Abstract
How do brain mechanisms create maladaptive attractions? Here intense maladaptive attractions are created in laboratory rats by pairing optogenetic channelrhodopsin (ChR2) stimulation of central nucleus of amygdala (CeA) in rats with encountering either sucrose, cocaine, or a painful shock-delivering object. We find that pairings make the respective rats pursue either sucrose exclusively, or cocaine exclusively, or repeatedly self-inflict shocks. CeA-induced maladaptive attractions, even to the painful shock-rod, recruit mesocorticolimbic incentive-related circuitry. Shock-associated cues also gain positive incentive value and are pursued. Yet the motivational effects of paired CeA stimulation can be reversed to negative valence in a Pavlovian fear learning situation, where CeA ChR2 pairing increases defensive reactions. Finally, CeA ChR2 valence can be switched to neutral by pairing with innocuous stimuli. These results reveal valence plasticity and multiple modes for motivation via mesocorticolimbic circuitry under the control of CeA activation.
Highlights
How do brain mechanisms create maladaptive attractions? Here intense maladaptive attractions are created in laboratory rats by pairing optogenetic channelrhodopsin (ChR2) stimulation of central nucleus of amygdala (CeA) in rats with encountering either sucrose, cocaine, or a painful shock-delivering object
Control rats with optically inactive virus in CeA (‘eYFP’) chose about between sucrose and cocaine regardless of which was paired with laser (Fig. 2b, c)
Pairing CeA ChR2 stimulation with sucrose, cocaine, or shock encounters produced strong motivation that switched between positive valence and negative valence, depending on situation
Summary
Intense maladaptive attractions are created in laboratory rats by pairing optogenetic channelrhodopsin (ChR2) stimulation of central nucleus of amygdala (CeA) in rats with encountering either sucrose, cocaine, or a painful shock-delivering object. Intense and narrowly focused attractions have been induced in laboratory rats by pairing of optogenetic channelrhodopsin (ChR2) stimulation of neurons in central nucleus of amygdala (CeA) with sensory rewards, intensifying appetitive motivation (e.g., effort breakpoints) and narrowing pursuit to the paired reward in choice tasks[9,10,11]. The value of motivation produced by CeA ChR2 pairings can switch to negative valence in a traditional Pavlovian fear learning context, oppositely increasing conditioned defensive reactions to cues for the uncontrollable footshock. CeA ChR2 control of mesocorticolimbic circuitry can create either maladaptive attractions, exaggerated fear reactions, or become relatively neutral by interacting with situational factors
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