Referenced in: none

Automatically associated channels: Kir2.3

Title: Fear response failed to return in AAB extinction paradigm accompanied with increased NR2B and GluR1 per845 in hippocampal CA1.

Authors: L Xue, Z D Li, Z X Chen, X G Wang, Y W Shi, H Zhao

Journal, date & volume: Neuroscience, 2014 Feb 28 , 260, 1-11

PubMed link: http://www.ncbi.nlm.nih.gov/pubmed/24342568

Abstract
Extinction is a well-known and important behavioral phenomenon that allows an organism to adapt its behavior to its environment. Previous studies have shown that the expression of extinction is highly context dependent, meanwhile, conditioning context, as part of fear memory, might have influence on extinction formation. To this end, we have conducted four different extinction paradigms in this study: extinction conducted in the conditioning context but tested in another, novel context (AAB); conditioning in one context and extinction and testing in the second (ABB); conditioning in context A, extinction training in context B, but test back to context A (ABA); and extinction training in a third context, context C (ACB). Additionally, a low dose of the GABAA agonist muscimol was used to temporarily inactivate CA1 to observe its effect in extinction. Our results showed that rats under the AAB, but not the ACB or ABA condition, showed a similar level of freezing compared with the typical ABB extinction paradigm. Moreover, muscimol infused into CA1 before extinction training resulted in impaired extinction and down-regulation of NR2B activity and phosphorylated GluR1 (at Ser845) in CA1, and the expression levels of NR2B and GluR1 were decreased significantly in the basolateral amygdala (BLA). Thus, CA1 may play an important role in the context-specific expression of fear extinction, and Ser845 may be a phosphorylation site in GluR1 in CA1, triggering the context-specific response of extinction memory.