The first half of this figure should be straightforward for students: The first four panels of the figure contain linear place fields along with voltage traces from their neurons. It is worth noting that the researchers filtered their traces to remove spiking activity and isolate the slower changes in the signal—the long-lasting depolarizations that persist in the cells. They found that both naturally occurring and experimentally induced (via stimulation) plateau potentials caused a measurable depolarization of the membrane and the initiation of a place field. Interestingly, you can find a subthreshold signature of a place field earlier (in time and space) than the place where the plateau was evoked, suggesting that this plasticity begins seconds earlier.
The second half of Figure 1 is a little trickier to parse. Keeping in mind that mice are running on a treadmill, and that place fields are already formed in upstream hippocampal area CA3, the authors show that the size of the induced place field size depends on how fast the animal is running during the trial. Understanding why this is the case may furrow your brow a bit (it did mine, at least). Essentially, because CA1 is inheriting place fields from CA3, more cells from CA3 fire when the mouse covers more distance. More strengthened inputs over longer distances (which you can see illustrated as lots of Gaussian bumps underneath the mouse in 1E and 1F) leads to longer voltage ramps.
In Figure 2, the authors used modeling to determine whether their data demonstrate typical Hebbian plasticity (within milliseconds) or longer plasticity. You could skip this figure altogether if you’re not interested in dissecting the model; the take-home message is this: When you use CA3 place-field inputs based on the animal’s movement, you can model the CA1 data and estimate a time frame over which plasticity occurs. Importantly, the model showed that plasticity could arise seconds before and after the initiation of a plateau potential, a much longer timescale than Hebb’s rule.
In Figure 3, the authors used electrical stimulation in brain slices to see if they could observe this plasticity while precisely controlling the timing of both the pre- and post-synaptic activity. By varying the timing of the stimulation of CA3 axons or input into the CA1 cell itself to generate plateau potentials, they showed that they could increase synaptic strength even when the plateau potential was initiated seconds before or after the CA3 axons were stimulated. Remarkably, and also in opposition to Hebb’s rule, they could do this with just five electrical stimulations. The data in Figure 3D nicely mirror Figure 2G, demonstrating how modeling and experimental work can go hand in hand.
Finally, the authors used pharmacological approaches to demonstrate that it really, truly is the plateau potentials that drive plasticity. Magee’s group had previously shown that NMDA receptors and Ca+2 channels are essential for dendritic plateaus. In the 2017 paper, they showed that blocking either prevents the increase in synaptic strength and that blocking Ca+2 channels in vivo stops formation of place fields in CA1 neurons.