TY - JOUR
T1 - Effects of a muscarinic agonist on octopamine-stimulated cyclic AMP production in American Cockroach (Periplaneta americana) nerve cords
AU - Hirashima, Akinori
AU - Oyama, Kazuhiko
AU - Eto, Morifusa
N1 - Copyright:
Copyright 2016 Elsevier B.V., All rights reserved.
PY - 1991/10
Y1 - 1991/10
N2 - In the presence of 0.5 mM EGT A (a calcium chelator), the muscarinic agonist carbachol at 0.1 mM inhibited octopamine-stimulated cyclic AMP (cAMP) production in intact ventral nerve cords of Periplaneta americana. This effect was reduced by the addition of 0.1 mM atropine (a muscarinic antagonist), suggesting that the effect is mediated via muscarinic acetylcholine receptors (mAChR). This inhibitory effect of carbachol was not observed in the synaptosomes of nerve cords, suggesting that the inhibitory effect was not due to direct coupling of the mAChR to adenylate cyclase but mediated by other second messengers. The inhibitory effect seems to be due to an increase in the intracellular calcium level. In the presence of exogeneous extracellular 0.25 mM Ca2 +the octopamine-stimulated cAMP production was lower than that in the absence of extracellular Ca2 +, and the cAMP levels were not further reduced by adding carbachol to the octopamine-stimulated cAMP production system. Washing did not remove all of the inhibitory activity of carbachol in intact nerve cords, indicating that carbachol modulated octopaminergic neurotransmission irreversibly.
AB - In the presence of 0.5 mM EGT A (a calcium chelator), the muscarinic agonist carbachol at 0.1 mM inhibited octopamine-stimulated cyclic AMP (cAMP) production in intact ventral nerve cords of Periplaneta americana. This effect was reduced by the addition of 0.1 mM atropine (a muscarinic antagonist), suggesting that the effect is mediated via muscarinic acetylcholine receptors (mAChR). This inhibitory effect of carbachol was not observed in the synaptosomes of nerve cords, suggesting that the inhibitory effect was not due to direct coupling of the mAChR to adenylate cyclase but mediated by other second messengers. The inhibitory effect seems to be due to an increase in the intracellular calcium level. In the presence of exogeneous extracellular 0.25 mM Ca2 +the octopamine-stimulated cAMP production was lower than that in the absence of extracellular Ca2 +, and the cAMP levels were not further reduced by adding carbachol to the octopamine-stimulated cAMP production system. Washing did not remove all of the inhibitory activity of carbachol in intact nerve cords, indicating that carbachol modulated octopaminergic neurotransmission irreversibly.
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U2 - 10.1080/00021369.1991.10871003
DO - 10.1080/00021369.1991.10871003
M3 - Article
AN - SCOPUS:84909930204
VL - 55
SP - 2547
EP - 2552
JO - Bioscience, Biotechnology and Biochemistry
JF - Bioscience, Biotechnology and Biochemistry
SN - 0916-8451
IS - 10
ER -