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PMID:10801976

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Citation

Saegusa, H, Kurihara, T, Zong, S, Minowa, O, Kazuno, A, Han, W, Matsuda, Y, Yamanaka, H, Osanai, M, Noda, T and Tanabe, T (2000) Altered pain responses in mice lacking alpha 1E subunit of the voltage-dependent Ca2+ channel. Proc. Natl. Acad. Sci. U.S.A. 97:6132-7

Abstract

alpha(1) subunit of the voltage-dependent Ca(2+) channel is essential for channel function and determines the functional specificity of various channel types. alpha(1E) subunit was originally identified as a neuron-specific one, but the physiological function of the Ca(2+) channel containing this subunit (alpha(1E) Ca(2+) channel) was not clear compared with other types of Ca(2+) channels because of the limited availability of specific blockers. To clarify the physiological roles of the alpha(1E) Ca(2+) channel, we have generated alpha(1E) mutant (alpha(1E)-/-) mice by gene targeting. The lacZ gene was inserted in-frame and used as a marker for alpha(1E) subunit expression. alpha(1E)-/- mice showed reduced spontaneous locomotor activities and signs of timidness, but other general behaviors were apparently normal. As involvement of alpha(1E) in pain transmission was suggested by localization analyses with 5-bromo-4-chloro-3-indolyl beta-d-galactopyranoside staining, we conducted several pain-related behavioral tests using the mutant mice. Although alpha(1E)+/- and alpha(1E)-/- mice exhibited normal pain behaviors against acute mechanical, thermal, and chemical stimuli, they both showed reduced responses to somatic inflammatory pain. alpha(1E)+/- mice showed reduced response to visceral inflammatory pain, whereas alpha(1E)-/- mice showed apparently normal response compared with that of wild-type mice. Furthermore, alpha(1E)-/- mice that had been presensitized with a visceral noxious conditioning stimulus showed increased responses to a somatic inflammatory pain, in marked contrast with the wild-type mice in which long-lasting effects of descending antinociceptive pathway were predominant. These results suggest that the alpha(1E) Ca(2 +) channel controls pain behaviors by both spinal and supraspinal mechanisms.

Links

PubMed PMC18570 Online version:10.1073/pnas.100124197

Keywords

Acetic Acid/toxicity; Animals; Anxiety/genetics; Calcium/physiology; Calcium Channels, R-Type/deficiency; Calcium Channels, R-Type/genetics; Calcium Channels, R-Type/physiology; Exploratory Behavior; Fear; Formaldehyde/toxicity; Gene Expression; Inflammation/chemically induced; Inflammation/physiopathology; Ion Transport; Mice; Mice, Inbred C57BL; Mice, Knockout; Nociceptors/physiopathology; Pain/physiopathology; Pain Insensitivity, Congenital/etiology; Pain Insensitivity, Congenital/genetics; Pain Insensitivity, Congenital/physiopathology; Pain Measurement; Peritonitis/chemically induced; Peritonitis/physiopathology; Recombinant Fusion Proteins/physiology; Reverse Transcriptase Polymerase Chain Reaction; Startle Reaction/genetics

Significance

Annotations

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

MOUSE:CAC1E

acts_upstream_of_or_within

GO:0007626: locomotory behavior

ECO:0000315: mutant phenotype evidence used in manual assertion

MGI:MGI:2179732

P

Seeded From UniProt

complete

MOUSE:CAC1E

acts_upstream_of_or_within

GO:0048266: behavioral response to pain

ECO:0000315: mutant phenotype evidence used in manual assertion

MGI:MGI:2179732

P

Seeded From UniProt

complete

MOUSE:CAC1E

acts_upstream_of_or_within

GO:0042596: fear response

ECO:0000315: mutant phenotype evidence used in manual assertion

MGI:MGI:2179732

P

Seeded From UniProt

complete


See also

References

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