I’ve been interested in vicarious/social fear learning since I first took the Neuropsychology of Fear in Spring 2017. I’ve been interested in how fear can be passed down through observational learning and the things that influence it. As each of the papers this week build on one another, I want to consider the role of other sensory stimuli in the ACC -> BLA circuit. Ana Pereira from Marta Moita’s lab published a paper a few years ago about the role of silence in the social transmission of fear. They did a similar behavioral paradigm as the Allsop and had an experienced observer watch another rat undergo fear conditioning. They concluded that the rats relied on auditory cues in the environment, namely the silence resulting from the absence of movement in the conditioned rat. Given the necessity of ACC cells in the social transmission of fear as Allsop concluded, I’m wondering if these two notions relate to one another. The cingulate cortex is related to many autonomic and cognitive functions, one being hearing and attention. I’d be interested to see if there could be a way to study the connection of the role of auditory cues and the ACC -> BLA pathway. Perhaps one could replicate the Pereira methodology of conducting observed conditioning in the dark and playing/stopping recorded sounded of rat movements at various times while stimulating or inhibiting the ACC -> BLA pathway in both conditions. This could determine if and what role auditory cues play in the transmission of fear. If the cingulate to BLA pathway is modulated in some part by auditory cues, then freezing would be affected in the absence of silence but not in the absence of visual cues. I’d be interested to see if there is a way to understand how the transference and recognition of other sensory stimuli affect this particular pathway.
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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