The central amygdala recruits mesocorticolimbic circuitry for pursuit of reward or pain

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.

Cellular, circuit and transcriptional framework for modulation of itch in the central amygdala

“…Neural circuits in the central amygdala are implicated in pruritic process (Chen et al, 2016;Mu et al, 2017;Sanders et al, 2019), but cells and circuits that can alter pruritic processing in the CeA has been unclear. The CeA is well known to regulate a wide variety of aversive (Carrasquillo and Gereau, 2007;Ciocchi et al, 2010;Crock et al, 2012;Ehrlich et al, 2009;Haubensak et al, 2010;Tovote et al, 2016) and appetitive behaviors (Cai et al, 2014;Carter et al, 2013;Douglass et al, 2017;Hardaway et al, 2019;Kim et al, 2017;Robinson et al, 2014;Warlow et al, 2020). Here, we propose a cellular and circuit framework of the CeA in pruritis and its associated affect modulation.…”

“…Our additional experiments also suggest that the CeA chloroquine responsive neurons do not have any effect on feeding, reward seeking, motor and freezing behaviors. It is possible these behaviors are driven by distinct molecularly defined cell types in the CeA (Cai et al, 2014;Carter et al, 2013;Ciocchi et al, 2010;Douglass et al, 2017;Ehrlich et al, 2009;Hardaway et al, 2019;Haubensak et al, 2010;Kim et al, 2017;Robinson et al, 2014;Tovote et al, 2016;Warlow et al, 2020) that are distinct from the chloroquine-activated CeA neurons we have studied here.…”

'Liking' as a First Draft of the Affective Future

“…The full range of learning anomalies to which this leads has yet to be mined. Furthermore, there are various experimental procedures which can make persistently dis-'liked' goods strongly 'wanted' (Myers and Sclafani, 2003;Warlow et al, 2020).…”

Cellular, Circuit and Transcriptional Framework for Modulation of Itch in the Central Amygdala

“…Neural circuits in the central amygdala are implicated in pruritic process (Chen et al, 2016; Mu et al, 2017), but cells and circuits that can alter pruritic processing in the CeA has been unclear. The CeA is well known to regulate a wide variety of aversive (Carrasquillo and Gereau, 2007; Ciocchi et al, 2010; Crock et al, 2012; Ehrlich et al, 2009; Haubensak et al, 2010; Tovote et al, 2016) and appetitive behaviors (Cai et al, 2014; Carter et al, 2013; Douglass et al, 2017; Hardaway et al, 2019; Kim et al, 2017; Robinson et al, 2014; Warlow et al, 2020). Here, we propose a cellular and circuit framework of the CeA in pruritis and its associated affect modulation.…”

“…Our additional experiments also suggest that the CeA itch responsive neurons do not have any effect on feeding, reward seeking, motor and freezing behaviors. It is possible these behaviors are driven by distinct molecularly defined cell types in the CeA (Cai et al, 2014; Carter et al, 2013; Ciocchi et al, 2010; Douglass et al, 2017; Ehrlich et al, 2009; Hardaway et al, 2019; Haubensak et al, 2010; Kim et al, 2017; Robinson et al, 2014; Tovote et al, 2016; Warlow et al, 2020) that are distinct from the itch-activated CeA neurons we have studied here.…”