This
week’s papers were both related to the effects of neuronal excitability on fear
memory expression. Han et al., 2009 showed that increased CREB levels during
fear learning are critical to the stability of that memory by deleting neurons
showing overexpressed CREB levels, which blocked expression of fear memories by
decreasing transgenic mice’s freezing levels. I thought the researchers did a
very impressive job in finding the neurons in the LA that are actually involved
in the fear learning process because instead of being in a small cluster they
are widely spread out. There could have been more experiments in disrupting
CREB, however, to further show that it is indeed involved.
Yiu
et al., 2014 used the knowledge from the first paper to show that increasing
neuronal excitability biases recruitment into the memory trace, enhancing
memory formation. I thought this experiment was more comprehensive than the
first one because they not only showed the involvement of CREB, but also
numerous other molecules such as dnKCNQ2, hM3Dq + CNO, and ChR2 in neuronal
excitability and memory formation enhancement. Furthermore, I like how they
used Kir2.1 to show opposite effects in mice. They also used a wide-ranging set
of control experiments, including the anxiety test and the anatomical
specificity test.
From
a clinical aspect, these experiments can be very valuable for the treatment of
fear disorders such as PTSD. Clearly, these experiments are not exactly feasible
in humans, but knowing that you can manipulate neurons in your lateral amygdala
during fear memory expression is very important. These papers show that you
need to excite neurons prior to training the fear memory, but perhaps researchers
can next dive into ways you can manipulate fear memories after it has been
encoded.
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