Autism Spectrum Disorders (ASDs) are thought to be caused by the abnormal development or dysfunction of synapses. Consistent with these many genes that code for key synaptic proteins confer increased risk for ASD. Adding to story, a new study shows that deleting an ASD-risk gene called Sema5A causes neurons to form more connections in mice, and also alters how these mutant mice interact with one another. Justin Kenney wrote a commentary on this paper, and it is published in eLife.
Clockwise from top left: Axel, Chen, Liz, Leo and Asim.
From top left: 1) Steve Ramirez and Karim Nader; 2) Kiriana Cowansage and Josh Johansen; 3) Jonathan Britt and Kay Tye; 4) Jaideep Bains and Shernaz Bamji; 5) Natalie Tronson and Satoshi Kida; 6) Megan and Hayley from the Matt Hill lab.
Jonathan fielding questions at his posters in 2013 and 2014. Left, 2013 without Karl Deisseroth as co-author. Right, 2014 with Karl Deisseroth as co-author.
And so it begins. 30,000 neuroscientists descend on Washington DC.
They keep coming (this is #2 of 3 in quick succession…). This one is on a new Nature paper from the Sweatt lab on histone acetylation and long-term memory. The first author– Eva Zovkic– is a new faculty here at the University of Toronto, Mississauga. A pdf of the commentary is available here.
For the 0.000015 % of people who might care, on the left is legendary British football commentator Brian Moore at Wembley, sometime in the 1970s.
We had a baby shower for Adelaide last week. Adelaide is almost the longest standing member of the Frankland/Josselyn lab, having joined first as an undergrad in 2005. She then completed her PhD and now is a postdoc. Adelaide is pictured with the longest serving member of the lab- Toni (lab manager). We’ll miss you and we wish you the best with baby Ng!
More pictures from the shower here.
There’s plenty of debate, but the classical view is that memory traces for events are laid down in cell ensembles across distributed hippocampal-cortical networks. Then the hippocampus is necessary, at least temporarily after encoding, for successful retrieval of these event memories via reinstatement of the patterns of activity within these cortical ensembles. According to this view, the hippocampus contains indices or pointers to cortical cell assemblies that collectively represent a given event. Observations of retrograde amnesia following hippocampal damage in human patients (such as H.M.), as well as in experimental animals, provide broad support for this view. However, they tell us little about how specific hippocampal and cortical cell ensembles interact to support memory retrieval. Two new studies (from Kazu Tanaka in the Wiltgen lab and Kiriana Cowansage in the Mayford lab) begin to shed light on this interaction. Both studies used a genetic strategy to tag active cells at the time of memory encoding with light-sensitive opsins and then optogenetically manipulate the activity of these ‘engram’ cells during retrieval.
These papers have just been published in Neuron. We were asked to write a commentary on these studies, and a pdf is available here.
We celebrated Liz’s cocaine paper last week with champagne and cake. In this study, Liz explored how rewarding things (in this case cocaine, not cake) become associated with particular places. Liz was able to show that a key population of neurons in the amygdala represent the association between a place and a reward, and that killing or silencing this population of cells effectively “erases” the drug memory. The paper is published in the Journal of Neuroscience. A pdf is available here.