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Glutamate NMDA receptors within the amygdala participate in the modulatory effect of glucocorticoids on extinction of conditioned fear in rats.
Neuropsychopharmacology. 2007 May; 32(5):1042-51.N

Abstract

Recent results show that brain glucocorticoids are involved in the dysregulation of fear memory extinction in post-traumatic stress disorder patients. The present study was aimed to elucidate the possible mechanism of glucocorticoids on the conditioned fear extinction. To achieve these goals, male SD rats, fear-potentiated startle paradigm, and Western blot were used. We found that (1) systemic administration of the synthetic glucocorticoid agonist dexamethasone (DEX) facilitated extinction of conditioned fear in a dose-dependent manner (0.05, 0.1, 0.5, or 1.0 mg/kg, i.p.); (2) systemic administration of the glutamate NMDA receptor antagonist (+/-)-HA966 (6.0 mg/kg, i.p.) and intra-amygdala infusion of the NMDA receptor antagonists MK801 (0.5 ng/side, bilaterally) or D,L-2-amino-5-phosphonovaleric acid (AP5, 2.0 ng/side, bilaterally) blocked the DEX facilitation effect; (3) the corticosteroid synthesis inhibitor metyrapone (25 mg/kg. s.c.) blocked extinction and this was prevented by co-administration of NMDA receptor agonist D-cycloserine (DCS, 5.0 mg/kg, i.p.); (4) co-administration of DEX and DCS in subthreshold doses provided a synergistic facilitation effect on extinction (0.2 and 5 mg/kg, respectively). Control experiments indicated that co-administration of DEX and DCS did not alter the expression of conditioned fear and the effect was not due to lasting damage to the amygdala. These results suggest that glutamate NMDA receptors within the amygdala participate in the modulatory effect of glucocorticoids on extinction.

Authors+Show Affiliations

Institute of Biotechnology, National Chia-Yi University, Chia-Yi, Taiwan.No affiliation info availableNo 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

17047672

Citation

Yang, Yi-Ling, et al. "Glutamate NMDA Receptors Within the Amygdala Participate in the Modulatory Effect of Glucocorticoids On Extinction of Conditioned Fear in Rats." Neuropsychopharmacology : Official Publication of the American College of Neuropsychopharmacology, vol. 32, no. 5, 2007, pp. 1042-51.
Yang YL, Chao PK, Ro LS, et al. Glutamate NMDA receptors within the amygdala participate in the modulatory effect of glucocorticoids on extinction of conditioned fear in rats. Neuropsychopharmacology. 2007;32(5):1042-51.
Yang, Y. L., Chao, P. K., Ro, L. S., Wo, Y. Y., & Lu, K. T. (2007). Glutamate NMDA receptors within the amygdala participate in the modulatory effect of glucocorticoids on extinction of conditioned fear in rats. Neuropsychopharmacology : Official Publication of the American College of Neuropsychopharmacology, 32(5), 1042-51.
Yang YL, et al. Glutamate NMDA Receptors Within the Amygdala Participate in the Modulatory Effect of Glucocorticoids On Extinction of Conditioned Fear in Rats. Neuropsychopharmacology. 2007;32(5):1042-51. PubMed PMID: 17047672.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Glutamate NMDA receptors within the amygdala participate in the modulatory effect of glucocorticoids on extinction of conditioned fear in rats. AU - Yang,Yi-Ling, AU - Chao,Po-Kuan, AU - Ro,Long-Sun, AU - Wo,Yu-Yuan P, AU - Lu,Kwok-Tung, Y1 - 2006/10/18/ PY - 2006/10/19/pubmed PY - 2007/6/6/medline PY - 2006/10/19/entrez SP - 1042 EP - 51 JF - Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology JO - Neuropsychopharmacology VL - 32 IS - 5 N2 - Recent results show that brain glucocorticoids are involved in the dysregulation of fear memory extinction in post-traumatic stress disorder patients. The present study was aimed to elucidate the possible mechanism of glucocorticoids on the conditioned fear extinction. To achieve these goals, male SD rats, fear-potentiated startle paradigm, and Western blot were used. We found that (1) systemic administration of the synthetic glucocorticoid agonist dexamethasone (DEX) facilitated extinction of conditioned fear in a dose-dependent manner (0.05, 0.1, 0.5, or 1.0 mg/kg, i.p.); (2) systemic administration of the glutamate NMDA receptor antagonist (+/-)-HA966 (6.0 mg/kg, i.p.) and intra-amygdala infusion of the NMDA receptor antagonists MK801 (0.5 ng/side, bilaterally) or D,L-2-amino-5-phosphonovaleric acid (AP5, 2.0 ng/side, bilaterally) blocked the DEX facilitation effect; (3) the corticosteroid synthesis inhibitor metyrapone (25 mg/kg. s.c.) blocked extinction and this was prevented by co-administration of NMDA receptor agonist D-cycloserine (DCS, 5.0 mg/kg, i.p.); (4) co-administration of DEX and DCS in subthreshold doses provided a synergistic facilitation effect on extinction (0.2 and 5 mg/kg, respectively). Control experiments indicated that co-administration of DEX and DCS did not alter the expression of conditioned fear and the effect was not due to lasting damage to the amygdala. These results suggest that glutamate NMDA receptors within the amygdala participate in the modulatory effect of glucocorticoids on extinction. SN - 0893-133X UR - https://www.unboundmedicine.com/medline/citation/17047672/Glutamate_NMDA_receptors_within_the_amygdala_participate_in_the_modulatory_effect_of_glucocorticoids_on_extinction_of_conditioned_fear_in_rats_ L2 - https://medlineplus.gov/steroids.html DB - PRIME DP - Unbound Medicine ER -