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Alterations of excitatory transmission in the lateral amygdala during expression and extinction of fear memory.
Int J Neuropsychopharmacol. 2010 Apr; 13(3):335-45.IJ

Abstract

Understanding the neurophysiology of fear extinction has important implications for the treatment of post-traumatic stress disorders. Here we report that fear conditioning resulted in an increase in AMPA/NMDA ratio as well as depression of paired-pulse facilitation (PPF) in neurons of the lateral nucleus of amygdala. These conditioning-induced changes in synaptic transmission were not affected by extinction training. D-cycloserine (DCS), a partial agonist at the glycine-binding site of the NMDA receptor, facilitated extinction and reversed the increase in AMPA/NMDA ratio without altering the depression of PPF when administered before extinction training. Extinction training, however, significantly increased the frequency and amplitude of miniature inhibitory post-synaptic currents and these effects were unaffected by the DCS treatment. Disruption of AMPA receptor endocytosis with a synthetic peptide containing a short C-terminal sequence of GluR2 (869YKEGYNVYG877, GluR23Y) specifically blocked DCS-induced reversal of AMPA/NMDA ratio and the facilitation of extinction. These results suggest that extinction training mainly increases inhibitory transmission leaving conditioning-induced excitatory association unaltered. DCS does not affect inhibitory transmission but reverses the conditioning-induced post-synaptic memory trace when administered before extinction training.

Authors+Show Affiliations

Institute of Basic Medical Sciences and Department of Pharmacology, Center for Gene Regulation and Signal Transduction Research, National Cheng-Kung University, Tainan, Taiwan.No affiliation info availableNo affiliation info availableNo affiliation info available

Pub Type(s)

Journal Article
Research Support, Non-U.S. Gov't

Language

eng

PubMed ID

19775504

Citation

Lin, Hui-Ching, et al. "Alterations of Excitatory Transmission in the Lateral Amygdala During Expression and Extinction of Fear Memory." The International Journal of Neuropsychopharmacology, vol. 13, no. 3, 2010, pp. 335-45.
Lin HC, Mao SC, Su CL, et al. Alterations of excitatory transmission in the lateral amygdala during expression and extinction of fear memory. Int J Neuropsychopharmacol. 2010;13(3):335-45.
Lin, H. C., Mao, S. C., Su, C. L., & Gean, P. W. (2010). Alterations of excitatory transmission in the lateral amygdala during expression and extinction of fear memory. The International Journal of Neuropsychopharmacology, 13(3), 335-45. https://doi.org/10.1017/S1461145709990678
Lin HC, et al. Alterations of Excitatory Transmission in the Lateral Amygdala During Expression and Extinction of Fear Memory. Int J Neuropsychopharmacol. 2010;13(3):335-45. PubMed PMID: 19775504.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Alterations of excitatory transmission in the lateral amygdala during expression and extinction of fear memory. AU - Lin,Hui-Ching, AU - Mao,Sheng-Chun, AU - Su,Chun-Lin, AU - Gean,Po-Wu, Y1 - 2009/09/24/ PY - 2009/9/25/entrez PY - 2009/9/25/pubmed PY - 2010/6/25/medline SP - 335 EP - 45 JF - The international journal of neuropsychopharmacology JO - Int J Neuropsychopharmacol VL - 13 IS - 3 N2 - Understanding the neurophysiology of fear extinction has important implications for the treatment of post-traumatic stress disorders. Here we report that fear conditioning resulted in an increase in AMPA/NMDA ratio as well as depression of paired-pulse facilitation (PPF) in neurons of the lateral nucleus of amygdala. These conditioning-induced changes in synaptic transmission were not affected by extinction training. D-cycloserine (DCS), a partial agonist at the glycine-binding site of the NMDA receptor, facilitated extinction and reversed the increase in AMPA/NMDA ratio without altering the depression of PPF when administered before extinction training. Extinction training, however, significantly increased the frequency and amplitude of miniature inhibitory post-synaptic currents and these effects were unaffected by the DCS treatment. Disruption of AMPA receptor endocytosis with a synthetic peptide containing a short C-terminal sequence of GluR2 (869YKEGYNVYG877, GluR23Y) specifically blocked DCS-induced reversal of AMPA/NMDA ratio and the facilitation of extinction. These results suggest that extinction training mainly increases inhibitory transmission leaving conditioning-induced excitatory association unaltered. DCS does not affect inhibitory transmission but reverses the conditioning-induced post-synaptic memory trace when administered before extinction training. SN - 1469-5111 UR - https://www.unboundmedicine.com/medline/citation/19775504/Alterations_of_excitatory_transmission_in_the_lateral_amygdala_during_expression_and_extinction_of_fear_memory_ L2 - https://academic.oup.com/ijnp/article-lookup/doi/10.1017/S1461145709990678 DB - PRIME DP - Unbound Medicine ER -