In the April 18 issue of Science, scientists from the Scuola Normale Superiore in Pisa, Italy and the Neuroscience Centre at the University of Helsinki, Finland, provide new information about the mechanism of action of antidepressant drugs.
In addition, the study suggests that antidepressants could also be used for the treatment of amblyopia. However, to produce a functional effect, antidepressant treatment also seems to require environmental stimuli, such as rehabilitation or therapy
According to Professor Eero Castrén at the University of Helsinki, the original objective of the study was to learn more about why the antidepressant effect of fluoxetine (also known as Prozac) and other selective serotonin reuptake inhibitors develops so slowly, many weeks after starting treatment.
Castrén’s research group has approached this question by examining the growth factor, brain-derived neurotrophic factor (BDNF), which influences plasticity of the nervous system or in other words, the ability of brain cells to change their structure or function in response to stimuli. Antidepressants seem to act through BDNF, thus enhancing the plasticity of the nervous system, at least in certain brain areas. However, it has been unclear how antidepressant-induced increases in BDNF could relieve depression.
Neuronal plasticity of the developing visual cortex has been well characterised. Therefore, this classical model of the visual cortex was utilised to examine the effect of fluoxetine on neuronal plasticity, although there was previously no evidence that antidepressants would act on the visual system. During early childhood, if one eye remains weaker than the other eye, the neuronal connections of the stronger eye take over the visual cortex while the connections of the weaker eye retract. During a critical period of early childhood, neuronal connections are in a highly plastic state, and the vision of the weaker eye can be strengthened by covering the better eye, thus reinforcing the connections of the weaker eye to the visual cortex. In adolescence however, after the critical period has closed, plasticity is reduced and covering the better eye no longer strengthens the connections of the weaker eye which remains poor in vision throughout adulthood.