Sunday, April 5, 2015

Burrow et al.

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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