BDNF vs. serotonin in depression theory

highlighted by the discovery that stress can decrease the expression of brain-derived neurotrophic factor and lead to atrophy of these same populations of stressvulnerable hippocampal neurons. The possibility that the decreased size and impaired function of these neurons may be involved in depression is supported by recent clinical imaging studies, which demonstrate a decreased volume of certain brain structures. These findings constitute the framework for an updated molecular and cellular hypothesis of depression, which posits that stressinduced vulnerability and the therapeutic action of antidepressant treatments occur via intracellular mechanisms that decrease or increase, respectively, neurotrophic factors necessary for the survival and function of particular 

neurons. 

 you all knew that the hippocampus is associated with learning and memory, but it is ALSO associated with depression. Or, more specifically, withantidepressants. We used to think that antidepressants worked because they increased the neurotransmitter serotonin in the brain. But there was a disconnect between the way the drugs were supposed to work and the onset of the actual antidepressant effects. Traditional antidepressants like Prozac produce peak serotonin levels in the brain in within about 6-8 hours. But the antidepressant effects take longer. WAY longer, up to several weeks. So if the increases in serotonin themselves weren't causing the antidepressant effects, what was?

Well, it turns out that, if you treat an animal with a drug like Prozac for a few weeks, long enough to get a clinical effect in humans, you also get neurogenesis in the hippocampus, along with increases in BDNF. So the idea is that, somehow, antidepressants increase BDNF, which helps to increase neurogenesis, and this produces antidepressant effects.