Week 1 Articles

Reading these articles in light of one another clearly demonstrated the complexity of how scientific knowledge evolves over time.  Santarelli asked the question of whether an increase in neurogenesis is mechanistically required for antidepressants to take action, and therefore proceeded to experimentally test the efficacy of antidepressants under manipulation of neurogenic capacity.  Six years later Bessa explored the context that neurogenesis is not critical to antidepressant efficacy, and that synaptic remodeling and neuronal plasticity underlie such ramifying behavioral effects.  Across both studies it is agreed that pharmacological intervention has direct physiological effects in the hippocampus, and causes the reversal of symptomatic depression.  Santarelli concludes that antidepressant induced behavioral remediation will not be obtained in the absence of proliferating progenitor cells, which is backed by irradiation experimentation in the hippocampus.  Bessa provided evidence in favor of antidepressant efficacy in coadministration with the antiproliferation agent MAM, to block neurogenesis, and shift focus to how synaptic plasticity is the critical factor at play.  Bessa was successful in discrediting the claims made in the Santarelli article, providing clearly contrasting data, and after reading the two I felt this needed to be done.  However, being that neurogenesis and synaptic plasticity are self conceived processes regarding similar cognitive function, I wonder why instead of discrediting neurogenesis in terms of causation, one wouldn’t focus on neurogenesis for all its correlations to the mechanisms at hand.  For example, Bessa demonstrated that the increased latency times to feed resulting from exposure to CMS was reversed by antidepressant drugs, but also demonstrated that the efficacy was increased when given in co-administration with MAM.  Why the observed increase?  Also Bessa claimed that neurons produced in response to antidepressant help modulate anxiety by growing into pre-established neuronal networks controlling behavior.  I wonder if the growth of neurons produced by antidepressant induced neurogenesis is conditioned by the environment they are born into, and does synaptic plasticity vary based on the age of the neuron?  These facts indicate to me that neurogenesis is a specialized process that should be explored as a key function in the fight against depressive disorders in definitive conjunction to neuronal plasticity.  Previous studies should be examined from more collaborative than competitive standpoints!