Incentive motivation that is dissociated from actual outcome value can lead to maladaptive attractions, such as in the case of a rat that pursues a painful shock-delivering object. We have previously shown that optogenetic channelrhodopsin (ChR2) stimulation of the central nucleus of the amygdala (CeA), when paired with the presence of a painful shockrod, causes laboratory rats to repeatedly self-inflict shocks. However, the CeA is a heterogeneous structure and the contributions of its individual neuronal subpopulations in creating shockrod attraction is not known. Here, in laboratory rats, CeA neurons expressing D1, adenosine 2a (A2a), or corticotropin releasing factor (CRF) receptors were optogenetically stimulated via ChR2 in the presence of a shockrod. In another group, CeA neurons were targeted non-selectively with the hSyn promoter. Over multiple test days, hSyn and D1 ChR2-stimulated rats displayed intense attraction for the shockrod, repeatedly self-inflicting shocks and even overcoming an occluding barrier to do so. In a separate experiment, we tested whether CeA ChR2 activation is capable of controlling preference for a laser-paired over a non-laser-paired reward in a choice test scenario. Here, CeA ChR2 activation paired with remifentanil was preferred over sucrose alone, and sucrose paired with CeA ChR2 activation was preferred over remifentanil alone. Together, these results reveal that CeA ChR2 activation can make particular rewards ‘wanted’ over available alternative rewards, and can even make harmful stimuli attractive and desirable. Our findings may have important implications for understanding the brain mechanisms of disorders in which individuals maladaptively pursue particular stimuli, such as in addictions, obsessive compulsion, and self-harm.
Tuesday, April 5, 2022
4448 East Hall
Dr. David Nguyen, Research Fellow working with Dr. Kent Berridge is giving a talk titled: "Amygdala neuronal mechanisms of 'wanting what hurts' "