Interactions between the prefrontal cortex and amygdala during delay discounting and reversal.

Abstract

Interactions between the prefrontal cortex and amygdala are thought to be critical for reward anticipation. Alterations in reward anticipation that lead to an inability to wait for rewards or a diminished capacity to change behavior when doing so would be optimal is often termed impulsivity and compulsivity, respectively. Distinct regions of the prefrontal cortex may support decreased impulsivity through self-control and decreased compulsivity through flexibility. However, both self-control and flexibility appear to involve the amygdala. Using a delay discounting paradigm, the present investigation found that inactivation and disconnection of the medial prefrontal cortex and basolateral amygdala led rats to become more impulsive by affecting preference for smaller immediate over larger delayed rewards. Conversely, inactivation and disconnection of the orbitofrontal cortex and amygdala led rats to become more compulsive as demonstrated by an inability to flexibly reverse stimulus reward relationships in an odor reversal task. The present findings support a double dissociation between orbitofrontal cortex - amygdala interactions for odor reversal and medial prefrontal cortex - amygdala interactions for delay discounting.

Differential Modifications of Synaptic Weights During Odor Rule Learning: Dynamics of Interaction Between the Piriform Cortex with Lower and Higher Brain Areas

“…In particular, key roles have been suggested for the OB (Wilson and Sullivan 1994;Linster et al 2001;Fletcher and Wilson 2003;Churchwell et al 2009), the entorhinal cortex (Xu and Wilson 2012), and the OFC MacDonald 2008;Churchwell et al 2009). Indeed, we showed previously that both the ascending and descending synaptic inputs to the PC, from the OB and OFC are enhanced 3 days after learning (Cohen et al 2008).…”

Acute nicotine increases both impulsive choice and behavioural disinhibition in rats

“…Of particular relevance in the present context, nAChRs are present in many brain regions implicated in the modulation of impulsivity (e.g. the ventral tegmental area, striatum, nucleus accumbens, prefrontal cortex and amygdala; Aron et al 2004;Cardinal et al 2001;Christakou et al 2004;Churchwell et al 2009;Eagle et al 2008;Hariri et al 2006;Koob and Volkow 2010;Winstanley et al 2004). Extensive research on smokers suggests a strong association between nicotine dependence and impulsivity.…”

Future Directions in Emotion Dysregulation and Youth Psychopathology

“…Children and adolescents with anxiety disorders exhibit less functional connectivity in amygdalar-ventrolateral prefrontal connections than controls (e.g., Monk et al, 2008), and adolescents with externalizing disorders exhibit less functional connectivity in striatal-anterior cingulate connections than controls (e.g., Shannon, Sauder, Beauchaine, & Gatzke-Kopp, 2009). Deficient top-down control of the amygdala by the medial PFC, and reduced functional connectivity between the amygdala and the orbitofrontal cortex, are implicated in emotional lability and deficient self-regulation (see Churchwell, Morris, Heurtelou, & Kesner, 2009;Hilt, Hanson, & Pollak, 2011). Among typically developing individuals, the PFC reaches peak volume around ages 10-11, with gradual reductions observed thereafter (see Lenroot & Giedd, 2006).…”