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BDNF regulates eating behavior and locomotor activity in mice
Author(s) -
Kernie Steven G.,
Liebl Daniel J.,
Parada Luis F.
Publication year - 2000
Publication title -
the embo journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 7.484
H-Index - 392
eISSN - 1460-2075
pISSN - 0261-4189
DOI - 10.1093/emboj/19.6.1290
Subject(s) - tropomyosin receptor kinase b , biology , neurotrophic factors , neurotrophin , brain derived neurotrophic factor , endocrinology , medicine , tropomyosin receptor kinase c , phenotype , tropomyosin receptor kinase a , central nervous system , neuroscience , receptor , gene , genetics , growth factor , platelet derived growth factor receptor
Brain‐derived neurotrophic factor (BDNF) was studied initially for its role in sensory neuron development. Ablation of this gene in mice leads to death shortly after birth, and abnormalities have been found in both the peripheral and central nervous systems. BDNF and its tyrosine kinase receptor, TrkB, are expressed in hypothalamic nuclei associated with satiety and locomotor activity. In heterozygous mice, BDNF gene expression is reduced and we find that all heterozygous mice exhibit abnormalities in eating behavior or locomotor activity. We also observe this phenotype in independently derived inbred and hybrid BDNF mutant strains. Infusion with BDNF or NT4/5 can transiently reverse the eating behavior and obesity. Thus, we identify a novel non‐neurotrophic function for neurotrophins and indicate a role in behavior that is remarkably sensitive to alterations in BDNF activity.