The study revealed that PL contributes towards fear expression whereas IL facilitates the extinction of fear memory. Therein it was revealed that the inactivation of PL reduced fear expression while stimulation lead to increased fear expression. Inactivation of IL lead to impaired acquisition of extinction suggesting its role in the inhibition of fear responses during the process of extinction. These findings were comparable to that found by Milad and Quirk (2002). Numerous studies (Sierra-Mercado, Corcoran, Lebrón-Milad, & Quirk, 2006; Burgos-Robles et al., 2007; Mueller, Porter, & Quirk, 2008; Santini, Ge, Ren, Pena, & Quirk, 2004) show that the long-term fear memory extinction that takes place in IL is due to the uptick of calcium mediated channels which trigger protein kinases and protein synthesis. Thus, the previous studies which considered vmPFC to have one function gathered confounding results as PL and IL have very different functions that contribute towards fear …show more content…
The inactivation of vHPC lead to reduced fear expression and created disrupted extinction memory during extinction training. The study suggests that activity in vHPC during extinction training is required for subsequent expression of extinction memory. This could be through the potentiation of vHPC inputs to vmPFC (Sierra-Mercado et al., 2010). This study did not differentiate the role of the vHPC in the extinction of context versus tone fears. Furthermore, it was found that the basolateral amygdala (BLA) was necessary for extinction of fear memory. Thus, it was established that the inactivation of BLA leads to impaired recollection extinction memory and reduces fear expression (Sierra-Mercado et al.,