Week 4 (Han et al, Yiu et al)

            Like last week’s set of papers, this weeks pair of papers (Han et al. 2009, Yiu et al. 2014) dealt with the formation of memories and the specific neuronal processes and cell types that can alter formation of especially fearful memories. Han et al. set about this by determining the effect that CREB (cyclic adenosine monophosphate response element–binding protein) had on amygdalar cells during the formation of fear memories. By first overexpressing CREB in LA cells that already had higher levels in relation to fear memory, the team was able to show that greater levels of CREB could turn a weak memory-forming event into a robust memory that could affect behavior. Likewise, by ablating those very same neurons through a clever use of diphtheria toxin after those first tests, the team showed that those memories could be ablated by removing CREB-linked neurons without deleting prior memories or altering the formation of new memories. Deleting memories would be a convenient tactic especially in some post-traumatic disorders, however ethics and invasiveness aside, CREB’s systemic expression could make altering CREB levels and ablating CREB-active cells could lead to unintended consequences. 

          Yiu et al 2014 expanded upon those findings by adding that it is not only CREB expression that leads to robust memory formation, but also the excitability of those neurons, and by turning down excitability of memory-linked neurons via specially designed K+ channels, they could reduce fear memory recall, while reactivating those neurons and returning levels of excitability could also reactivate the memory. Together, these findings indicate CREB as a noteworthy factor in the formation of fear memories in the lateral amygdala, and a notable factor to be studied for possible therapeutic application.