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Facilitation of conditioned fear extinction by d-cycloserine is mediated by mitogen-activated protein kinase and phosphatidylinositol 3-kinase cascades and requires de novo protein synthesis in basolateral nucleus of amygdala.
Neuroscience. 2005; 134(1):247-60.N

Abstract

Recent results showed that either systemic or intra-amygdala administration of d-cycloserine, a partial agonist at the glycine modulatory site on the glutamate N-methyl-d-aspartate receptor facilitates the extinction of conditioned fear. Here we evaluated the role of mitogen-activated protein kinase and phosphatidylinositol 3-kinase in the basolateral nucleus of amygdala on the effect of d-cycloserine. The facilitation effect of d-cycloserine on fear extinction and mitogen-activated protein kinase activation was completely blocked by intra-amygdala administration of mitogen-activated protein kinase inhibitor PD98059 (500 ng/side, bilaterally) or U0-126 (20 microM/side, bilaterally). Furthermore, phosphatidylinositol 3-kinase inhibitor (wortmannin, 5.0 microg/side, bilaterally) infused into the basolateral nucleus of amygdala significantly reduced both facilitation effect of d-cycloserine and phosphatidylinositol 3-kinase activation. Intra-amygdala administration of a transcription inhibitor (actinomycin D, 10 microg dissolved in 1.6 microl vehicle; 0.8 microl per side) and a translation inhibitor (anisomycin, 125 microg dissolved in 1.6 microl vehicle; 0.8 microl per side) completely blocked the facilitation effect of d-cycloserine. Control experiments indicated the blockage by actinomycin D or anisomycin were not due to lasting damage to the basolateral nucleus of amygdala or state dependency. In addition, none of the active drugs used here altered the expression of conditioned fear. These results suggested that phosphatidylinositol 3-kinase and mitogen-activated protein kinase-dependent signaling cascades and new protein synthesis within the basolateral nucleus of amygdala played important roles in the d-cycloserine facilitation of the extinction of conditioned fear.

Authors+Show Affiliations

Yang YL
Institute of Biotechnology, Department of Molecular Biology and Biochemistry, National Chia-Yi University, 300 University Road, Chia-Yi, Taiwan.
Lu KT
No affiliation info available

MeSH

AmygdalaAnimalsBehavior, AnimalBlotting, WesternConditioning, PsychologicalCycloserineDrug InteractionsEnzyme InhibitorsExtinction, PsychologicalFearMaleMitogen-Activated Protein KinasesPhosphatidylinositol 3-KinasesRatsRats, Sprague-DawleyReflex, StartleTime Factors

Pub Type(s)

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

Language

eng

PubMed ID

15951121

Citation

Yang, Y L., and K T. Lu. "Facilitation of Conditioned Fear Extinction By D-cycloserine Is Mediated By Mitogen-activated Protein Kinase and Phosphatidylinositol 3-kinase Cascades and Requires De Novo Protein Synthesis in Basolateral Nucleus of Amygdala." Neuroscience, vol. 134, no. 1, 2005, pp. 247-60.
Yang YL, Lu KT. Facilitation of conditioned fear extinction by d-cycloserine is mediated by mitogen-activated protein kinase and phosphatidylinositol 3-kinase cascades and requires de novo protein synthesis in basolateral nucleus of amygdala. Neuroscience. 2005;134(1):247-60.
Yang, Y. L., & Lu, K. T. (2005). Facilitation of conditioned fear extinction by d-cycloserine is mediated by mitogen-activated protein kinase and phosphatidylinositol 3-kinase cascades and requires de novo protein synthesis in basolateral nucleus of amygdala. Neuroscience, 134(1), 247-60.
Yang YL, Lu KT. Facilitation of Conditioned Fear Extinction By D-cycloserine Is Mediated By Mitogen-activated Protein Kinase and Phosphatidylinositol 3-kinase Cascades and Requires De Novo Protein Synthesis in Basolateral Nucleus of Amygdala. Neuroscience. 2005;134(1):247-60. PubMed PMID: 15951121.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Facilitation of conditioned fear extinction by d-cycloserine is mediated by mitogen-activated protein kinase and phosphatidylinositol 3-kinase cascades and requires de novo protein synthesis in basolateral nucleus of amygdala. AU - Yang,Y L, AU - Lu,K T, PY - 2004/12/20/received PY - 2005/03/23/revised PY - 2005/04/01/accepted PY - 2005/6/14/pubmed PY - 2005/12/13/medline PY - 2005/6/14/entrez SP - 247 EP - 60 JF - Neuroscience JO - Neuroscience VL - 134 IS - 1 N2 - Recent results showed that either systemic or intra-amygdala administration of d-cycloserine, a partial agonist at the glycine modulatory site on the glutamate N-methyl-d-aspartate receptor facilitates the extinction of conditioned fear. Here we evaluated the role of mitogen-activated protein kinase and phosphatidylinositol 3-kinase in the basolateral nucleus of amygdala on the effect of d-cycloserine. The facilitation effect of d-cycloserine on fear extinction and mitogen-activated protein kinase activation was completely blocked by intra-amygdala administration of mitogen-activated protein kinase inhibitor PD98059 (500 ng/side, bilaterally) or U0-126 (20 microM/side, bilaterally). Furthermore, phosphatidylinositol 3-kinase inhibitor (wortmannin, 5.0 microg/side, bilaterally) infused into the basolateral nucleus of amygdala significantly reduced both facilitation effect of d-cycloserine and phosphatidylinositol 3-kinase activation. Intra-amygdala administration of a transcription inhibitor (actinomycin D, 10 microg dissolved in 1.6 microl vehicle; 0.8 microl per side) and a translation inhibitor (anisomycin, 125 microg dissolved in 1.6 microl vehicle; 0.8 microl per side) completely blocked the facilitation effect of d-cycloserine. Control experiments indicated the blockage by actinomycin D or anisomycin were not due to lasting damage to the basolateral nucleus of amygdala or state dependency. In addition, none of the active drugs used here altered the expression of conditioned fear. These results suggested that phosphatidylinositol 3-kinase and mitogen-activated protein kinase-dependent signaling cascades and new protein synthesis within the basolateral nucleus of amygdala played important roles in the d-cycloserine facilitation of the extinction of conditioned fear. SN - 0306-4522 UR - https://www.unboundmedicine.com/medline/citation/15951121/Facilitation_of_conditioned_fear_extinction_by_d_cycloserine_is_mediated_by_mitogen_activated_protein_kinase_and_phosphatidylinositol_3_kinase_cascades_and_requires_de_novo_protein_synthesis_in_basolateral_nucleus_of_amygdala_ DB - PRIME DP - Unbound Medicine ER -