Herry et al. and Reznikov et al.

Both articles this week discuss fear conditioning and fear extinction, but with different applications. Herry et. Al. explore the rapid switch between fear and extinction neurons located in the basolateral complex of the amygdala and how they trigger the behavioral transitions between extinction and context dependent fear renewal (the recovery of previously conditioned fear response). The paper also touches upon the circuitry and efferent and afferent interactions between extinction and fear neurons and the amygdala, hippocampus, and mPFC. Reznikov was searching for a better model of PTSD in animals that can be translated to clinical settings. To do this, they conducted fear conditioning and extinction training, and then segregated the animals based on their rate of extinction. Animals with impaired extinction of a conditioned fear response were coined “weak extinction” animals. Reznikov et. Al. also measured the level of plasma corticosterone before the animals went through fear conditioning and found that mice with low levels of plasma corticosterone exhibited the weak extinction phenotype. Through experiments, Reznikov et Al. showed that these weak extinction animals exhibit traits similar to PTSD in humans such as exposure to a traumatic event, induction of long lasting fear/anxiety responses to conditioned fear cues, and signs of increased freezing.

After reading through both of these papers, I found myself enjoying Reznikov’s paper more. On a purely formatting level, Reznikov et. Al. presented the materials and methods in a very clear concise manner, illustrating and narrating exactly what was administered and tested before and after and in what order. After reading, I had little question of the experimental method, a problem we noticed in the last papers. The graphs diagrams were also easy to navigate. I think experiment two also strengthened their argument particularly by showing that the weak and strong extinction mice had no significant difference before fear conditioning, showing that it was the traumatic event that caused the weakening of extinction. I also think to improve the validity of the findings, this experiment should be conducted using more mice.

I also thought that the way Reznikov et. Al. approached the experiment was different than the previous papers we have discussed. This experiment was conducted with clinical applications in mind, while the other papers we read briefly mentioned in the end vaguely how this could have clinical applications. In the discussion, the weak extinction model is described as a “valid correlate of human PTSD” and parallels between the two were highlighted. I think that the weak extinction model is promising, but the experiment did not really touch upon the hyporesponsiveness (emotional blunting or social withdrawal) criteria mentioned. I would like to see an extension of this study in which they measure this criteria.

Despite my preference for the Reznikov paper, I found the data from Herry’s paper convincing and thorough. I especially found Figure 3 intriguing, which illustrates that the behavioral change occurs after the switch from fear neuron to extinction neuron activity. This paper touches upon the necessity of the basolateral amygdala for the behavioral transitions, and I think that this could be a new potential area of interest for pharmacological interventions.