Drug and alcohol abuse presents major and increasing costs to individuals across society. Abuse of alcohol and other drugs has been suggested to alter multiple aspects of motivation and affect related processes. These changes include alterations in the motivational value of cues in the environment, exaggerated negative affect and anxiety, and disruption of top-down cognitive control. Improvements in our long-term treatment of drug and alcohol addiction require major advancements of our understanding of the underlying neural mechanisms of these processes. The central goal of the Richard lab is to understand the neural signaling and circuit mechanisms that drive motivation, affect and decision-making in both healthy brains and in models of addiction.
Cues that have been paired with rewards like food and drugs can gain the ability to induce motivational states like craving, and to invigorate reward-seeking behaviors. A major objective of the Richard lab is to identify neural populations that encode the motivational value of cues, and determine the neural building blocks of this encoding. We use in vivo electrophysiology in awake, behaving rats to identify neurons in the brain that encode the motivational value of cues, and to compare the timing of these representations across brain regions in order to constrain and develop circuit hypotheses. We then characterize these representations in specific neural circuit projection populations using genetically-encoded fluorescent activity indicators. Finally, we can test the role of specific neural populations in driving downstream representations of motivation using optogenetics. Another major goal of the Richard lab is to determine how alcohol and other drugs recruit and disrupt adaptive brain mechanisms underlying motivation and affect. To do so, we are investigating alterations in activity patterns in neural circuits that represent motivation, value and choice in models of alcohol abuse and exposure.
- Richard JM. Metabotropic glutamate receptor 5 signaling and appetitive Pavlovian behavior: implications for the treatment of addiction. Neuropsychopharmacology. 2019 Apr 9. doi: 10.1038/s41386-019-0375-y
- Ottenheimer D, Richard JM, Janak PH. Ventral pallidum encodes relative reward value earlier and more robustly than nucleus accumbens. Nat Commun. 2018;9:4350.
- Saunders BT, Richard JM, Margolis EB, Janak PH. Dopamine neurons create Pavlovian conditioned stimuli with circuit defined motivational properties. Nat Neurosci. 2018;21:1072-1083.
- Richard JM, Stout N, Acs D, Janak PH. Ventral pallidal encoding of reward seeking depends on the underlying associative structure. eLife. 2018;7:e33107.
- Richard JM, Ambroggi F, Janak PH, Fields HL. Ventral pallidum neurons encode incentive value and promote cue-elicited instrumental actions. Neuron. 2016;90:1165-1173.
- Richard JM, Fields HL. Mu-opioid receptor activation in the medial shell of nucleus accumbens promotes alcohol consumption, self-administration and cue-induced reinstatement. Neuropharmacology. 2016;108:14-23.
- Richard JM, Plawecki AM, Berridge KC. Nucleus accumbens GABAergic inhibition generates intense eating and fear that resists environmental retuning and needs no local dopamine. Eur J Neurosci. 2013;37:1789-1802.
- Richard JM, Castro DC, DiFeliceantonio AG, Robinson MJF, Berridge KC. Mapping brain circuits of reward and motivation: In the footsteps of Ann Kelley. Neurosci Biobehav Rev. 2013;37:1919-1931.
- Richard JM, Berridge KC. Prefrontal cortex modulates desire and dread generated by nucleus accumbens glutamate disruption. Biol Psychiatry. 2013;73:360-370.
- Richard JM, Berridge KC. Nucleus accumbens dopamine/glutamate interaction switches mode to generate desire versus dread: D1 alone for appetitive eating but D1 and D2 together for fear. J Neurosci. 2011;31:12866-12897.