Skip to main content

Week 3: Memory Engrams


In 2012, Ramirez et al. made an astounding discovery when they were successful in using optogenetic techniques to manipulate memory engram-bearing hippocampal neurons for the recollection of artificially implanted memories. Using this first experiment as a precursor, they proposed exploiting this model as a potential alleviation for stress response and depressive-like behavior three years later. Both studies used transgenic c-fos-tTA mice injected with an AAV encoding ChR2-mCherry to specifically label cells in the dentate gyrus, which were then reactivated during a behavioral fear conditioning paradigm in different contexts to control for memory. After exposure to context “A” and a subsequent foot shock paired with electrical light pulses while in context “B”, mice demonstrated freezing response when placed back in context “A”. The data elicits the idea that fear can be activated regardless of whether the aversive foot shock was provided in that context, hence the induction of false memories if encoded in the same engram. The second publication especially stood out to me, being that the overall results indicate that chronic stimulation of DG cells associated with positive memory leads to significant stress-induced behaviors as well as an increase in neurogenesis.

After reading both papers, I also watched Ramirez’s TED Talk (2017) where he explained how he derived his motivation behind the experiments. It brought me to thinking what would happen if we could indeed erase traumatic and stressful memories in humans as a “cure” for anxiety and mood related disorders. The translational implications of this is tremendous, being that this means a potential alternative to traditional corrective methods such as antidepressants. Neuroscientists have toyed with the idea of altering and destroying memories for sometime now, especially with the radical electroconvulsive therapy. An optogenetic alternative poses a (much) more specific and direct target of engram disruption, which could be quite useful in a clinical setting. And although it is accompanied by ethical and moral dilemmas—for instance, would “deleting” a traumatic event prevent our past from informing our present selves—it achieves plasticity at a faster rate than any medication would. The data is exciting, but we certainly still have ways to make before reconfiguring the mnemonic memory circuit becomes the standard for treating maladaptive behavior.

Comments

Popular posts from this blog

Buffington et al (2016) and Reber et al. (2016)

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...

Gut-brain axis

This weeks papers Reber et al. 2016 and Buffington et al. 2016 present a super interesting look into the gut-brain axis. Regarding both of these papers, it was amazing to see how potent favorable or unfavorable gut microbiome compositions are in affecting neuronal signaling and overall behavior. Reber et al. shows how immunoregulatory immunization with specifically heat killed M.vaccae can serve as a protective factor against chronic subordinate stress induce colotis as well as behavioral symptoms due to chronic stress as such. Interestringly, this paper depleted regulatory T cell activity via the anti CD25 antibody in order to show that the antiinflammatory mechanism induced by m vaccae immunization is depented on the secondary regulatory mechanisms offered by Treg proliferation and signaling. But, when T reg signaling was removed, this did not seem to cause a significant change in behavior . Therefore, this begs the consideration of what othe rmechanisms may be at play in order ...

Gut-Brain Interactions: Buffington et al, Reber et al 2016

April 13 Papers (Buffington et. al, Reber et. al) I found this week’s papers to be quite novel in that they both proposed potential treatments for neurodevelopmental or psychiatric disorders that target bacterial or microbial abnormalities and how these give rise to certain behavioral and physical symptoms associated with the disorders. I thought this was a very unusual yet interesting approach, and as I have not previously studied the gut-brain axis, these papers offered me a fresh perspective on researching psychiatric and neurodevelopmental disorders. They were also unconventional in their focus of the physical symptoms that often accompany mental disorders, as this is not something that I have seen many other papers touch upon very much. Particularly, I was surprised by the Reber et al paper’s focus on the link between psychiatric disorders and inflammation in organs other than the brain, such as the colon, and the Buffington et al paper’s description of a relationship between ...