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Serotonin deficiency and prolonged bleeding in beige mice.

Abstract
Beige mice have been observed to bleed excessively from small wounds. Platelets obtained from these mice were deficient in adenine nucleotides and serotonin and in vivo uptake of labeled serotonin was impaired. Heterozygotes of beige and C57BL/6 mice have adenine nucleotide and serotonin levels comparable to control and do not manifest a bleeding tendency, consistent with the recessive mode of inheritance of the beige mouse syndrome. Morphologic confirmation of the observed biochemical defects was obtained by the demonstration that serotonin storage organelles were not observed in electron photomicrographs of beige mouse platelets. The demonstration that small doses of serotonin were effective in reversing the bleeding tendency in beige mice suggested a causal role for defective storage and release of endogenous serotonin as the basis for the bleeding tendency, acting either independently or synergistically with impaired release of adenine nucleotides.
AuthorsJ M Holland
JournalProceedings of the Society for Experimental Biology and Medicine. Society for Experimental Biology and Medicine (New York, N.Y.) (Proc Soc Exp Biol Med) Vol. 151 Issue 1 Pg. 32-9 (Jan 1976) ISSN: 0037-9727 [Print] United States
PMID1250853 (Publication Type: Journal Article, Research Support, U.S. Gov't, Non-P.H.S.)
Chemical References
  • Adenine Nucleotides
  • Serotonin
Topics
  • Adenine Nucleotides (blood, deficiency)
  • Animals
  • Blood Coagulation Disorders (metabolism, pathology, therapy)
  • Blood Platelets (metabolism, pathology)
  • Chediak-Higashi Syndrome (blood, metabolism, pathology)
  • Disease Models, Animal
  • Mice
  • Mice, Inbred C57BL
  • Mice, Inbred Strains
  • Mutation
  • Serotonin (blood, deficiency, therapeutic use)

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