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.
|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|
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 number||Funding sponsor||Acronym|
|Baqyiatallah University of Medical Sciences||BMSU|
This work was supported by a grant from Neuroscience Research Center, Baqyiatallah (a.s.) University of Medical Sciences.
Zarrindast, M.-R.; Institute for Cognitive Science Studies (ICSS), Tehran, Iran; email:[email protected]
© Copyright 2017 Elsevier B.V., All rights reserved.