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Effects of ablation of N- and R-type Ca(2+) channels on pain transmission

Hironao Saegusa1, Yoshihiro Matsuda, Tsutomu Tanabe

  • 1Department of Pharmacology and Neurobiology, Graduate School of Medicine, Tokyo Medical and Dental University, and CREST, Japan Science and Technology Corporation, Tokyo, Japan.

Neuroscience Research
|June 21, 2002
PubMed

Insights

Mice lacking voltage-dependent calcium channels (VDCCs) show altered pain responses. Gene-targeted knockout mice reveal insights into pain transmission and antinociceptive mechanisms, offering new models for pain research.

Area of Science:

  • Neuroscience
  • Pharmacology
  • Genetics

Background:

  • Voltage-dependent calcium channels (VDCCs) are crucial for neuronal function and pain signaling.
  • Mutant mouse lines lacking specific VDCC subtypes (Ca(v)2.2 and Ca(v)2.3) have been generated using gene targeting.
  • Understanding the role of these channels in pain is essential for developing novel analgesics.

Purpose of the Study:

  • To investigate the role of Ca(v)2.2 and Ca(v)2.3 channels in pain transmission and modulation.
  • To analyze pain-related behaviors in knockout mice lacking these specific VDCCs.
  • To evaluate the utility of these mutant mice as models for studying nociception and antinociception.

Main Methods:

  • Generation of gene-targeted embryonic stem cells to create knockout mice for Ca(v)2.2 and Ca(v)2.3.
  • Assessment of acute nociception, inflammatory pain (somatic and visceral), and neuropathic pain in wild-type and mutant mice.
  • Evaluation of descending antinociceptive mechanisms using behavioral tests (e.g., acetic acid injection, formalin test).

Main Results:

  • Ca(v)2.3 knockout mice exhibited normal acute pain responses but reduced somatic inflammatory pain and visceral pain.
  • Ca(v)2.2 knockout mice showed reduced inflammatory pain (formalin test) and significantly diminished neuropathic pain.
  • Both Ca(v)2.2 and Ca(v)2.3 deficient mice displayed impaired antinociception, indicating a role in descending pain inhibitory pathways.

Conclusions:

  • Mice lacking Ca(v)2.2 or Ca(v)2.3 channels display distinct and overlapping alterations in pain processing.
  • These mutant mouse lines serve as valuable models for dissecting the complex mechanisms of nociception and antinociception.
  • The findings highlight the therapeutic potential of targeting VDCCs for pain management.

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