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Attenuation of reserpine-induced pain/depression dyad by gentiopicroside through downregulation of GluN2B receptors in the amygdala of mice.
Neuromolecular Med 2014; 16(2):350-9NM

Abstract

Epidemiological studies demonstrate that pain frequently occurs comorbid with depression. Gentiopicroside (Gent) is a secoiridoid compound isolated from Gentiana lutea that exhibits analgesic properties and inhibits the expression of GluN2B-containing N-methyl-D-aspartate (NMDA) receptors in the anterior cingulate cortex of mice. However, the effects of Gent on the reserpine-induced pain/depression dyad and its underlying mechanisms are unclear. Reserpine administration (1 mg/kg subcutaneous daily for 3 days) caused a significant decrease in the nociceptive threshold as evidenced by the reduced paw withdrawal latency in response to a radiant heat source and mechanical allodynia. Behavioral detection indicated a significant increase in immobility time during a forced swim test, as well as decreased time in the central area and total travel distance in an open field test. Furthermore, reserpinized animals exhibited increased oxidative stress. Systemic Gent administration dose-dependently ameliorated the behavioral deficits associated with reserpine-induced pain/depression dyad. At the same time, the decrease in biogenic amine levels (norepinephrine, dopamine, and serotonin) was integrated with the increase in caspase-3 levels and GluN2B-containing NMDA receptors in the amygdala of the reserpine-injected mice. Gent significantly reversed the changes in the levels of biogenic amines, caspase-3, and GluN2B-containing NMDA receptors in amygdala. However, Gent did not affect the expression of GluN2A-containing NMDA receptors. The inhibitory effects of Gent on oxidative stress were occluded by simultaneous treatment of GluN2B receptors antagonist Ro25-6981. Our study provides strong evidence that Gent inhibits reserpine-induced pain/depression dyad by downregulating GluN2B receptors in the amygdala.

Authors+Show Affiliations

Department of Pharmacology, School of Pharmacy, The Fourth Military Medical University, Xi'an, 710032, China.No affiliation info availableNo affiliation info availableNo affiliation info availableNo 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

24584520

Citation

Liu, Shui-bing, et al. "Attenuation of Reserpine-induced Pain/depression Dyad By Gentiopicroside Through Downregulation of GluN2B Receptors in the Amygdala of Mice." Neuromolecular Medicine, vol. 16, no. 2, 2014, pp. 350-9.
Liu SB, Zhao R, Li XS, et al. Attenuation of reserpine-induced pain/depression dyad by gentiopicroside through downregulation of GluN2B receptors in the amygdala of mice. Neuromolecular Med. 2014;16(2):350-9.
Liu, S. B., Zhao, R., Li, X. S., Guo, H. J., Tian, Z., Zhang, N., ... Zhao, M. G. (2014). Attenuation of reserpine-induced pain/depression dyad by gentiopicroside through downregulation of GluN2B receptors in the amygdala of mice. Neuromolecular Medicine, 16(2), pp. 350-9. doi:10.1007/s12017-013-8280-8.
Liu SB, et al. Attenuation of Reserpine-induced Pain/depression Dyad By Gentiopicroside Through Downregulation of GluN2B Receptors in the Amygdala of Mice. Neuromolecular Med. 2014;16(2):350-9. PubMed PMID: 24584520.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Attenuation of reserpine-induced pain/depression dyad by gentiopicroside through downregulation of GluN2B receptors in the amygdala of mice. AU - Liu,Shui-bing, AU - Zhao,Rong, AU - Li,Xu-sheng, AU - Guo,Hong-ju, AU - Tian,Zhen, AU - Zhang,Nan, AU - Gao,Guo-dong, AU - Zhao,Ming-gao, Y1 - 2014/03/01/ PY - 2013/07/30/received PY - 2013/11/20/accepted PY - 2014/3/4/entrez PY - 2014/3/4/pubmed PY - 2015/1/6/medline SP - 350 EP - 9 JF - Neuromolecular medicine JO - Neuromolecular Med. VL - 16 IS - 2 N2 - Epidemiological studies demonstrate that pain frequently occurs comorbid with depression. Gentiopicroside (Gent) is a secoiridoid compound isolated from Gentiana lutea that exhibits analgesic properties and inhibits the expression of GluN2B-containing N-methyl-D-aspartate (NMDA) receptors in the anterior cingulate cortex of mice. However, the effects of Gent on the reserpine-induced pain/depression dyad and its underlying mechanisms are unclear. Reserpine administration (1 mg/kg subcutaneous daily for 3 days) caused a significant decrease in the nociceptive threshold as evidenced by the reduced paw withdrawal latency in response to a radiant heat source and mechanical allodynia. Behavioral detection indicated a significant increase in immobility time during a forced swim test, as well as decreased time in the central area and total travel distance in an open field test. Furthermore, reserpinized animals exhibited increased oxidative stress. Systemic Gent administration dose-dependently ameliorated the behavioral deficits associated with reserpine-induced pain/depression dyad. At the same time, the decrease in biogenic amine levels (norepinephrine, dopamine, and serotonin) was integrated with the increase in caspase-3 levels and GluN2B-containing NMDA receptors in the amygdala of the reserpine-injected mice. Gent significantly reversed the changes in the levels of biogenic amines, caspase-3, and GluN2B-containing NMDA receptors in amygdala. However, Gent did not affect the expression of GluN2A-containing NMDA receptors. The inhibitory effects of Gent on oxidative stress were occluded by simultaneous treatment of GluN2B receptors antagonist Ro25-6981. Our study provides strong evidence that Gent inhibits reserpine-induced pain/depression dyad by downregulating GluN2B receptors in the amygdala. SN - 1559-1174 UR - https://www.unboundmedicine.com/medline/citation/24584520/Attenuation_of_reserpine_induced_pain/depression_dyad_by_gentiopicroside_through_downregulation_of_GluN2B_receptors_in_the_amygdala_of_mice_ L2 - https://dx.doi.org/10.1007/s12017-013-8280-8 DB - PRIME DP - Unbound Medicine ER -