Our focus is on characterizing the unique role of neuromodulators, like acetylcholine and dopamine, in encoding reward and motivation, altering circuit activity, and ultimately influencing perceptions and decisions.
REWARD/ADDICTION: Can we induce plasticity in neural circuits by optogenetically recreating the activity in neuromodulatory neurons that exist during rewarding (or aversive) events? What are the behavioral consequences of such plasticity? Conversely, can we optogenetically introduce patterns of activity that counteract the plasticity induced by rewarding stimuli, such as drugs of abuse, and can such paradigms be employed to counteract addiction?
COGNITION: How does neuromodulation support cognitive processes, such as attention and working memory? Can we improve or disrupt behavioral measures of attention or working memory through the manipulation of neuromodulatory systems? At what site do the neuromodulators act, and what are the downstream changes in the neural circuitry that mediate the behavioral changes?

Figure 1 (adapted from Witten et al, Science 2010): Cholinergic interneurons of the nucleus accumbens control local circuit activity and cocaine reward. A. Expression of eNphR3.0, an inhibitory opsin activated by yellow light, specifically in cholinergic interneurons. B. Recording in a cholinergic interneuron expressing eNpHR3.0 reveals large inhibitory response to yellow light. C. In vivo recording demonstrates excitation of a surrounding neuron in response to inhibition of the cholinergic interneurons. D. Conditioning with cocaine in a place preference paradigm is disrupted in mice that express eNpHR3.0 in cholinergic interneurons (ChAT::Cre+), but is unaffected in the absence of cocaine.