PVALB and post-traumatic stress disorder: In this study, we examined neuronal activity in the MD and its causality with impaired fear memory extinction employing a well‐established mouse model of PTSD.[16] Using a combination of approaches, including optogenetics, chemogenetics, and electrophysiology, we found that hyperactivity in the MD preferentially overactivated downstream parvalbumin‐expressing (PV+) interneurons, impairing the local excitatory and inhibitory (E/I) balance in the ACC microcircuitry and consequently leading to delayed fear memory extinction.