Consequences at adulthood of transient inactivation of the parahippocampal and prefrontal regions during early development: new insights from a disconnection animal model for schizophrenia

Abstract

Memory reconsolidation has been observed across species and in a number of behavioral paradigms. The majority of memory reconsolidation studies have been carried out in Pavlovian fear conditioning and other aversive memory settings, with potential implications for the treatment of post-traumatic stress disorder. However, there is a growing literature on memory reconsolidation in appetitive reward-related memory paradigms, including translational models of drug addiction. While there appears to be substantial similarity in the basic phenomenon and underlying mechanisms of memory reconsolidation across unconditioned stimulus valence, there are also notable discrepancies. These arise both when comparing aversive to appetitive paradigms and also across different paradigms within the same valence of memory. We review the demonstration of memory reconsolidation across different aversive and appetitive memory paradigms, the commonalities and differences in underlying mechanisms and the conditions under which each memory undergoes reconsolidation. We focus particularly on whether principles derived from the aversive literature are applicable to appetitive settings, and also whether the expanding literature in appetitive paradigms is informative for fear memory reconsolidation.

Anisomycin in the medial prefrontal cortex reduces reconsolidation of cocaine-associated memories in the rat self-administration model

“…However, there remains the possibility that boundary conditions existed, and additional reactivation sessions may have produced reconsolidation disruption in rats given abstinence. Rats not allowed to undergo extinction sessions may have stronger memories, and stronger memories do not generally undergo reconsolidation disruption as easily (Reichelt and Lee, 2013) so that longer or additional reactivation sessions may have been required to decrease reinstated lever-pressing behavior (Suzuki et al, 2004). Thus, extinction may weaken the memory and make it more susceptible to disruption by anisomycin.…”

“…Repeated drug use establishes drug-related memories. It is believed that each time these drug-related memories are recalled, as occurs when the organism is re-exposed to drug-associated cues, context, or the drug itself, those memories are reconsolidated to maintain or strengthen them (Milton and Everitt, 2010; Reichelt and Lee, 2013; Tronson and Taylor, 2007, 2013). After memory reactivation, the memory is thought to become destabilized so that it is susceptible to disruption by amnestic agents for a short period of time (typically, approximately 6 hr).…”

“…In animal models of addiction, we can exploit this window of vulnerability to disrupt drug-associated memories by providing appropriate amnestic agents, such as protein synthesis inhibitors, to dampen the memories that influence the motivation to seek and take drugs. The vast majority of studies on reconsolidation have been conducted on fear-conditioned memories (Alberini, 2005; Dudai, 2004, 2006; Dudai and Eisenberg, 2004; Nader and Einarsson, 2010; Reichelt and Lee, 2013), although an increasing number of studies have focused on reconsolidation of appetitive memories (see (Milton and Everitt, 2010; Reichelt and Lee, 2013; Sorg, 2012; Tronson and Taylor, 2013) for review). Of these latter studies, the majority have tested the impact of amnestic agents in the conditioned place preference (CPP) model of addiction, while only a relative handful of studies have examined reconsolidation using the drug self-administration model.…”

Persistent cognitive and morphological alterations induced by repeated exposure of adolescent rats to the abused inhalant toluene

“…Previous exposure to a non-reinforced cue has been repeatedly shown to block future conditioning to that cue, a phenomenon called latent inhibition. Although latent inhibition has traditionally been studied using Pavlovian conditioning paradigms, this idea can be conceptualized as “learned irrelevance” of cues in an operant conditioning scenario (although this definition is simplistic, for review: see (Meyer & Louilot, 2014)). Blunted latent inhibition has been observed in serotonin knockout (5HTT−/−) mice (Nonkes et al, 2012) and in spontaneously hypertensive rats, which are used as a in a rodent model of ADHD (Calzavara et al, 2009).…”

Reconsolidation and psychopathology: Moving towards reconsolidation-based treatments

“…Memories do not appear to be universally reconsolidated upon recall, which suggests the existence of certain boundary conditions that define whether or not a memory will undergo reconsolidation (Nader and Einarsson 2010; Reichelt and Lee 2013; Tronson and Taylor 2007). These boundary conditions that preclude reconsolidation are likely mirrored neurobiologically by downregulation of mechanisms that are critical for lability (Wang et al 2009).…”