Nonetheless, even a cursory inspection of Figure 3 highlights the fact that different animals offer very complementary opportunities: insects are tremendously useful for the study of highly specific social behaviors and their genetic basis; rodents are ideal for optogenetic manipulation; monkeys offer the best glimpse at the neurophysiology underlying complex group behaviors most similar to those of humans; and of course humans are indispensable because they can tell us about
ourselves most directly. We conclude by asking where should we invest our effort, PI3K Inhibitor Library chemical structure thinking ahead to the next 25 years (see Tables 2 and 3). We highlight three especially exciting avenues for the future. Arguably, one of the most exciting methods currently in neurobiology is optogenetics. This approach, especially suitable to the circuit and small-systems level, permits inhibition or excitation
of activity across large populations of cells but with precision at the level of single cells (Deisseroth, 2011 and Zhang et al., 2007). As such, very precise patterns of neural activity can be manipulated in space and time—so precisely, in fact, that in principle they can perfectly emulate the patterns that actually occur in the brain normally. It is thus not just the causal aspect of the method Doxorubicin datasheet that is so impressive but the (future) ability literally to replay the neural
events that would normally constitute a cognitive event. In the near future, these techniques will likely reveal with unprecedented detail the causal relationships between sequences of neural events and social behaviors in many social species including nonhuman primates (Gerits and Vanduffel, 2013). Indeed, although optogenetic approaches are currently too invasive 4-Aminobutyrate aminotransferase for use with humans, it is no longer in the realm of science fiction to consider that tools of this nature may be available for human research in the not-too-distant future as well, a prospect that opens up some very exciting possibilities (Alivisatos et al., 2012). For instance, we could (in principle) reinstantiate the neural state that corresponds to social anxiety; it would not be caused so much as constituted. One could imagine tweaking the neural state slightly, mapping out the boundaries of what people subjectively report as social anxiety, replaying the neural state as modulated by anxiolytic drugs, and so forth. There is little question that these advances will play a large role in helping to biologically constrain theories of social cognition over the next 25 years.