It looks like the reason the “switch” montage I’ve been working with is effective is because it inadvertently provides stimulation along both the ventral and dorsal hippocampal axis. More specifically, it differentially targets both the CA1 and CA3 regions.
The reason for the efficacy of PFC targeted TMS and tDCS targeted stimulation looks like it’s because most individuals are ventral dominant, and most types of “depression” can be seen in the hippocampus as lower CA1 activation. By targeting the PFC, we are inadvertently also activating the dorsal CA1 which is on the same axis. The dlPFC is exactly where we’d need to be targeting for a ventral dominant hippocampal transform, and would have likely no effect at all for a dorsal dominant type. At the same time stimulation just below the inion is aligned with the CA3, with similar effects.
My initial assumption that we were re-establishing plasticity along the entire stream is probably not quite an accurate description of the noted effects, instead we are differentially targeting the hippocampal transform. This is kind of exciting because it gives a lot more insight into how we might use this to manage conditions like hallucinations or apathy. By managing hyperpolization/depolarization in these specific regions, we should be able to reduce or eliminate these effects.
Edit: I’m thinking the closer we align the orientation of stimulation with the appropriate hippocampal axis, the more significant the effect we should see. I’m sure there is some math that should give us an angle/efficacy correlate if this proves out in testing.