Abnormally strong memories underlie common disorders including addiction and post-traumatic stress disorder (PTSD). Memory disruption would therefore be beneficial for treatment of these disorders. Evidence reveals that cocaine conditioned place preference (CPP) memories are susceptible to long-lasting disruption during memory retrieval. For example, inhibition of β-adrenergic receptor (β-AR) activity within the prelimbic medial prefrontal cortex (PL-mPFC) prevents cocaine CPP memory retrieval, and this retrieval impairment is both long-lasting and prevents subsequent reinstatement of the CPP. Despite this, whether PL-mPFC β-AR activity is a fundamental mechanism required to maintain retrieval of other memories is unclear. Furthermore, how PL-mPFC β-AR activity maintains memory retrieval is unknown. Thus, here I use a combination of behavioral and electrophysiological techniques to 1) evaluate how PL-mPFC β-AR activity regulates retrieval of memories related to a natural reward and to an aversive stimulus and 2) to determine the mechanism of memory retrieval deficits
