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

Neuroreport. 2009 Mar 25;20(5):517-20. doi: 10.1097/WNR.0b013e328329412d.

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.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Adrenergic alpha-Antagonists / pharmacology
  • Amygdala / drug effects
  • Amygdala / physiology*
  • Animals
  • Butadienes / pharmacology
  • Cycloheximide / pharmacology
  • Electric Stimulation
  • Enzyme Inhibitors / pharmacology
  • Extinction, Psychological / drug effects
  • Extinction, Psychological / physiology
  • Fear / drug effects
  • Fear / physiology
  • In Vitro Techniques
  • Long-Term Synaptic Depression / drug effects
  • Long-Term Synaptic Depression / physiology*
  • Male
  • Microelectrodes
  • Mitogen-Activated Protein Kinases / metabolism*
  • Nitriles / pharmacology
  • Piperidines / pharmacology
  • Protein Biosynthesis* / drug effects
  • Protein Synthesis Inhibitors / pharmacology
  • Rats
  • Rats, Sprague-Dawley
  • Receptors, N-Methyl-D-Aspartate / antagonists & inhibitors

Substances

  • Adrenergic alpha-Antagonists
  • Butadienes
  • Enzyme Inhibitors
  • Nitriles
  • Piperidines
  • Protein Synthesis Inhibitors
  • Receptors, N-Methyl-D-Aspartate
  • U 0126
  • Cycloheximide
  • Mitogen-Activated Protein Kinases
  • ifenprodil