Physiology and PharmacologyVolume 20, Issue 4, December 2016, Pages 220-230

Transient inactivation of the central amygdala modulates metabolic and hormonal responses to acute stress in female rats(Article)

  • aInstitute for Cognitive Science Studies (ICSS), Tehran, Iran
  • bNeuroscience Research Center, Baqiyatallah (a.S) University of Medical Sciences, Tehran, Iran
  • cDepartment of Endodontics, School of dentistry, AJA University of Medical Sciences, Tehran, Iran
  • dCognitive and Neuroscience Research Center (CNRC), Medical Genomic Research Center and Scholl of Advanced Siences in Medicine, Islamic Azad University, Tehran Medical Science Branch, Tehran, Iran
  • eDepartment of Pharmacology, School of Medicine, Tehran University of Medical Sciences, Tehran, Iran
  • fSchool of Cognitive Sciences, Institute for Research in Fundamental Sciences (IPM), Tehran, Iran
  • gIranian National Center for Addiction Studies, Tehran University of Medical Sciences, Tehran, Iran
  • hSubstance Abuse and Dependence Research Center, University of School Welfare and Rehabilitation Sciences, Tehran, Iran

Abstract

Introduction: Current study examined the possible role of the central nucleus of amygdala (CeA) transient inactivation on the metabolic and hormonal disturbances induced by acute electro foot shock stress in female rats. Considering the differences between female and male in responses to stress, this study attempts to reveal possible mechanisms underlying these differences. Methods: Uni-or bilateral CeA nucleus cannulation of female Wistar rats (W: 200±20 g) was preformed seven days before stress induction. Lidocaine hydrochloride (2%) administered five minutes before electro foot shock. Food and water intake, time of delaying the onset of eating, plasma glucose, corticosterone, estradiol and progesterone were measured after stress termination. Results: Stress caused an increase in food intake and time of delaying the onset of eating whereas had no effect on the water intake. In addition, plasma glucose, corticosterone and progesterone concentrations were increased. The CeA inactivation in the right and left sides results in reduced water intake and increased delay times to eating. However, bilaterally inactivation of the CeA results in reducing time that elapsed before eating. Lidocaine administration in the both sides of nucleus had no effect on food intake. Transient inactivation of the bilateral sides of CeA augmented the stress effect on the plasma glucose and estradiol but had no significant effect on the corticosterone and progesterone hormones. Conclusion: It could be concluded that inhibition of the CeA by lidocaine modulate certain metabolic and hormonal responses to acute stress in female rats. The CeA influence seems to be asymmetrical. © 2016, Iranian Society of Physiology and Pharmacology. All rights reserved.

Author keywords

  • Acute stress
  • Central amygdalaamygdala
  • Corticosterone
  • Estradiol
  • Female rat
  • Progesterone

Indexed keywords

EMTREE drug terms:corticosteroneestradiolglucoselidocaineprogesterone
EMTREE medical terms:acute stressadultanimal experimentanimal tissueArticlecannulationcentral nucleus (amygdala)controlled studyenzyme linked immunosorbent assayestrus cyclefemalefluid intakefood intakefootshockgene expressiongene inactivationhistologyhormone releasehormone responsemetabolic regulationmicroscopynonhumanproestrusrat

Chemicals and CAS Registry Numbers:

corticosterone, 50-22-6; estradiol, 50-28-2; glucose, 50-99-7, 84778-64-3; lidocaine, 137-58-6, 24847-67-4, 56934-02-2, 73-78-9; progesterone, 57-83-0

Funding details

Funding numberFunding sponsorAcronym
Baqyiatallah University of Medical SciencesBMSU

Funding text

This work was supported by a grant from Neuroscience Research Center, Baqyiatallah (a.s.) University of Medical Sciences.

  • ISSN: 17350581
  • Source Type: Journal
  • Original language: English
  • Document Type: Article
  • Publisher: Iranian Society of Physiology and Pharmacology

  Zarrindast, M.-R.; Institute for Cognitive Science Studies (ICSS), Tehran, Iran; email:[email protected]
© Copyright 2017 Elsevier B.V., All rights reserved.

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