Abstract
Visual recognition memory relies on long-term depression-like mechanisms within the perirhinal cortex and the activation of the lateral amygdala can enhance visual recognition memory. How the lateral amygdala regulates recognition memory is not known, but synaptic plasticity at amygdala-perirhinal synapses may provide a mechanism for the emotional enhancement of recognition memory. In this study, we investigate the mechanisms of long-term depression (LTD) at the amygdala-perirhinal synapse in male Lister Hooded rats. We demonstrate that LTD at this input relies on NR2A-containing NMDARs, located presynaptically. Therefore, the underlying mechanisms of LTD, at the amygdala-perirhinal input, which may regulate the emotional context for recognition memory, are different to previously described postsynaptic NR2B-NMDAR mechanisms of intraperirhinal LTD that subserve recognition memory.
Highlights
Since the perirhinal cortex can utilise NMDARs for the induction of long-term depression (LTD) (Cho et al, 2000), we questioned whether amygdalaϪperirhinal LTD may be NMDAR-dependent
The mechanisms by which the lateral amygdala modulates long-term potentiation (LTP) in the perirhinal cortex have only recently been described (Laing and Bashir, 2014), and this paper expands our understanding of these mechanistic processes by studying the receptor mechanisms required for amygdalaϪperirhinal LTD
We observed that LTD between the lateral amygdala and layer II/III of the perirhinal cortex is NMDARdependent and does not rely on -ADRs or voltage-gated calcium channels (VGCCs)
Summary
There is a clear evidence that synaptic plasticity in the perirhinal cortex may provide the cellular mechanisms underlying recognition memory (Warburton et al, 2003; Griffiths et al, 2008; Massey et al, 2008). The strong reciprocal connectivity between the lateral amygdala and the perirhinal cortex (Pitkänen et al, 2000; Kajiwara et al, 2003) provides an anatomical basis by which the lateral amygdala may profoundly influence mechanisms of recognition memory. Inputs from the lateral nucleus of the amygdala (Furtak et al, 2007) directly influence perirhinal cortex activity and regulate synaptic transmission between the perirhinal cortex and the entorhinal cortex (Paz et al, 2006). The receptor mechanisms by which the lateral amygdala might modulate synaptic plasticity, and learning and memory, have not yet been fully elucidated
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