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.
The Chaudhury et al paper explored the neural circuit mechanisms involved in the dopamine modulation of certain symptoms of depression. In this study, the researchers looked at social interaction and sucrose preference as part of their social-defeat paradigm, which has been shown in the past to be indicative of depressive-like behaviors. Although I initially did not completely see the connection between the social-defeat stress model of depression and the tonic vs phasic firing of dopamine neurons, it seemed that susceptibility and resilience to stress played a role in the functional/behavioral effects of dopamine firing. It was interesting to see how chronic mild stress with phasic firing of VTA dopamine neurons converted even resilient mice into susceptible mice. The Tye et al paper similarly looked at the dopamine modulation of depressive-like behaviors, focusing on motivation with the forced swim tests and open field tests, followed by measurement of anhedonia by quantifyi...
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