Cholinergic-opioidergic interaction in the central amygdala induces antinociception in the guinea pig

Several studies have demonstrated the involvement of the central nucleus of the amygdala (CEA) in the modulation of defensive behavior and in antinociceptive regulation. In a previous study, we demonstrated the existence of a cholinergic-opioidergic interaction in the CEA, modulating the defensive r...

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Main Authors: Leite-Panissi C.R.A., Brentegani M.R., Menescal-de-Oliveira L.
Format: Article
Language:English
Published: Associação Brasileira de Divulgação Científica 2004-01-01
Series:Brazilian Journal of Medical and Biological Research
Subjects:
Online Access:http://www.scielo.br/scielo.php?script=sci_arttext&pid=S0100-879X2004001000018
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author Leite-Panissi C.R.A.
Brentegani M.R.
Menescal-de-Oliveira L.
author_facet Leite-Panissi C.R.A.
Brentegani M.R.
Menescal-de-Oliveira L.
author_sort Leite-Panissi C.R.A.
collection DOAJ
description Several studies have demonstrated the involvement of the central nucleus of the amygdala (CEA) in the modulation of defensive behavior and in antinociceptive regulation. In a previous study, we demonstrated the existence of a cholinergic-opioidergic interaction in the CEA, modulating the defensive response of tonic immobility in guinea pigs. In the present study, we investigated a similar interaction in the CEA, but now involved in the regulation of the nociceptive response. Microinjection of carbachol (2.7 nmol) and morphine (2.2 nmol) into the CEA promoted antinociception up to 45 min after microinjection in guinea pigs as determined by a decrease in the vocalization index in the vocalization test. This test consists of the application of a peripheral noxious stimulus (electric shock into the subcutaneous region of the thigh) that provokes the emission of a vocalization response by the animal. Furthermore, the present results demonstrated that the antinociceptive effect of carbachol (2.7 nmol; N = 10) was blocked by previous administration of atropine (0.7 nmol; N = 7) or naloxone (1.3 nmol; N = 7) into the same site. In addition, the decrease in the vocalization index induced by the microinjection of morphine (2.2 nmol; N = 9) into the CEA was prevented by pretreatment with naloxone (1.3 nmol; N = 11). All sites of injection were confirmed by histology. These results indicate the involvement of the cholinergic and opioidergic systems of the CEA in the modulation of antinociception in guinea pigs. In addition, the present study suggests that cholinergic transmission may activate the release of endorphins/enkephalins from interneurons of the CEA, resulting in antinociception.
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spelling doaj.art-1dc78763cca84219b3aa125278de73402022-12-22T02:06:30ZengAssociação Brasileira de Divulgação CientíficaBrazilian Journal of Medical and Biological Research0100-879X0034-73102004-01-01371015711579Cholinergic-opioidergic interaction in the central amygdala induces antinociception in the guinea pigLeite-Panissi C.R.A.Brentegani M.R.Menescal-de-Oliveira L.Several studies have demonstrated the involvement of the central nucleus of the amygdala (CEA) in the modulation of defensive behavior and in antinociceptive regulation. In a previous study, we demonstrated the existence of a cholinergic-opioidergic interaction in the CEA, modulating the defensive response of tonic immobility in guinea pigs. In the present study, we investigated a similar interaction in the CEA, but now involved in the regulation of the nociceptive response. Microinjection of carbachol (2.7 nmol) and morphine (2.2 nmol) into the CEA promoted antinociception up to 45 min after microinjection in guinea pigs as determined by a decrease in the vocalization index in the vocalization test. This test consists of the application of a peripheral noxious stimulus (electric shock into the subcutaneous region of the thigh) that provokes the emission of a vocalization response by the animal. Furthermore, the present results demonstrated that the antinociceptive effect of carbachol (2.7 nmol; N = 10) was blocked by previous administration of atropine (0.7 nmol; N = 7) or naloxone (1.3 nmol; N = 7) into the same site. In addition, the decrease in the vocalization index induced by the microinjection of morphine (2.2 nmol; N = 9) into the CEA was prevented by pretreatment with naloxone (1.3 nmol; N = 11). All sites of injection were confirmed by histology. These results indicate the involvement of the cholinergic and opioidergic systems of the CEA in the modulation of antinociception in guinea pigs. In addition, the present study suggests that cholinergic transmission may activate the release of endorphins/enkephalins from interneurons of the CEA, resulting in antinociception.http://www.scielo.br/scielo.php?script=sci_arttext&pid=S0100-879X2004001000018AntinociceptionVocalization testCholinergic-opioidergic interactionAmygdalaNaloxoneAtropine
spellingShingle Leite-Panissi C.R.A.
Brentegani M.R.
Menescal-de-Oliveira L.
Cholinergic-opioidergic interaction in the central amygdala induces antinociception in the guinea pig
Brazilian Journal of Medical and Biological Research
Antinociception
Vocalization test
Cholinergic-opioidergic interaction
Amygdala
Naloxone
Atropine
title Cholinergic-opioidergic interaction in the central amygdala induces antinociception in the guinea pig
title_full Cholinergic-opioidergic interaction in the central amygdala induces antinociception in the guinea pig
title_fullStr Cholinergic-opioidergic interaction in the central amygdala induces antinociception in the guinea pig
title_full_unstemmed Cholinergic-opioidergic interaction in the central amygdala induces antinociception in the guinea pig
title_short Cholinergic-opioidergic interaction in the central amygdala induces antinociception in the guinea pig
title_sort cholinergic opioidergic interaction in the central amygdala induces antinociception in the guinea pig
topic Antinociception
Vocalization test
Cholinergic-opioidergic interaction
Amygdala
Naloxone
Atropine
url http://www.scielo.br/scielo.php?script=sci_arttext&pid=S0100-879X2004001000018
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AT brenteganimr cholinergicopioidergicinteractioninthecentralamygdalainducesantinociceptionintheguineapig
AT menescaldeoliveiral cholinergicopioidergicinteractioninthecentralamygdalainducesantinociceptionintheguineapig