作者: M. W. Coryell , A. M. Wunsch , J. M. Haenfler , J. E. Allen , M. Schnizler
DOI: 10.1523/JNEUROSCI.0360-09.2009
关键词:
摘要: No animal models replicate the complexity of human depression. However, a number behavioral tests in rodents are sensitive to antidepressants and may thus tap important underlying biological factors. Such also offer best opportunity discover novel treatments. Here, we used several these test hypothesis that acid-sensing ion channel-1a (ASIC1a) might be targeted reduce Genetically disrupting ASIC1a mice produced antidepressant-like effects forced swim test, tail suspension following unpredictable mild stress. Pharmacologically inhibiting had test. The disruption were independent additive those commonly antidepressants. Furthermore, interfered with an biochemical marker depression, ability stress BDNF hippocampus. Restoring amygdala ASIC1a−/− viral vector reversed effects, suggesting is key site action depression-related behavior. These data consistent clinical studies emphasizing importance mood regulation, suggest antagonists effectively combat