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Systemic and intra-amygdala administration of glucocorticoid agonist and antagonist modulate extinction of conditioned fear.
Neuropsychopharmacology. 2006 May; 31(5):912-24.N

Abstract

We examined the effect of glucocorticoid agonists on the extinction of conditioned fear in rats by using fear-potentiated startle. Systemic injection of glucocorticoid receptor agonists dexamethasone (DEX) (0.1, 0.5, and 1.0 mg/kg) and intra-amygdala infusion of RU28362 (0.5, 1.0, and 3.0 ng/side) prior to extinction training facilitated extinction of conditioned fear in a dose-dependent manner. Extinction of conditioned fear and circulating corticosterone levels were attenuated by administration of corticosteroid synthesis inhibitor metyrapone (25 mg/kg s.c.) 90 min before extinction training. The facilitation effect of DEX was dependent on repeated presentation of the conditioned stimulus rather than exposure to the experimental context, indicating this effect did not result from impaired expression of conditioned fear or accelerated forgetting. Intra-amygdaloid administration of the glucocorticoid receptor antagonist mifepristone (0.1, 0.2, and 0.5 ng/side, bilaterally) blocked extinction of conditioned fear and the facilitation effect of DEX in a dose-dependent manner. Mifepristone (2 ng/side) did not affect extinction but blocked the facilitating effect of DEX. Systemic administration of DEX after extinction training also facilitated extinction, suggesting that DEX may influence the memory consodilation phase of extinction. The Dose of dexamethsone or metyrapone used here did not influence fear-potentiated startle when administered before testing. Thus, it is unlikely that these drugs influenced extinction by increasing or disrupting CS processing. All results suggested that amygdaloid glucocorticoid receptors were involved in the extinction of conditioned fear.

Authors+Show Affiliations

Department of Molecular Biology and Biochemistry, Institute of Biotechnology, National Chia-Yi University, Chia-Yi, Taiwan.No affiliation info availableNo affiliation info available

Pub Type(s)

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

Language

eng

PubMed ID

16205786

Citation

Yang, Yi-Ling, et al. "Systemic and Intra-amygdala Administration of Glucocorticoid Agonist and Antagonist Modulate Extinction of Conditioned Fear." Neuropsychopharmacology : Official Publication of the American College of Neuropsychopharmacology, vol. 31, no. 5, 2006, pp. 912-24.
Yang YL, Chao PK, Lu KT. Systemic and intra-amygdala administration of glucocorticoid agonist and antagonist modulate extinction of conditioned fear. Neuropsychopharmacology. 2006;31(5):912-24.
Yang, Y. L., Chao, P. K., & Lu, K. T. (2006). Systemic and intra-amygdala administration of glucocorticoid agonist and antagonist modulate extinction of conditioned fear. Neuropsychopharmacology : Official Publication of the American College of Neuropsychopharmacology, 31(5), 912-24.
Yang YL, Chao PK, Lu KT. Systemic and Intra-amygdala Administration of Glucocorticoid Agonist and Antagonist Modulate Extinction of Conditioned Fear. Neuropsychopharmacology. 2006;31(5):912-24. PubMed PMID: 16205786.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Systemic and intra-amygdala administration of glucocorticoid agonist and antagonist modulate extinction of conditioned fear. AU - Yang,Yi-Ling, AU - Chao,Po-Kuan, AU - Lu,Kwok-Tung, PY - 2005/10/6/pubmed PY - 2006/6/7/medline PY - 2005/10/6/entrez SP - 912 EP - 24 JF - Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology JO - Neuropsychopharmacology VL - 31 IS - 5 N2 - We examined the effect of glucocorticoid agonists on the extinction of conditioned fear in rats by using fear-potentiated startle. Systemic injection of glucocorticoid receptor agonists dexamethasone (DEX) (0.1, 0.5, and 1.0 mg/kg) and intra-amygdala infusion of RU28362 (0.5, 1.0, and 3.0 ng/side) prior to extinction training facilitated extinction of conditioned fear in a dose-dependent manner. Extinction of conditioned fear and circulating corticosterone levels were attenuated by administration of corticosteroid synthesis inhibitor metyrapone (25 mg/kg s.c.) 90 min before extinction training. The facilitation effect of DEX was dependent on repeated presentation of the conditioned stimulus rather than exposure to the experimental context, indicating this effect did not result from impaired expression of conditioned fear or accelerated forgetting. Intra-amygdaloid administration of the glucocorticoid receptor antagonist mifepristone (0.1, 0.2, and 0.5 ng/side, bilaterally) blocked extinction of conditioned fear and the facilitation effect of DEX in a dose-dependent manner. Mifepristone (2 ng/side) did not affect extinction but blocked the facilitating effect of DEX. Systemic administration of DEX after extinction training also facilitated extinction, suggesting that DEX may influence the memory consodilation phase of extinction. The Dose of dexamethsone or metyrapone used here did not influence fear-potentiated startle when administered before testing. Thus, it is unlikely that these drugs influenced extinction by increasing or disrupting CS processing. All results suggested that amygdaloid glucocorticoid receptors were involved in the extinction of conditioned fear. SN - 0893-133X UR - https://www.unboundmedicine.com/medline/citation/16205786/Systemic_and_intra_amygdala_administration_of_glucocorticoid_agonist_and_antagonist_modulate_extinction_of_conditioned_fear_ L2 - https://medlineplus.gov/steroids.html DB - PRIME DP - Unbound Medicine ER -