Journal
ACTA PHARMACOLOGICA SINICA
Volume 33, Issue 1, Pages 5-10Publisher
NATURE PUBLISHING GROUP
DOI: 10.1038/aps.2011.184
Keywords
obstructive sleep apnea; intermittent hypoxia; synaptic plasticity; long-term potentiation; brain-derived neurotrophic factor
Funding
- Research Grants Council of Hong Kong, China [478308]
Ask authors/readers for more resources
Obstructive sleep apnea (OSA) is well known for its metabolic as well as neurobehavioral consequences. Chronic intermittent hypoxia (IH) is a major component of OSA. In recent years, substantial advances have been made in elucidating the cellular and molecular mechanisms underlying the effect of chronic IH on neurocognitive functions, many of which are based on studies in animal models. A number of hypotheses have been put forward to explain chronic IH-induced neurological dysfunctions. Among these, the roles of oxidative stress and apoptosis-related neural injury are widely accepted. Here, focusing on results derived from animal studies, we highlight a possible role of reduced expression of brain-derived neurotrophic factor (BDNF) in causing impairment in long-term synaptic plasticity and neurocognitive functions during chronic IH. The possible relationship between BDNF and previous findings on this subject will be elucidated.
Authors
I am an author on this paper
Click your name to claim this paper and add it to your profile.
Reviews
Recommended
No Data Available