Amygdala depotentiation ex vivo requires mitogen-activated protein kinases and protein synthesis.

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

Neuroreport

journal_title

Neuroreport

authors

Kim J,Park S,Lee S,Choi S

doi

10.1097/WNR.0b013e328329412d

subject

Has Abstract

pub_date

2009-03-25 00:00:00

pages

517-20

issue

5

eissn

0959-4965

issn

1473-558X

journal_volume

20

pub_type

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