Both research papers read for this
week, Bessa et al and Santarelli et al, study how antidepressants work by
administering several different ones along with either MAM or irradiation on
some groups, respectively. They agree on the fact that stress is a trigger of
depression and reduces neurogenesis, and can lead to cell shrinkage in areas
such as the PFC and the hippocampus.
Both studies are based on common
ideas and use in fact common antidepressant drugs to test their ideas. For example, both use fluoxetine (serotonin
uptake inhibitor) and imipramine. In fact Bessa et al cites authors that have
studied serotonin such as Santarelli et al, but does not directly mention the
role of serotonin specifically.
In 2003, Santarelli et al
concluded that antidepressants increase neurogenesis, understanding it is the
factor on the mood improving actions of the drugs. Bessa in fact states Santarelli conclusion
but challenges it by administering some with MAM. He understands the behavior changes seen
after the drugs are administered occur independently of their ability to
stimulate hippocampal neurogenesis since they were observed for the group with
the MAM and the one without it. Instead,
he concluded the drugs had an effect of neuroplasticity and connectivity in the
hippocampus and PFC which lead to the behavior change.
The fact that Santarelli was focused
on looking at leads me to believe that there has to be a relationship between
these. Who knows if the growth of the
neurons are also involved in the synaptic plasticity and connections observed
by Bessa et al? I also wonder how this
works for anti anxiety drugs only , and if there is any difference from the combination
of both depression and anxiety tests?
No comments:
Post a Comment