THURSDAY, Aug. 24 (HealthDay News) -- Transgenic brain-derived neurotrophic factor (BDNF) over-expression increases anxiety, which may be mediated by increased spine density in the amygdala. But it also reduces depression, according to an animal study published online Aug. 21 in the Proceedings of the National Academy of Sciences Early Edition.
Susumu Tonegawa, Ph.D., of the Massachusetts Institute of Technology in Cambridge, and colleagues created genetically-modified mice producing high levels of BDNF in excitatory neurons. Previous research had suggested that neurotrophins such as BDNF may resolve the brain remodeling that occurs after prolonged and severe stress, according to the authors.
The researchers found that the mice showed higher levels of anxiety, even in the absence of chronic stress, as well as enhanced synaptic connectivity in the basolateral amygdala. The high levels of BDNF also acted as an antidepressant and protected mice from chronic stress-induced hippocampal atrophy.
"These results with BDNF suggest that, unless antidepressants have a differential effect in the hippocampus and amygdala, they would not be expected to be effective anxiolytic drugs," the authors wrote. "Consistent with this view, some clinical reports indicate that anxiety actually increases upon initiation of certain types of antidepressant treatments. Based on our cellular data, we suggest that differences in the action of such drugs on depression versus anxiety are a consequence of their differential actions on the hippocampus and amygdala."
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