This study is about localizing components of the fear memory engram. Although it was well established that the amygdala is involved in fear processing, it had not yet been shown that this was a site of fear memory storage. Specifically, it was debated whether or not the lateral amygdala (LA) stored memories.
To test this, the Schafe et al. injected the lateral amygdala with MAP Kinase, which inhibits the consolidation of fear memories into a long-term store. Three hours after learning the cue-shock association, an increase in LA activity was seen as measured by the local field potential (LFP) both in the group with the MAPK inhibitor and in controls. Further, these groups did not differ from each other in LFP amplitude or on short-term memory performance. However, after 24 hours, the experimental group showed a very small LFP as compared to controls and was not much different from baseline recordings. These animals also showed a deficit in cue-evoked fear memory at this time point. In animals that were infused with the MAPK inhibitor, memory strength strongly correlated with the cue evoked-LFP magnitude (r=.92, p<.01). Thus, the authors have demonstrated that the same pharmacological agents that block fear memory consolidation have reduced synaptic plasticity in LA.
In the next set of experiments, the authors tested the auditory thalamic area that projects to the LA with a similar experiment. Inhibiting MAPK in the LA did not affect short-term plasticity in the thalamus, as was the case with the LA. However, unlike the LA which showed a reduced potential 24hr after MAPK inhibition, the thalamus showed no such reduction in long-term plasticity. Further, while memory strength correlated very strongly (r=.89, p<.05) with cue-evoked LFP amplitude in the LA, it showed essentially no correlation with the LFP of the thalamic area, demonstrating that LTP of the LA, but not of the auditory thalamus is necessary for the consolidation of an auditory-shock association. It took me a minute to understand why the MAPK inhibitor was infused into the LA, rather than the thalamus if they were testing the thalamus as the site of consolidation. It seems that the argument against consolidation in the LA was that the deficits seen in consolidation when MAP K inhibitors were fused into the LA could be due to other areas in the fear memory processing stream. So, the authors replicated this scenario with an LA injection and then showed that plasticity here in the thalamus was unaffected.
So, if you want to test whether or not a structure is important for memory consolidation, inhibit MAPK, wait, and then test plasticity and behavior.
As a non-amygdala person, it would be interesting to learn more about how consolidation of fear memories compares to consolidation of contextual (hippocampal) memories. For instance, how might a trace stored in the LA be modulated as the hippocampal traces described by Denny et al.? I would think that only neurogenesis in the ventral hippocampus would modulate amygdala traces, as the ventral is more involved in mood and anxiety regulation, whereas the dorsal is more involved in spatial memory.
But that’s another paper for another day.