The Endogenous Opioids Related with Antinociceptive Effects Induced by Electrical Stimulation into the Amygdala
Takami Nakamura 1, 2, *, Mihoko Tomida 2, Toshiharu Yamamoto 3, Hiroshi Ando 2, Tetsuya Takamata 1, Eiji Kondo 4, Ikufumi Kurasawa 5, Naokazu Asanuma 2
Identifiers and Pagination:Year: 2013
First Page: 27
Last Page: 35
Publisher ID: TODENTJ-7-27
Article History:Received Date: 17/12/2012
Revision Received Date: 8/2/2013
Acceptance Date: 9/2/2013
Electronic publication date: 8/3/2013
Collection year: 2013
open-access license: This is an open access article licensed under the terms of the Creative Commons Attribution Non-Commercial License (http://creativecommons.org/licenses/by-nc/3.0/) which permits unrestricted, non-commercial use, distribution and reproduction in any medium, provided the work is properly cited.
Pain relief is necessary and essential for dental treatments. Recently, the relationships of pain and emotion were studied, and electrical stimulation applied to the amygdala depressed the nociceptive response in the anterior cingulate cortex (ACC). Thus, the antinociceptive effects of the amygdala are elucidated, but its mechanism is not yet clarified. The present study was performed to investigate whether endogenous opioid system is related to the depression, and the quantitative changes of endogenous opioids induced by electrical stimulation to the amygdala. We investigated immunohistologically c-Fos expression to confirm the activated neurons, as well as the distribution and the amount of endogenous opioids (β-endorphin, enkephalin and dynorphin A) in the brain using male Wistar rats, when electrical stimulation was applied to the central nucleus of the amygdala (CeA) or noxious stimulation was delivered to the peripheral tissue. c-Fos expression in the ipsilateral ACC was increased by electrical stimulation to the CeA. However, only a small amount of endogenous opioids was observed in the ACC when noxious stimulation or electrical stimulation was applied. In contrast, the amount of dynorphin A in the periaqueductal gray (PAG) was increased by electrical stimulation to the CeA, and the amount of β-endorphin in the PAG was increased by noxious stimulation to the peripheral tissue. The results suggest that dynorphin A in the PAG induced by electrical stimulation to the CeA activate the descending antinociceptive system, and suggest that the nociceptive response in the ACC is depressed indirectly.