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Reduced nociceptive behavior in islet amyloid polypeptide (amylin) knockout mice
S Gebre-Medhin1, H Mulder, Y Zhang
1Department of Medical Biochemistry, Göteborg University, Box 440 SE 405 30, Göteborg, Sweden. samuel.gebre-medlem.gu.se
Brain Research. Molecular Brain Research
|December 5, 1998
Summary
Islet amyloid polypeptide (IAPP), also known as amylin, plays a role in pain perception. Mice lacking IAPP showed a reduced pain response, suggesting it acts in sensory neurons to promote pain.
Area of Science:
- Neuroscience
- Pain research
- Molecular biology
Background:
- Islet amyloid polypeptide (IAPP), or amylin, is primarily produced by pancreatic beta cells.
- IAPP has also been identified in primary sensory neurons in rats.
- The role of IAPP in sensory neurons and pain pathways is not fully understood.
Purpose of the Study:
- To investigate the expression and function of IAPP in murine sensory neurons.
- To determine the role of IAPP in pain perception using a knockout mouse model.
- To explore the potential involvement of IAPP in inflammatory pain.
Main Methods:
- Generation of mice with a null mutation in the IAPP gene.
- Analysis of IAPP distribution in the spinal cord and dorsal root ganglion.
- Assessment of pain response using the paw formalin test.
- Evaluation of adjuvant-induced joint inflammation.
Main Results:
- Murine IAPP is expressed in sensory neurons, co-localizing with calcitonin gene-related peptide.
- IAPP-mutant mice exhibited a significantly reduced pain response in the formalin test.
- No alterations were observed in joint inflammation in IAPP-mutant mice.
Conclusions:
- IAPP is present in sensory neurons in mice, similar to rats.
- IAPP appears to have a pro-nociceptive function, contributing to pain signaling.
- The pro-nociceptive role of IAPP is likely independent of peripheral inflammatory processes.