Abstract:
:We have recently characterized a form of ex vivo depotentiation (depotentiationex vivo), which correlates tightly with fear extinction, at thalamic input synapses onto the lateral amygdala. Here, we examined the effects of learning-attenuating drugs, reported to impair fear extinction when microinjected into the basolateral amygdala, on depotentiationex vivo. U0126, a mitogen-activated protein kinase inhibitor, and cycloheximide, a protein synthesis inhibitor, blocked depotentiationex vivo. However, ifenprodil, an NR2B-containing NMDA receptor inhibitor, did not alter depotentiationex vivo, although it blocked amygdala long-term potentiation. These findings indicate that amygdala depotentiation shares some molecular processes with learning and further suggest that different forms of synaptic plasticity in the basolateral amygdala mediate fear extinction.
journal_name
Neuroreportjournal_title
Neuroreportauthors
Kim J,Park S,Lee S,Choi Sdoi
10.1097/WNR.0b013e328329412dsubject
Has Abstractpub_date
2009-03-25 00:00:00pages
517-20issue
5eissn
0959-4965issn
1473-558Xjournal_volume
20pub_type
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