All function ascribed to the CA2 is an artifact of prediction accuracy management, including social memory. Social behavior as a whole is a predictive exercise.
I’m thinking the blindspot for the CA2 is because it’s function might be better described as an “expectation manager”. Until we get a better system level model going, expectation is always going to hard to quantify and present like magic. How do we understand what our animal model “expects”, when expectation is a real time computed property of both CA3b/DG input and CA1/Sub? The CA2 having so many hot reciprocal circuits to the valence centers, and a hot circuit straight to the brain stem via the SuM means this calculation has ton of moving parts.
Testable condition: novelty stimulates the brainstem, particularly the pedunculopontine or or ventral tegmental areas. Let’s call this a null case, if highly novel stimuli does not stimulate these areas, this hypothesis is null. Because I’m too chicken this won’t be part of the null, but the expectation should be that dorsal stream novelty should be associated with VTA stimulation, ventral stream novelty should be associated with PPN stimulation.
Edit 02/26/2022: Pondering this a bit more, I’m getting really interested in the LEC->CA2 circuits as the enabler for “declarative” memory as a whole. One really interesting experiment I would like to see is if we could manipulate the internal perception of time with stimulation changes in the LEC. Messing with output in the LEC->CA2 circuit and SuM->CA2 circuit should be able to modify how prediction accuracy is calculated, and as such present some pretty dramatic modifications to perceived experiences. My thinking here is that we may even be able to induce or suppress “psychotic” states by synchronizing/desynchronizing these inputs against our prediction accuracy module.
I think it might be worth the time to take a look at what it would take to build a decent spatial resolution functional ultrasound stimulation device.