Octopamine and cyclic AMP mediate release of adipokinetic hormone I and II from isolated locust neuroendocrine tissue

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Abstract

Octopamine serves as a neurotransmitter in the glandular lobe of the locust corpus cardiacum where it regulates adipokinetic hormone (AKH) secretion from intrinsic neurosecretory cells. Two AKHs (AKH I and II) from the corpus cardiacum of Locusta have been sequenced and synthesized. We have now demonstrated that octopamine mediates release of both AKH I and II from Locusta corpora cardiaca in vitro. Octopamine, IBMX, and forskolin have previously been shown to elevate levels of cAMP in the glandular lobe. In this paper we demonstrate that IBMX and forskolin mediate secretion of AKH I and AKH II thus mimicking the effects of octopamine in this tissue. The cAMP analogs dibutyryl cAMP and 8-bromo cAMP also elicit release of AKH and a subthreshold concentration of IBMX potentiates the effects of octopamine. These observations demonstrate that cAMP participates in regulating AKH release and support the hypothesis that octopamine mediates hormone release at least in part via changes in intracellular levels of cAMP. The release of AKH I and AKH II is apparently regulated by similar mechanisms. The hyperlipemic activity of AKH II released into the perfusates following stimulation by octopamine and agents which elevate cAMP levels is significantly lower than that of AKH I. This differential response is probably due both to the reduced lipid-mobilizing effect of AKH II relative to AKH I, as well as to the release of greater amounts of AKH I.

Original languageEnglish (US)
Pages (from-to)153-159
Number of pages7
JournalMolecular and Cellular Endocrinology
Volume48
Issue number2-3
DOIs
StatePublished - 1986
Externally publishedYes

Fingerprint

Octopamine
Grasshoppers
Cyclic AMP
Tissue
Corpora Allata
1-Methyl-3-isobutylxanthine
Colforsin
adipokinetic hormone
8-Bromo Cyclic Adenosine Monophosphate

Keywords

  • adipokinetic hormone
  • corpus cardiacum
  • cyclic AMP
  • forskolin
  • locust
  • octopamine

ASJC Scopus subject areas

  • Endocrinology
  • Endocrinology, Diabetes and Metabolism

Cite this

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title = "Octopamine and cyclic AMP mediate release of adipokinetic hormone I and II from isolated locust neuroendocrine tissue",
abstract = "Octopamine serves as a neurotransmitter in the glandular lobe of the locust corpus cardiacum where it regulates adipokinetic hormone (AKH) secretion from intrinsic neurosecretory cells. Two AKHs (AKH I and II) from the corpus cardiacum of Locusta have been sequenced and synthesized. We have now demonstrated that octopamine mediates release of both AKH I and II from Locusta corpora cardiaca in vitro. Octopamine, IBMX, and forskolin have previously been shown to elevate levels of cAMP in the glandular lobe. In this paper we demonstrate that IBMX and forskolin mediate secretion of AKH I and AKH II thus mimicking the effects of octopamine in this tissue. The cAMP analogs dibutyryl cAMP and 8-bromo cAMP also elicit release of AKH and a subthreshold concentration of IBMX potentiates the effects of octopamine. These observations demonstrate that cAMP participates in regulating AKH release and support the hypothesis that octopamine mediates hormone release at least in part via changes in intracellular levels of cAMP. The release of AKH I and AKH II is apparently regulated by similar mechanisms. The hyperlipemic activity of AKH II released into the perfusates following stimulation by octopamine and agents which elevate cAMP levels is significantly lower than that of AKH I. This differential response is probably due both to the reduced lipid-mobilizing effect of AKH II relative to AKH I, as well as to the release of greater amounts of AKH I.",
keywords = "adipokinetic hormone, corpus cardiacum, cyclic AMP, forskolin, locust, octopamine",
author = "Pannabecker, {Thomas L} and Ian Orchard",
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TY - JOUR

T1 - Octopamine and cyclic AMP mediate release of adipokinetic hormone I and II from isolated locust neuroendocrine tissue

AU - Pannabecker, Thomas L

AU - Orchard, Ian

PY - 1986

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N2 - Octopamine serves as a neurotransmitter in the glandular lobe of the locust corpus cardiacum where it regulates adipokinetic hormone (AKH) secretion from intrinsic neurosecretory cells. Two AKHs (AKH I and II) from the corpus cardiacum of Locusta have been sequenced and synthesized. We have now demonstrated that octopamine mediates release of both AKH I and II from Locusta corpora cardiaca in vitro. Octopamine, IBMX, and forskolin have previously been shown to elevate levels of cAMP in the glandular lobe. In this paper we demonstrate that IBMX and forskolin mediate secretion of AKH I and AKH II thus mimicking the effects of octopamine in this tissue. The cAMP analogs dibutyryl cAMP and 8-bromo cAMP also elicit release of AKH and a subthreshold concentration of IBMX potentiates the effects of octopamine. These observations demonstrate that cAMP participates in regulating AKH release and support the hypothesis that octopamine mediates hormone release at least in part via changes in intracellular levels of cAMP. The release of AKH I and AKH II is apparently regulated by similar mechanisms. The hyperlipemic activity of AKH II released into the perfusates following stimulation by octopamine and agents which elevate cAMP levels is significantly lower than that of AKH I. This differential response is probably due both to the reduced lipid-mobilizing effect of AKH II relative to AKH I, as well as to the release of greater amounts of AKH I.

AB - Octopamine serves as a neurotransmitter in the glandular lobe of the locust corpus cardiacum where it regulates adipokinetic hormone (AKH) secretion from intrinsic neurosecretory cells. Two AKHs (AKH I and II) from the corpus cardiacum of Locusta have been sequenced and synthesized. We have now demonstrated that octopamine mediates release of both AKH I and II from Locusta corpora cardiaca in vitro. Octopamine, IBMX, and forskolin have previously been shown to elevate levels of cAMP in the glandular lobe. In this paper we demonstrate that IBMX and forskolin mediate secretion of AKH I and AKH II thus mimicking the effects of octopamine in this tissue. The cAMP analogs dibutyryl cAMP and 8-bromo cAMP also elicit release of AKH and a subthreshold concentration of IBMX potentiates the effects of octopamine. These observations demonstrate that cAMP participates in regulating AKH release and support the hypothesis that octopamine mediates hormone release at least in part via changes in intracellular levels of cAMP. The release of AKH I and AKH II is apparently regulated by similar mechanisms. The hyperlipemic activity of AKH II released into the perfusates following stimulation by octopamine and agents which elevate cAMP levels is significantly lower than that of AKH I. This differential response is probably due both to the reduced lipid-mobilizing effect of AKH II relative to AKH I, as well as to the release of greater amounts of AKH I.

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