But I can look past this.

Seriously though, the only reason there was an effect in CA3 in the Frankland poster was because of dentate dysfunction (!). No seriously though, I agree that it can’t be that the dentate is the only region performing a pattern separation function. To some degree or another all circuits are doing this. There is a nice series of papers from the Guzowski, Knierem, and Moser labs (summarized here) that talk about the dual separation/completion role of CA3, depending on whether there are more/fewer differences between stimuli.

As far as architecture goes, I think a lot of the interest in a pattern separation role for DG-CA3 is based purely on architecture (if architecture can mean or include wiring), specifically the divergent nature of afferent inputs and sparse connectivity.

I think it’s interesting how many people don’t acknowledge ACSF-LTP in the DG. In a lot of papers they apply a GABA blocker (BIC or PICRO) but don’t factor this blockade of GABA into the interpretations of their findings.

It seems to me the focus in pattern separation research is shifting. Many of the posters I looked at (not just Franklab) really emphasized CA3 over the DG. It’s a little refreshing to see people taking a look somewhere else, particularly CA3, which I think is hands-down the most poorly understood part of the hippocampus. It’s a little surprising all the evidence of pattern separation in CA3 population code.

A number of posters I saw looked at changes in dendritic architecture, not just plasticity. These I think are important too – I think pattern separation relies on far more than just strong plasticity (otherwise how could there be any selectively?)