Memory retrieval has been considered as requisite to initiate memory reconsolidation; however, some studies indicate that blocking retrieval does not prevent memory from undergoing reconsolidation. Since N-methyl-D-aspartate (NMDA) and aamino-3-hydroxy-5-methyl-4-isoxazolepropionic acid (AMPA) glutamate receptors in the perirhinal cortex have been involved in object recognition memory formation, the present study evaluated whether retrieval and reconsolidation are independent processes by manipulating these glutamate receptors. The results showed that AMPA receptor antagonist infusions in the perirhinal cortex blocked retrieval, but did not affect memory reconsolidation, although NMDA receptor antagonist infusions disrupted reconsolidation even if retrieval was blocked. Importantly, neither of these antagonists disrupted short-term memory. These data suggest that memory underwent reconsolidation even in the absence of retrieval.Retrieval has been held as an indispensable condition to trigger memory reconsolidation (Nader et al. 2000;Dudai 2006). However, recent reports showed that inhibition of retrieval does not disrupt memory reconsolidation in several memory paradigms (Ben Mamou et al. 2006;Rodriguez-Ortiz et al. 2012;Balderas et al. 2013;Barreiro et al. 2013;Milton et al. 2013;Garcia-Delatorre et al. 2014). Some of these studies have shown that inhibition of the a-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid (AMPA) receptors of the basolateral amygdala impairs retrieval of aversive memories, without affecting its reconsolidation (Ben Mamou et al. 2006;Rodriguez-Ortiz et al. 2012;Milton et al. 2013; GarciaDelatorre et al. 2014). Conversely, inhibition of N-methyl-Daspartate (NMDA) receptors disrupts reconsolidation of aversive memories but spare retrieval (Garcia-Delatorre et al. 2014).A recent study evaluated the capacity of retrieval to trigger memory reconsolidation in a nonaversive task, i.e., the object recognition task (Balderas et al. 2013). The object recognition task is widely used to evaluate recognition memory in rodents, since it has been suggested that it maintains a close analogy to the recognition memory task used in humans to assess impairments in declarative memories (Reed and Squire 1997). In this regard, muscimol (GABA A receptor agonist) infusions in the perirhinal cortex blocked retrieval, but this effect did not impede memory to undergo reconsolidation in a protocol of memory updating, suggesting that retrieval and reconsolidation of object recognition memory (ORM) are independent processes (Balderas et al. 2013).It has been reported that glutamate receptor activity in the perirhinal cortex has an important and dissociative role mediating synaptic transmission in several stages of ORM. In one study, it was showed that the AMPA receptor antagonist 6-cyano-7-nitroquinoxaline (CNQX) impaired ORM retrieval when infused 15 min before, since rats did not show preference for the new object. On the other hand, the group infused 15 min before reactivation with the NMDA receptor antagonist A...

In addition to numerous metabolic comorbidities, obesity is associated with several adverse neurobiological outcomes, especially learning and memory alterations. Obesity prevalence is rising dramatically in youth and is persisting in adulthood. This is especially worrying since adolescence is a crucial period for the maturation of certain brain regions playing a central role in memory processes such as the hippocampus and the amygdala. We previously showed that periadolescent, but not adult, exposure to obesogenic high-fat diet (HFD) had opposite effects on hippocampus-and amygdala-dependent memory, impairing the former and enhancing the latter. However, the causal role of these two brain regions in periadolescent HFD-induced memory alterations remains unclear.Here, we first showed that periadolescent HFD induced long-term, but not short-term, object recognition memory deficits, specifically when rats were exposed to a novel context. Using chemogenetic approaches to inhibit targeted brain regions, we then demonstrated that recognition memory deficits are dependent on the activity of the ventral hippocampus, but not the basolateral amygdala. On the contrary, the HFD-induced enhancement of conditioned odor aversion specifically requires amygdala activity. Taken together, these findings suggest that HFD consumption throughout adolescence impairs long-term object recognition memory through alterations of ventral hippocampal activity during memory acquisition. Moreover, these results further highlight the bidirectional effects of adolescent HFD on hippocampal and amygdala functions.

1ABSTRACTIn addition to numerous metabolic comorbidities, obesity is associated with several adverse neurobiological outcomes, especially learning and memory alterations. Obesity prevalence is rising dramatically in youth and is persisting in adulthood. This is especially worrying since adolescence is a crucial period for the maturation of certain brain regions playing a central role in memory processes such as the hippocampus and the amygdala. We previously showed that periadolescent exposure to obesogenic high-fat diet (HFD) had opposite effects on hippocampus- and amygdala-dependent memory, impairing the former and enhancing the latter. However, the causal role of these two brain regions in periadolescent HFD-induced memory alterations remains unclear. Here, we first showed that periadolescent HFD induced long-term, but not short-term, object recognition memory deficits, specifically when rats were exposed to a novel context. Using chemogenetic approaches to inhibit targeted brain regions, we then demonstrated that recognition memory deficits are dependent on the activity of the ventral hippocampus, but not the basolateral amygdala. On the contrary, the HFD-induced enhancement of conditioned odor aversion requires specifically amygdala activity. Taken together, these findings suggest that HFD consumption throughout adolescence impairs long-term object recognition memory through the overactivation of the ventral hippocampus during memory acquisition. Moreover, these results further highlight the bidirectional effects of adolescent HFD on hippocampal and amygdala functions.