Dysfunction in amygdala-prefrontal plasticity and extinction-resistant avoidance: A model for XXXX vulnerability.

@entity3391 @entity4476 @entity148 @entity35 @entity12210
Individuals exhibiting an @entity148 are believed to possess an innate vulnerability that makes them susceptible to the disorder. @entity148 are also associated with abnormalities in the interconnected brain regions of the amygdala and prefrontal cortex (PFC). However, the link between @entity148 is currently unclear. Accordingly, the present study sought to determine if innate dysfunction within the amygdala to PFC projection underlies the susceptibility to develop @entity148 -like behavior, using an @entity148 vulnerable rodent model. The inbred @entity35 Kyoto (WKY) @entity35 was used to model vulnerability, as this strain naturally expresses extinction-resistant avoidance; a behavior that models the symptom of avoidance present in @entity148 . Synaptic plasticity was assessed within the projection from the basolateral nucleus of the amygdala (BLA) to the prelimbic cortical subdivision of the PFC in WKY and Sprague Dawley (SD) @entity35 . While WKY @entity35 exhibited normal paired-pulse plasticity, they did not maintain long-term potentiation (LTP) as SD @entity35 . Thus, impaired plasticity within the BLA-PL cortex projection may contribute to extinction resistant avoidance of WKY, as lesions of the PL cortex in SD @entity35 impaired extinction of avoidance similar to WKY @entity35 . Treatment with @entity12210 to reverse the impaired LTP in WKY @entity35 was unsuccessful. The lack of LTP in WKY @entity35 was associated with a significant reduction of @entity3391 receptors containing @entity4476 subunits in the PL cortex. Thus, dysfunction in amygdala-PFC plasticity is innate in @entity148 vulnerable @entity35 and may promote extinction-resistant avoidance by disrupting communication between the amygdala and prefrontal cortex.
