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PMID:12074836

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Citation

Saegusa, H, Matsuda, Y and Tanabe, T (2002) Effects of ablation of N- and R-type Ca(2+) channels on pain transmission. Neurosci. Res. 43:1-7

Abstract

Recently several mutant mouse lines lacking neuronal voltage-dependent Ca(2+) channels (VDCCs) have been established by the use of gene targeting in embryonic stem cells. Pain-related behaviors in Ca(v)2.2 (alpha(1B)) and Ca(v)2.3 (alpha(1E)) knockout mice were studied to gain further insight into the mechanism of pain transmission, where VDCCs are thought to play important roles. We review here the data from these recent studies. Ca(v)2.3-/- mice showed normal responses to acute painful stimuli, and reduced responses to the somatic inflammatory pain stimuli. Ca(v)2.3+/- mice exhibited reduced symptoms of visceral inflammatory pain. Ca(v)2.3-/- mice showed abnormal behavior related to the descending antinociceptive mechanism activated by the intraperitoneal injection of acetic acid. Ca(v)2.2-/- mice showed variable acute nociceptive responses depending on the mutant lines. However, all the lines of Ca(v)2.2-/- mice exhibited reduced responses in the phase 2 of the formalin test, suggesting a suppression of inflammatory pain. Furthermore Ca(v)2.2-/- mice showed markedly reduced neuropathic pain symptoms after spinal nerve ligation. Impaired antinociception, similar to that seen in the Ca(v)2.3-/- mice, was also observed in the Ca(v)2.2-/- mice. Therefore, it is suggested that these mutant mice could provide novel models to delineate the nociceptive and antinociceptive mechanisms.

Links

PubMed

Keywords

Acetic Acid/diagnostic use; Acetic Acid/pharmacology; Animals; Behavior, Animal/drug effects; Behavior, Animal/physiology; Calcium Channels, N-Type/deficiency; Calcium Channels, N-Type/genetics; Calcium Channels, R-Type/deficiency; Calcium Channels, R-Type/genetics; Central Nervous System/metabolism; Central Nervous System/physiopathology; Disease Models, Animal; Female; Hot Temperature/adverse effects; Inflammation/genetics; Inflammation/metabolism; Inflammation/physiopathology; Male; Mice; Mice, Knockout; Models, Neurological; Neural Pathways/metabolism; Neural Pathways/physiopathology; Neurons/metabolism; Nociceptors/drug effects; Nociceptors/metabolism; Pain/genetics; Pain/metabolism; Pain/physiopathology; Pain Measurement; Phenotype; Physical Stimulation; Synaptic Transmission/physiology

Significance

Annotations

Gene product Qualifier GO Term Evidence Code with/from Aspect Extension Notes Status

MOUSE:CAC1B

enables

GO:0005245: voltage-gated calcium channel activity

ECO:0000315: mutant phenotype evidence used in manual assertion

F

  • occurs_in:(CL:0000540)
  • occurs_in:(EMAPA:16668)

Seeded From UniProt

complete

MOUSE:CAC1B

acts_upstream_of_or_within

GO:0051924: regulation of calcium ion transport

ECO:0000315: mutant phenotype evidence used in manual assertion

P

  • regulates_o_occurs_in:(CL:0000540)
  • regulates_o_occurs_in:(EMAPA:16668)

Seeded From UniProt

complete

MOUSE:CAC1B

acts_upstream_of_or_within

GO:0048265: response to pain

ECO:0000315: mutant phenotype evidence used in manual assertion

P

Seeded From UniProt

complete

MOUSE:CAC1B

acts_upstream_of_or_within

GO:0070588: calcium ion transmembrane transport

ECO:0000315: mutant phenotype evidence used in manual assertion

P

  • occurs_in:(CL:0000540)
  • occurs_in:(EMAPA:16668)

Seeded From UniProt

complete

MOUSE:CAC1E

enables

GO:0005245: voltage-gated calcium channel activity

ECO:0000315: mutant phenotype evidence used in manual assertion

F

  • occurs_in:(CL:0000540)
  • occurs_in:(EMAPA:16668)

Seeded From UniProt

complete

MOUSE:CAC1E

acts_upstream_of_or_within

GO:0048265: response to pain

ECO:0000315: mutant phenotype evidence used in manual assertion

P

Seeded From UniProt

complete

MOUSE:CAC1E

acts_upstream_of_or_within

GO:0070588: calcium ion transmembrane transport

ECO:0000315: mutant phenotype evidence used in manual assertion

P

  • occurs_in:(CL:0000540)
  • occurs_in:(EMAPA:16668)

Seeded From UniProt

complete


See also

References

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