Format

Send to

Choose Destination
See comment in PubMed Commons below
PLoS One. 2013;8(3):e59032. doi: 10.1371/journal.pone.0059032. Epub 2013 Mar 14.

Lack of tryptophan hydroxylase-1 in mice results in gait abnormalities.

Author information

1
Immune Disease Institute, Boston, Massachusetts, United States of America.

Erratum in

  • PLoS One. 2013;8(8). doi:10.1371/annotation/49097405-57c1-4923-875a-9216de91d230.

Abstract

The role of peripheral serotonin in nervous system development is poorly understood. Tryptophan hydroxylase-1 (TPH1) is expressed by non-neuronal cells including enterochromaffin cells of the gut, mast cells and the pineal gland and is the rate-limiting enzyme involved in the biosynthesis of peripheral serotonin. Serotonin released into circulation is taken up by platelets via the serotonin transporter and stored in dense granules. It has been previously reported that mouse embryos removed from Tph1-deficient mothers present abnormal nervous system morphology. The goal of this study was to assess whether Tph1-deficiency results in behavioral abnormalities. We did not find any differences between Tph1-deficient and wild-type mice in general motor behavior as tested by rotarod, grip-strength test, open field and beam walk. However, here we report that Tph1 (-/-) mice display altered gait dynamics and deficits in rearing behavior compared to wild-type (WT) suggesting that tryptophan hydroxylase-1 expression has an impact on the nervous system.

PMID:
23516593
PMCID:
PMC3597584
DOI:
10.1371/journal.pone.0059032
[Indexed for MEDLINE]
Free PMC Article
PubMed Commons home

PubMed Commons

0 comments
How to join PubMed Commons

    Supplemental Content

    Full text links

    Icon for Public Library of Science Icon for PubMed Central
    Loading ...
    Support Center