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Muscarinic acetylcholine and proctolin receptors in the foregut of the locust Schistocerca gregaria: Role of inositol phosphates, protein kinase C and calcium in second messenger effects

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Muscarinic acetylcholine and proctolin receptors in the foregut of the locust Schistocerca gregaria : Role of inositol phosphates, protein kinase C and calcium in second messenger effects. / Hinton, J. M.; Nejad, M.; Issberner, J. P.; Hancock, J. T.; Osborne, R. H.

In: Insect Biochemistry and Molecular Biology, Vol. 28, No. 5-6, 01.05.1998, p. 331-343.

Research output: Contribution to journalArticle

Harvard

Hinton, JM, Nejad, M, Issberner, JP, Hancock, JT & Osborne, RH 1998, 'Muscarinic acetylcholine and proctolin receptors in the foregut of the locust Schistocerca gregaria: Role of inositol phosphates, protein kinase C and calcium in second messenger effects' Insect Biochemistry and Molecular Biology, vol. 28, no. 5-6, pp. 331-343. https://doi.org/10.1016/S0965-1748(98)00008-3

APA

Hinton, J. M., Nejad, M., Issberner, J. P., Hancock, J. T., & Osborne, R. H. (1998). Muscarinic acetylcholine and proctolin receptors in the foregut of the locust Schistocerca gregaria: Role of inositol phosphates, protein kinase C and calcium in second messenger effects. Insect Biochemistry and Molecular Biology, 28(5-6), 331-343. https://doi.org/10.1016/S0965-1748(98)00008-3

Vancouver

Hinton JM, Nejad M, Issberner JP, Hancock JT, Osborne RH. Muscarinic acetylcholine and proctolin receptors in the foregut of the locust Schistocerca gregaria: Role of inositol phosphates, protein kinase C and calcium in second messenger effects. Insect Biochemistry and Molecular Biology. 1998 May 1;28(5-6):331-343. https://doi.org/10.1016/S0965-1748(98)00008-3

Author

Hinton, J. M. ; Nejad, M. ; Issberner, J. P. ; Hancock, J. T. ; Osborne, R. H. / Muscarinic acetylcholine and proctolin receptors in the foregut of the locust Schistocerca gregaria : Role of inositol phosphates, protein kinase C and calcium in second messenger effects. In: Insect Biochemistry and Molecular Biology. 1998 ; Vol. 28, No. 5-6. pp. 331-343.

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@article{01decbb246c0497fbe579c7c89b59d32,
title = "Muscarinic acetylcholine and proctolin receptors in the foregut of the locust Schistocerca gregaria: Role of inositol phosphates, protein kinase C and calcium in second messenger effects",
abstract = "Acetylcholine (ACh) induced dose-dependent contraction of the locust (Schistocerca gregaria) foregut was antagonised by 4-DAMP (1,1-dimethyl-4- diphenylacetoxypiperidinium; 10 nM-10 μM) and Li+ (50- 100 mM). The inhibition by Li+, of ACh-induced gut contraction suggests that this muscarinic ACh receptor is linked to phosphatidylinositol second messenger systems. ACh (1 μM and 0.5 mM) stimulated concentration-dependent production of [3H]-inositol phosphates, including [3H]-inositol trisphosphate, from foregut homogenates incubated in Tris buffer containing [3H]-myo-inositol. Pre-incubation of homogenates with Li+ (50 mM) or atropine (10 μM) reduced ACh-stimulated inositol phosphate production by 95{\%}. The contractile effects of ACh, 1-oleoyl-2-sn-glycerol (OAG) and phorbol 12,13-dibutyrate (PDBu), but not those of proctolin, on the foregut, were reduced by the protein kinase C (PKC) inhibitor H7 (10 nM-10 μM) and the L-type Ca2+ channel blocker verapamil (1 μM-0.1 mM). In comparison, the contractile effects of proctolin, but not those of ACh, OAG and PDBu, were potentiated by H7 (10 nM- 10 μM) and attenuated by the inositol 1,4,5-trisphosphate (IP3) receptor blocker decavanadate (10 μM-0.5 mM) and ryanodine (1 μM-0.1 mM), an inhibitor of intracellular Ca2+ release. Decavanadate and ryanodine had no effect on ACh-induced tissue contraction. Proctolin-induced contraction was unaffected by the presence of verapamil at concentrations as high as 1 mM but was abolished by 10 mM Co2+ . These data suggest, that in the locust foregut, stimulation of ACh receptors causes activation of PKC, thereby promoting Ca2+ entry via the opening of L-type Ca2+ channels. However, the function of IP3 produced following activation of tissue muscarinic receptors is unclear. In contrast, activation of proctolin receptors causes verapamil-insensitive entry of extracellular Ca2+ as well as the generation of IP3 which causes release of Ca2+ from intracellular stores to bring about an increase in gut contractility.",
keywords = "Acetylcholine, Calcium, Inositol Phosphates, Proctolin, Protein Kinase C, Receptor, Schistocerca gregaria",
author = "Hinton, {J. M.} and M. Nejad and Issberner, {J. P.} and Hancock, {J. T.} and Osborne, {R. H.}",
year = "1998",
month = "5",
day = "1",
doi = "10.1016/S0965-1748(98)00008-3",
language = "English",
volume = "28",
pages = "331--343",
journal = "Insect Biochemistry and Molecular Biology",
issn = "0965-1748",
publisher = "Elsevier Science B.V.",
number = "5-6",

}

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TY - JOUR

T1 - Muscarinic acetylcholine and proctolin receptors in the foregut of the locust Schistocerca gregaria

T2 - Insect Biochemistry and Molecular Biology

AU - Hinton, J. M.

AU - Nejad, M.

AU - Issberner, J. P.

AU - Hancock, J. T.

AU - Osborne, R. H.

PY - 1998/5/1

Y1 - 1998/5/1

N2 - Acetylcholine (ACh) induced dose-dependent contraction of the locust (Schistocerca gregaria) foregut was antagonised by 4-DAMP (1,1-dimethyl-4- diphenylacetoxypiperidinium; 10 nM-10 μM) and Li+ (50- 100 mM). The inhibition by Li+, of ACh-induced gut contraction suggests that this muscarinic ACh receptor is linked to phosphatidylinositol second messenger systems. ACh (1 μM and 0.5 mM) stimulated concentration-dependent production of [3H]-inositol phosphates, including [3H]-inositol trisphosphate, from foregut homogenates incubated in Tris buffer containing [3H]-myo-inositol. Pre-incubation of homogenates with Li+ (50 mM) or atropine (10 μM) reduced ACh-stimulated inositol phosphate production by 95%. The contractile effects of ACh, 1-oleoyl-2-sn-glycerol (OAG) and phorbol 12,13-dibutyrate (PDBu), but not those of proctolin, on the foregut, were reduced by the protein kinase C (PKC) inhibitor H7 (10 nM-10 μM) and the L-type Ca2+ channel blocker verapamil (1 μM-0.1 mM). In comparison, the contractile effects of proctolin, but not those of ACh, OAG and PDBu, were potentiated by H7 (10 nM- 10 μM) and attenuated by the inositol 1,4,5-trisphosphate (IP3) receptor blocker decavanadate (10 μM-0.5 mM) and ryanodine (1 μM-0.1 mM), an inhibitor of intracellular Ca2+ release. Decavanadate and ryanodine had no effect on ACh-induced tissue contraction. Proctolin-induced contraction was unaffected by the presence of verapamil at concentrations as high as 1 mM but was abolished by 10 mM Co2+ . These data suggest, that in the locust foregut, stimulation of ACh receptors causes activation of PKC, thereby promoting Ca2+ entry via the opening of L-type Ca2+ channels. However, the function of IP3 produced following activation of tissue muscarinic receptors is unclear. In contrast, activation of proctolin receptors causes verapamil-insensitive entry of extracellular Ca2+ as well as the generation of IP3 which causes release of Ca2+ from intracellular stores to bring about an increase in gut contractility.

AB - Acetylcholine (ACh) induced dose-dependent contraction of the locust (Schistocerca gregaria) foregut was antagonised by 4-DAMP (1,1-dimethyl-4- diphenylacetoxypiperidinium; 10 nM-10 μM) and Li+ (50- 100 mM). The inhibition by Li+, of ACh-induced gut contraction suggests that this muscarinic ACh receptor is linked to phosphatidylinositol second messenger systems. ACh (1 μM and 0.5 mM) stimulated concentration-dependent production of [3H]-inositol phosphates, including [3H]-inositol trisphosphate, from foregut homogenates incubated in Tris buffer containing [3H]-myo-inositol. Pre-incubation of homogenates with Li+ (50 mM) or atropine (10 μM) reduced ACh-stimulated inositol phosphate production by 95%. The contractile effects of ACh, 1-oleoyl-2-sn-glycerol (OAG) and phorbol 12,13-dibutyrate (PDBu), but not those of proctolin, on the foregut, were reduced by the protein kinase C (PKC) inhibitor H7 (10 nM-10 μM) and the L-type Ca2+ channel blocker verapamil (1 μM-0.1 mM). In comparison, the contractile effects of proctolin, but not those of ACh, OAG and PDBu, were potentiated by H7 (10 nM- 10 μM) and attenuated by the inositol 1,4,5-trisphosphate (IP3) receptor blocker decavanadate (10 μM-0.5 mM) and ryanodine (1 μM-0.1 mM), an inhibitor of intracellular Ca2+ release. Decavanadate and ryanodine had no effect on ACh-induced tissue contraction. Proctolin-induced contraction was unaffected by the presence of verapamil at concentrations as high as 1 mM but was abolished by 10 mM Co2+ . These data suggest, that in the locust foregut, stimulation of ACh receptors causes activation of PKC, thereby promoting Ca2+ entry via the opening of L-type Ca2+ channels. However, the function of IP3 produced following activation of tissue muscarinic receptors is unclear. In contrast, activation of proctolin receptors causes verapamil-insensitive entry of extracellular Ca2+ as well as the generation of IP3 which causes release of Ca2+ from intracellular stores to bring about an increase in gut contractility.

KW - Acetylcholine

KW - Calcium

KW - Inositol Phosphates

KW - Proctolin

KW - Protein Kinase C

KW - Receptor

KW - Schistocerca gregaria

UR - http://www.scopus.com/inward/record.url?scp=0032078503&partnerID=8YFLogxK

U2 - 10.1016/S0965-1748(98)00008-3

DO - 10.1016/S0965-1748(98)00008-3

M3 - Article

VL - 28

SP - 331

EP - 343

JO - Insect Biochemistry and Molecular Biology

JF - Insect Biochemistry and Molecular Biology

SN - 0965-1748

IS - 5-6

ER -

ID: 255578081