies for pain management.