TrkB-deficient mice show diminished phase shifts of the circadian activity rhythm in response to light. Academic Article

abstract

• Brain-derived neurotrophic factor (BDNF) has been implicated in the mechanism underlying the circadian sensitivity of the clock in the hypothalamic suprachiasmatic nucleus (SCN) to the phase-shifting effects of light. In the present study, we examined the role of the cognate receptor for BDNF, the TrkB tyrosine kinase, in the photic regulation of the SCN clock by determining whether the phase-shifting action of light is impaired in mice with targeted mutation of the TrkB gene. In comparison with wild-type littermates, heterozygous TrkB mutant mice (trkB(+/-)) showed marked reductions in SCN and cortical levels of this neurotrophin receptor that were accompanied by decreases in the amplitude of light-induced phase shifts during the subjective night. These results provide further evidence indicating that BDNF-mediated signaling through the TrkB receptor is an important process in the gating of SCN responses to light and its phase-shifting effects on circadian rhythms.

authors

• Allen, Gregg
• Earnest, David

published proceedings

• Neurosci Lett

author list (cited authors)

• Allen, G. C., Qu, X., & Earnest, D. J.

citation count

• 32

complete list of authors

• Allen, Gregg C||Qu, Xiaoyu||Earnest, David J

publication date

• January 2005

publisher

• Elsevier  Publisher

published in

• NEUROSCIENCE LETTERS  Journal

keywords

• Animals
• Biological Clocks
• Brain-derived Neurotrophic Factor
• Cerebral Cortex
• Circadian Rhythm
• Down-Regulation
• Female
• Light
• Male
• Mice
• Mice, Knockout
• Photic Stimulation
• Receptor, TrkB
• Suprachiasmatic Nucleus
• Time Factors

PubMed Central ID

• 15781149

Digital Object Identifier (DOI)

• 10.1016/j.neulet.2004.12.023

start page

• 150

end page

• 155

volume

• 378

issue

• 3

URL

• http://dx.doi.org/10.1016/j.neulet.2004.12.023