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"This disparity between simple pharmacological effects and clinical experience might be due to the time it takes for serotonin axons to grow," Koliatsos said.

"For the patient, this hypothesis provides more tangible evidence of a real effect in the brain," he added.

In the Hopkins study, Koliatsos and his team gave either the selective serotonin reuptake inhibitor fluoxetine (Prozac), the selective serotonin reuptake enhancer tianeptine (a drug approved only for human use in France) or the selective norepineprine reuptake inhibitor desipramine, a so-called tricyclic antidepressant, to groups of rats for four weeks and studied anatomical patterns of serotonin stimulation on various parts of the brain. The results showed that fluoxetine and tianeptine, but not desipramine, increased the density of serotonin axons in the frontal and parietal neocortex and certain limbic cortical and subcortical areas.

One possible explanation for this action is the brain-derived growth factor (BDNF). BDNF is regulated by levels of serotonin and is known to be a prime candidate for causing serotonin axon growth, Koliatsos said.

In general, the relationships between brain serotonin concentrations and BDNF expression are very complex, but previous studies have suggested that both higher (such as caused by serotonin reuptake inhibitors) and lower (such as effected by tianeptine) concentrations of free serotonin might induce BDNF expression in such brain regions as the frontal and parietal cortex.

The researchers caution that since a previous study failed to show a correlation between tianeptine treatment and BDNF levels, further investigation of the complex regulations of BDNF by antidepressants is needed.

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Contact: Eric Vohr
evohr1@jhmi.edu
410-955-8665
Johns Hopkins Medical Institutions
19-Dec-2005