The amygdala modulates prefrontal cortex activity relative to conditioned fear

Abstract

Animals learn that a tone can predict the occurrence of an electric shock through classical conditioning. Mice or rats trained in this manner display fear responses, such as freezing behaviour, when they hear the conditioned tone. Studies using amygdalectomized rats have shown that the amygdala is required for both the acquisition and expression of learned fear responses. Freezing to a conditioned tone is enhanced following damage to the dorsal part of the medial prefrontal cortex, indicating that this area may be involved in fear reduction. Here we show that prefrontal neurons reduce their spontaneous activity in the presence of a conditioned aversive tone as a function of the degree of fear. The depression in prefrontal spontaneous activity is related to amygdala activity but not to the freezing response itself. These data indicate that, in the presence of threatening stimuli, the amygdala controls both fear expression and prefrontal neuronal activity. They suggest that abnormal amygdala-induced modulation of prefrontal neuronal activity may be involved in the pathophysiology of certain forms of anxiety disorder.

Limbic-Cortical-Ventral Striatal Activation during Retrieval of a Discrete Cocaine-Associated Stimulus: A Cellular Imaging Study with γ Protein Kinase C Expression

“…Conditioned stimuli generally produce decreases in the activity of neurons in the anterior cingulate cortex and the PrL regions, whether predictive of a natural food reward or an aversive footshock (Garcia et al, 1999;Takenouchi et al, 1999). Although there is no clear evidence that the direction of a change in gene expression is directly correlated with neuronal activity, the decrease in expression of ␥ PKC in medial prefrontal cortical regions in response to the cocaine-associated cue shown here may reflect a similar conditioned decrease in neuronal activity.…”

Systemic administration of the benzodiazepine receptor partial inverse agonist FG‐7142 disrupts corticolimbic network interactions

“…Conditioned stressors alter activity in mPFC neurons and this effect is abolished by lesions (Garcia et al, 1999) or pharmacological inactivation (Laviolette et al, 2005) of BLA. Unconditioned stress also blocks long-term potentiation in mPFC, an effect mimicked by BLA stimulation (Maroun and Richter-Levin, 2003).…”

Glucocorticoids in the prefrontal cortex enhance memory consolidation and impair working memory by a common neural mechanism

“…Considerable evidence indicates that glucocorticoid-induced enhancement of memory consolidation of emotionally arousing experiences involves a neural circuitry of interacting brain regions that include the basolateral complex of the amygdala (BLA) and its projections to efferent brain regions (5-7), whereas glucocorticoid impairment of working memory depends primarily on influences within the medial prefrontal cortex (mPFC) (3), a brain region involved in higher-order cognitive and affective processing, as well as executive function (8,9). However, there is also extensive evidence that the BLA and mPFC are anatomically and functionally interconnected (10)(11)(12). Maintenance of mPFC activity is known to constrain BLA activity, whereas stress and glucocorticoids alter mPFC functioning, thereby increasing BLA responses to emotionally arousing stimuli (13).…”