The fragment of complement 3a lacking the primary 9 amino acids induces promoting activity on mouse voluntary running

Tohoku J Exp Med. 1999 Sep;189(1):21-7. doi: 10.1620/tjem.189.21.

Abstract

We have newly found that interleukin-2 (IL-2) increases mouse voluntary running 24 hours, but not 30 minutes, after the injection. We suspected that IL-2 induced a substance increasing the voluntary running for 24 hours after injection. Serum obtained from mice 24 hours after the IL-2 treatment was fractioned with the use of an ion-exchanger and an ultra-filtration method, and the amino acid sequence analysis indicated that the substance purified from the effective fraction was a fragment of mouse complement 3a (C3a) lacking the primary 9 amino acids. The 20 amino acid peptide synthesized according to the fragment showed the activity increasing the voluntary running, but the 20 amino acid peptide synthesized according to the C3a itself did not. The effect of the synthesized peptide was demuted by haloperidol but not by a specific dopamine 2 antagonist (-)sulpiride. The present findings clearly indicate that IL-2 produces the C3a fragment lacking the primary 9 amino acids which directly promotes the voluntary running, and that the effect of the fragment is mediated by an activity of haloperidol on the neurons, except for the dopamine 2 antagonism.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Amino Acid Sequence
  • Animals
  • Complement C3a / chemical synthesis
  • Complement C3a / pharmacology*
  • Interleukin-2 / pharmacology
  • Male
  • Mice
  • Molecular Sequence Data
  • Peptide Fragments / chemical synthesis
  • Peptide Fragments / pharmacology
  • Physical Exertion*
  • Running
  • Sequence Deletion
  • Structure-Activity Relationship

Substances

  • Interleukin-2
  • Peptide Fragments
  • Complement C3a