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TNAP and Pain Control.

Sarah E Street1, Nathaniel A Sowa

  • 1Department of Cell Biology and Physiology, University of North Carolina at Chapel Hill, Chapel Hill, NC, USA, Sarah_street@med.unc.edu.

Sub-Cellular Biochemistry
|July 30, 2015
PubMed
Summary
This summary is machine-generated.

New research explores how tissue non-specific alkaline phosphatase (TNAP) and other ectonucleotidases can generate adenosine, a natural pain inhibitor. This offers potential for novel chronic pain therapeutics with fewer side effects.

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Area of Science:

  • Neuroscience
  • Pharmacology
  • Biochemistry

Background:

  • Chronic pain is a widespread, costly disease with inadequate treatments.
  • Current pain therapies often have limited efficacy and significant side effects.
  • Adenosine is a known pain inhibitor, but its broad receptor distribution limits its use.

Purpose of the Study:

  • To investigate the role of ectonucleotidases, specifically tissue non-specific alkaline phosphatase (TNAP), in generating endogenous adenosine.
  • To explore the potential of targeting these enzymes for novel chronic pain therapies.

Main Methods:

  • Review of existing literature on adenosine signaling and ectonucleotidases in nociceptive circuits.
  • Discussion of the biochemical pathways involving 5' ectonucleotidases and nucleotide hydrolysis.

Main Results:

  • Ectonucleotidases, including TNAP, can convert pronociceptive nucleotides (e.g., ATP) into antinociceptive adenosine in the spinal cord.
  • This enzymatic activity occurs within the nociceptive circuitry of the dorsal spinal cord.

Conclusions:

  • TNAP and other ectonucleotidases represent promising therapeutic targets for chronic pain management.
  • Targeting these enzymes could lead to new analgesics with improved efficacy and reduced side effects.