>The BMI decodes the onset of nociception via a state-space model on the basis of the analysis of online-sorted spikes recorded from the anterior cingulate cortex (which is critical for pain processing) and couples real-time pain detection with optogenetic activation of the prelimbic prefrontal cortex (which exerts top–down nociceptive regulation). In rats
>Example ChR2 expression in the prelimbic PFC. Highmagnification (100x) view of the expression of YFP-ChR2 in the prelimbic PFC demonstrated the co-staining of pyramidal neuron markers (CaMKII) with YFP. Arrows point to examples of co-stained neurons.
(from abstract and supplementary info, scihub is kind of down)
On their own (generally speaking!), very few neurons "respond" to low intensity light. "Optogenetics" stuff like this inserts a gene encoding a light sensitive ion channel in order to make cells responsive to a specific wavelength of light.
So there's two types of targeting here: Targeting gene expression to a certain population of cells, and then spatially targeting a group of those cells with the light - Blue light doesn't travel very far in tissue. (Also targeting multiple cell populations within a region using multiple colors of light + differently sensitive proteins).
Of course your comment still stands - Presumably not all the CamKII-positive PFC neurons are involved in nociception, and rats can't talk about their conscious experience so the answers there are limited to what questions researchers chose to ask using the limited tools available.