| 19247210 |
Kim J, Park S, Lee S, Choi S: Amygdala depotentiation ex vivo requires mitogen-activated protein kinases and protein synthesis. Neuroreport. 2009 Mar 25;20(5):517-20.
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. |
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