Abstract
Different lines of investigation suggest that the medial amygdala is causally involved in the processing of information linked to social behavior in rodents. Here we investigated the consequences of temporary inhibition of the medial amygdala by bilateral injections of lidocaine on long-term social recognition memory as tested in the social discrimination task. Lidocaine or control NaCl solution was infused immediately before learning or before retrieval. Our data show that lidocaine infusion immediately before learning did not affect long-term memory retrieval. However, intra-amygdalar lidocaine infusions immediately before choice interfered with correct memory retrieval. Analysis of the aggressive behavior measured simultaneously during all sessions in the social recognition memory task support the impression that the lidocaine dosage used here was effective as it—at least partially—reduced the aggressive behavior shown by the experimental subjects toward the juveniles. Surprisingly, also infusions of NaCl solution blocked recognition memory at both injection time points. The results are interpreted in the context of the importance of the medial amygdala for the processing of non-volatile odors as a major contributor to the olfactory signature for social recognition memory.
Highlights
Individual recognition in socially living rodents is primarily based on the acquisition and processing of the conspecifics’ body odors
Aggressive/Sexual Behavior We observed that the durations spent in aggressive behavior were—at least under treatment conditions—too low to allow for a reliable analysis
The present study was designed to investigate the impact of temporary inhibition of the medial amygdala on long-term social recognition memory (LTsrM)
Summary
Individual recognition in socially living rodents is primarily based on the acquisition and processing of the conspecifics’ body odors. The analysis of c-Fos synthesis (Ferguson et al, 2001; Richter et al, 2005; Noack et al, 2010), and genetic and pharmacological (Ferguson et al, 2001) studies revealed that this brain area may play a key Medial amygdala and social memory role for social recognition in mice In this context the MeA was shown to act as a relay station from the olfactory bulb to deeper brain areas, and to signal back to the accessory olfactory bulb thereby controlling the impact of the non-volatile fraction of the conspecific’s “olfactory signature” on approach-avoidance behavior (Martel and Baum, 2009). We investigated the effects of bilateral temporary suppression of action potential propagation in the MeA by injecting Lidocaine into the MeA prior to both learning and recall of the individual olfactory information
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