The two articles included this week continue our discussion of the nature of memory trace formation by exploring the role of the lateral amygdala in fear memories. Han et al followed up on a previous study done in their lab in which they found that lateral amygdala (LA) neurons which have increased levels of the CREB transcription factor were preferentially activated by auditory fear memory training. In this follow up study, they wanted to identify more specifically the neurons involved in the formation of the fear memory trace. By selectively inducing apoptosis in CREB-overexpressing vs control LA neurons, they supported the conclusion that levels of CREB dictate which neurons are recruited into a memory trace regardless of behavior. While this was an interesting finding, it is also important to take note of how they designed their experimental vs control groups. They chose a group of LA neurons that are “not preferentially activated by fear testing”. However, it seems like this is quite a vague set of criteria to include for a control. It also begs the question of whether this is the most representative control criteria because this description does not seem to allow for quantifiable data. I am not sure if this may have been included in supplemental methods or results, but it may have been worth defining a threshold for what the researchers consider “preferential activation” of the LA neurons. Another limitation is that the Han et al article does not describe in detail the specific techniques they defined with the “fear testing”, but it seems like this is expanded upon by the Yiu et al article, which is quite helpful. The Yiu et al article also expands on the finding that LA neurons are involved in fear memory traces by exploring the strength of the memory trace. They found that neuronal excitability during encoding determines the strength of the memory formation. This was a very interesting finding because it allows for future studies to explore this in a clinical context, such as PTSD or other memory-related disorders.
This week's articles were about the role of the gut-brain axis in neurodevelopment and stress. Reber and colleagues used a heat-killed version of the bacteria, M. vaccae, as a type of vaccine and found that administration to mouse models resulted in decreased response to chronic stress, prevented colitis related to stress, and reduced measures of anxiety. Reber et al. also used the inactivated M. vaccae in a mouse model of IBD and found that the bacteria prevented stress-induce flare-ups of colitis, but that this could be reversed by removing T cells. Buffington and colleagues instead examined the role of gut microbiota in maternal high-fat diets (MHFD) in the neurodevelopment and social behaviors of their offspring. Buffington et al. found that housing MHFD rats with the offspring of regular diet (MRD) rats prevented social deficits in their offspring. They also found that this co-housing arrangement prevented an imbalance in the gut bacteria Reber and colleagues' findings w...
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