The articles this week looked more closely at schizophrenia
like symptoms at a developmental perspective. Burrow et al takes an interesting
approach for supporting the glutamate hypothesis in schizophrenia by using the
environment enrichment paradigm. I had
heard of the environment enrichment paradigm when looking an synaptic
plasticity and memory enhancement, but I definitely think this was a valid
model while looking more at depth for schizophrenic symptoms. It was also clear
to me that the upregulations of NMDAR are only enhanced in these environments. Burrow et al. experiments on many behavioral
aspects of the environment enrichment which allows us to examine the need of
the NMDAR in this paradigm. Each shows a strong significance, whether it was
the behavioral test or the effects of hippocampal BDNF, only supporting that
this is a positive influence for the model. It also helps that the researchers examined
the rodents at an age where these symptoms of schizophrenia would begin to
develop since we’ve already observed what the effects would be like in the
embryonic stages. It would, however, be interesting to compare different groups
ranging at different ages of the rodents to see if there are any changes with
the expression.
The article contains strong data which could ultimate help
take a step further for clinical investigations in humans with these symptoms
at an early age. If we were ethically able to observe the NMDA receptors by
using the environment enrichment than we could possibly see some sort of
mediation for the behavioral impairments of schizophrenia. If anything, if we
are able to understand the use of mGlu5 and its modulation with NMDAR, then
perhaps there will be otherwise to upregulate this expression for patients with
schizophrenia. Also continuing research for the glutamate hypothesis could
become some sort of therapeutic way for treating this disorder.
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