| dc.description.abstract | Since the 1920s, it has been recognized that nonhuman animals are capable of forming expectations about rewards and exhibit emotional responses when those expectations are violated-- when obtained rewards have lower value than expected rewards. Our lab utilizes a rodent model for coping with unexpected reward loss with a specific interest in furthering our understanding of the underlying neural correlates. Frustration effects in rats are commonly and reliably produced using the consummatory successive negative contrast (cSNC) procedure, where rats are given access to a highly preferred 32% sucrose solution followed by an unexpected downshifted to 4% sucrose. Such surprising nonreward leads to a suppression of behavior compared to a control group that always received the less-preferred, 4% sucrose solution. Studies involving neurological manipulation indicate that permanent lesion or reversible deactivation of the central amygdala (CeA) and the basolateral amygdala (BLA) eliminate the cSNC effect. While these studies are important for identifying key structures, they provide little information about the underlying circuitry. The present research examined the role of the neural pathway between the BLA and CeA in the cSNC task using a chemogenetic approach known as Designer Receptor Exclusively Activated by Designer Drugs (DREADDs). Inhibitory DREADDs are intracranially infused into the key structures and later activated by intraperitoneal injections of clozapine N-oxide (CNO). Both groups of rats received unilateral inactivation of the BLA and CeA. The experimental (contralateral) group has one functioning area in each hemisphere, a procedure that disrupts communication between the two areas. The control (ipsilateral) group has one hemisphere disrupted while the other is left intact. Preliminary results indicate a disconnecting the BLA-CeA pathway reduces the cSNC effect in contralateral rats compared to ipsilateral rats. The BLA-CeA pathway is necessary to respond to surprising nonreward. These results add to the hypothesized model of circuity underlying unexpected reward loss in mammals. Because the amygdala circuitry is highly conserved across species, these results inform us about the neural circuitry engaged by similar instances of frustrative nonreward in the human brain. | |
