On Your Mind Neuroscience Podcast

We’ve got Rett syndrome on our mind this week and we’re discussing a paper that uses a clever gene editing technology in embryonic stem cells to study it.  We’re also talking about the allure of sexiness in science, the role of misfolded proteins in neurodegenerative disorders and what, if anything, distinguishes the brain of a genius.

We’ve got Rett syndrome on our mind this week and we’re discussing a paper that uses a clever gene editing technology in embryonic stem cells to study it.  We’re also talking about the allure of sexiness in science, the role of misfolded proteins in neurodegenerative disorders and what, if anything, distinguishes the brain of a genius.

This week at On Your Mind, we’re shedding some light on feeding behaviour with “The Inhibitory Circuit Architecture of the Lateral Hypothalamus Orchestrates Feeding” by Jennings et al.  It uses optogenetics and single cell gene expression to look at neural circuits in mice. 

We’ve also got stress and the state of academia on our minds and we discuss all this from two different time zones at once!

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/).

This week on On Your Mind:

It’s an OYM blast from the past with this week’s special-release, archived episode!  

This episode starts out with a well-deserved congratulation to our very own Liam, for acing his PhD candidacy exam.  Now he’s formally allowed to do more work for no change in pay!  We also talk about how frustrating it can be when your experiments don’t work and how nerve wracking it is waiting for a funding decision.  This is the first (and hopefully last) episode where the “Kath-eter of science” makes an appearance and then it’s onto this week’s paper.  

It’s called “Detection of Clinically Relevant Genetic Variants in Autism Spectrum Disorder by Whole-Genome Sequencing” by Jiang et al. doi:10.1016/j.ajhg.2013.06.012 This paper brings up some nostalgic flash-backs from Kat, who used to work in ASD research before taking the leap into grad school.  Autism spectrum disorders affect 1 in 88 children and are defined by deficits in social skills, communication and repetitive and restrictive interests.  Genome-wide association studies (GWAS) have identified genetic polymorphisms that contribute to the risk of ASD but these are common mutations that can’t explain the whole genetic landscape of the disease.  This week’s paper uses whole genome sequencing (for a video tutorial: http://www.youtube.com/watch?v=Rzmm57udYdk  ) to identify new, rare mutations that are found in 32 children with ASD.  These include single nucleotide changes (SNP or SNV), and larger alterations to the genetic sequence (indels and CNVs).  The authors attempt to prioritize future medical interventions and follow up for children based on their genetic findings.  Of course, this leads us to a rather epistemological discussion on personalized genomics and the pros and cons of putting disorders on a spectrum in the first place.

Finally, this week wraps up with a debate about predicting the impact of your research inspired by this article in Science. (http://www.sciencemag.org/content/340/6138/1265.full.pdf)