Blockade of amygdala metabotropic glutamate receptor subtype 1 impairs fear extinction

Jeongyeon Kim, Sukwon Lee, Heewoo Park, Beomjong Song, Ingie Hong, Dongho Geum, Kisoon Shin, Sukwoo Choi

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70 Citations (Scopus)

Abstract

The metabotropic glutamate receptor subtype 1 (mGluR1) is thought to be crucial for several forms of memory, but its role in memory extinction has not been determined. Here, we examined a role of mGluR1 in the extinction of conditioned fear using microinjection of an mGluR1 antagonist, CPCCOEt, into the lateral amygdala (LA), a critical structure for fear conditioning and extinction. Intra-LA injection of 3 μg CPCCOEt impaired extinction that was initiated 48 h after the conditioning, but not that initiated 2 h after the conditioning, indicating that the effectiveness of CPCCOEt depends upon the length of time since fear conditioning. The CPCCOEt injection failed to alter an mGluR1-like receptor (mGluR5)-dependent acquisition of fear memory, further supporting the specificity of the injected CPCCOEt on mGluR1. Together, our results suggest that amygdala mGluR1 plays a critical role in the extinction of learned fear, but not in the acquisition of fear memory.

Original languageEnglish
Pages (from-to)188-193
Number of pages6
JournalBiochemical and Biophysical Research Communications
Volume355
Issue number1
DOIs
Publication statusPublished - 30 Mar 2007

Bibliographical note

Funding Information:
This work was supported by the Korea Research Foundation grant funded by the Korean Government (MOEHRD) (KRF-2002-041-C00266, 2003-041-C20266, 2004-041-C00360), the Korea Science and Engineering Foundation (KOSEF) grant funded by the Korea government (MOST) (R01-2004-000-10613-0) and the Korea Health 21 R&D Project, Ministry of Health & Welfare, Republic of Korea (02-PJ1-PG1-CH06-0001). J. Kim, S. Lee, H. Park, B. Song, and I. Hong were supported by Brain Korea 21 Research Fellowships from the Korean Ministry of Education.

Keywords

  • Amygdala
  • CPCCOEt
  • Conditioning
  • Consolidation
  • Extinction
  • mGluR1

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