|
Description:
|
|
We’re changing things up this week at On Your Mind and taking a more critical look at a paper that we’ve developed strong opinions about. From the unnecessarily long title to the unfortunate lack of controls, we’ve got alot to say about “Reelin, an extracellular matrix protein linked to early onset psychiatric diseases, drives postnatal development of the prefrontal cortex via GluN2B-NMDARs and the mTOR pathway” by Iafrati et al. (doi: 10.1038/mp.2013.66). On the upside, this article is open access so we encourage you to download it and form your own opinions. The authors do a series of behavioural, electrophysiological and pharmacological experiments using a mouse model that’s heterozygous for a functioning reelin gene. Reelin is a protein that’s involved in guiding neural progenitors to their final destination, and seems to influence the maturation of NMDA receptors. It has also been indirectly associated with a number of psychiatric disorders, including schizophrenia. Mice that are heterozygous for reelin show an erasure of fear memory and impaired long term potentiation and dendritic spine formation in their pre frontal cortices. It seems that ketamine, an NDMA receptor antagonist and controversial new antidepressant, lessens some of these impairments in this model. Besides a thorough dissection of their experimental design, we also talk about issues with interpreting “negative” data, how lucky we are to have visualized science (www.benchfly.com; www.jove.com) and the concept of the impact factor. Finally, to end on a positive note, we talk about a really interesting pair of neuroscience blogs, from the same author, that take a look at the field from both sides (http://neurocritic.blogspot.ca/; http://neurocomplimenter.blogspot.ca/).
|