Abstract

Episodic memory, can be defined as the memory for unique events. The serotonergic system one of the main neuromodulatory systems in the brain appears to play a role in it. The serotonin 2a receptor (5-HT2aR) one of the principal post-synaptic receptors for 5-HT in the brain, is involved in neuropsychiatric and neurological disorders associated with memory deficits. Recognition memory can be defined as the ability to recognize if a particular event or item was previously encountered and is thus considered, under certain conditions, a form of episodic memory. As human data suggest that a constitutively decrease of 5-HT2A signaling might affect episodic memory performance we decided to compare the performance of mice with disrupted 5-HT2aR signaling (htr2a−/−) with wild type (htr2a+/+) littermates in different recognition memory and working memory tasks that differed in the level of proactive interference. We found that ablation of 5-HT2aR signaling throughout development produces a deficit in tasks that cannot be solved by single item strategy suggesting that 5-HT2aR signaling is involved in interference resolution. We also found that in the absence of 5-HT2aR signaling serotonin has a deleterious effect on recognition memory retrieval through the activation of 5-HT1aR in the medial prefrontal cortex.

Highlights

  • Serotonin (5-HT) is synthesized in neurons of the raphe nuclei localized in the brain stem

  • To study whether 5-HT2aR deficiency caused a deficit in recognition memory, we exposed htr2a+/+ and htr2a−/− mice to a spontaneous novel object recognition task (SNOR) task

  • We found that the constitutive blockade of 5-HT2aR signaling has not affect on how mice distributed

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Summary

Introduction

Serotonin (5-HT) is synthesized in neurons of the raphe nuclei localized in the brain stem. The serotonin 1a receptor (5HT1aR), a Gi coupled receptor, and 5-HT2aRs appear to be coexpressed in a large fraction of pyramidal cells (Araneda and Andrade, 1991; Amargos-Bosch et al, 2004; Béïque et al, 2004) in the medial Prefrontal Cortex (mPFC). They may regulate in a cooperative manner the way pyramidal neurons encode excitatory inputs into action potential firing.

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