Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound   Target Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound

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Query: EC:4.6.1.1 (adenylate cyclase)
19,190 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Octopamine is highly concentrated in neurones of several invertebrate species. Unlike in mammals, octopaminergic neurones in invertebrates are spatially separated from catecholaminergic neurons. In identified nerve cells of Aplysia, however, this amine coexists with other putative neurotransmitters. Octopamine is synthesized in nerves from tyrosine and tyramine and metabolised mainly by monoamine oxidase. When lobster nerves are depolarized, octopamine is liberated by a Ca2+-dependent process. A specific adenylate cyclase is stimulated by octopamine in several invertebrates to activate phosphorylase in the cockroach, induce a light-flash in firefly lattern or inhibit rhythm contractions in locust muscle. All of these observations provide compelling evidence that octopamine is a neurotransmitter in invertebrates. In mammals octopamine is localised in nerves in peripheral tissues and brain where it seems to coexist with noradrenaline, the catecholamine being present in much higher concentrations. Octopamine is released from nerves together with noradrenaline and it may under certain conditions modify the actions of the adrenergic neurotransmitter. Octopamine is present in unusually high concentrations in certain neurological and hepatic diseases and may have a pathophysiological role.
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PMID:Octopamine. 1 10

1. Octopamine (OA) (10(-7)-10(-5) M) relaxed isolated foreguts. Tyramine mimicked the effects of OA but was 64x less potent. 2. Proctolin (10(-8) M to 10(-6) M) induced contraction of isolated foreguts was antagonised non competitively by tyramine. 3. Mianserin (10(-6) M) was a non competitive antagonist of relaxation caused by tyramine but was without effect on proctolin induced contraction. 4. Caffeine (1 microM and 2 microM) caused non competitive inhibition of proctolin-induced tissue contraction. 5. It is concluded that tyramine antagonises proctolin-induced contraction of the foregut by activating an adenylate cyclase-linked OA2 receptor.
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PMID:Tyramine antagonizes proctolin-induced contraction of the isolated foregut of the locust Schistocerca gregaria by an interaction with octopamine2 receptors. 197 52

D,L-Octopamine elevates the cyclic AMP content of the lateral oviduct of the locust, Locusta migratoria, in a dose-dependent manner with a threshold of about 10(-8) M. The effect of octopamine is potentiated by the phosphodiesterase inhibitor 3-isobutyl-1-methylxanthine (IBMX). The response is specific for octopamine and synephrine with an order of potency being octopamine = synephrine greater than metanephrine greater than tyramine greater than norepinephrine = dopamine = 5-hydroxytryptamine and the effect of octopamine is inhibited by the alpha-adrenergic receptor antagonist phentolamine. The diterpene adenylate cyclase activator forskolin also elevates cyclic AMP levels and IBMX potentiates the action of forskolin. Stimulation of the two identified octopaminergic neurons which project to the lateral oviducts results in an elevation in cyclic AMP and again this effect is blocked by phentolamine. Elevation of cyclic AMP levels in the lateral oviducts by means of IBMX, forskolin or dibutyryl cyclic AMP mimics the physiological effects of octopamine on this preparation. The results indicate that the octopaminergic control of this insect's visceral muscle is mediated via cyclic AMP.
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PMID:Identified octopaminergic neurons modulate contractions of locust visceral muscle via adenosine 3',5'-monophosphate (cyclic AMP). 241 68

In the locust, cyclic adenosine monophosphate (cAMP) mediates at least part of the effects of octopamine, the neurotransmitter which regulates the release of two adipokinetic hormones (AKHs) from the glandular lobe of the corpus cardiacum (CC). We have examined the requirement for extracellular Ca2+ in the process of AKH release mediated by octopamine and by agents which artificially elevate intracellular cAMP levels. Octopamine and the adenylate cyclase activator forskolin elevate the cAMP content of the glandular lobe in normal saline, in normal saline with the Ca2+ channel blocker, methoxyverapamil, and in Ca2+-free saline during 10-min exposure periods. Octopamine, forskolin, and 8-bromo cAMP mediate release of AKHs in vitro in normal saline, but release is prevented in the absence of extracellular Ca2+. When glands are exposed to these agents in normal saline in the presence of methoxyverapamil, AKH release is curtailed in a similar manner. Lanthanum and EGTA dramatically reduce cAMP production elicited by octopamine and forskolin, and lanthanum prevents octopamine-mediated release of AKHs. The phosphodiesterase inhibitor, IBMX, elevates cAMP content in the presence and absence of extracellular Ca2+, and stimulates normal release of AKHs both in the presence and absence of extracellular Ca2+. However, following extensive washing in Ca2+-free saline, IBMX fails to evoke AKH release. Methoxyverapamil has no effect on IBMX-mediated secretion. These results suggest that IBMX may mobilize intracellular stores of Ca2+ to induce release. Extracellular Ca2+ is apparently required for the process of neurotransmitter-evoked release, as has been shown for release of other peptide hormones. Cyclic AMP is intimately associated with Ca2+ in mediating this process. The release of AKHs is more dependent upon extracellular Ca2+ than is cAMP production under the conditions examined in this study. Ca2+ may provide the signal which initiates the secretory response, although cAMP may modulate this signal or the cells' responsiveness to this signal in some way. Support for this hypothesis is provided by experiments with the Ca2+ ionophore, A23187. This agent provokes release of AKHs in a Ca2+-dependent manner, probably by elevating intracellular Ca2+ levels. A23187 does not elevate cAMP levels in the glandular lobe, indicating that cAMP elevation is not a prerequisite for secretion.
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PMID:Regulation of adipokinetic hormone release from locust neuroendocrine tissue: participation of calcium and cyclic AMP. 244 45

1. We analyzed the physiological effects of the adenylate cyclase activator forskolin, and other adenosine 3',5'-cyclic monophosphate (cAMP)-elevating agents, on neurons of the pyloric circuit from the stomatogastric ganglion of the lobster Panulirus interruptus. Agents were bath applied to pyloric neurons either in the synaptically intact pyloric circuit or following isolation from all known synaptic input. 2. Several cAMP-elevating agents, including forskolin, 3-isobutyl-1-methylxanthine, Ro20-1724, and 8-bromo-cAMP, generated similar motor patterns from the pyloric circuit. The motor patterns exhibited an increased cycle frequency and enhanced spike activity from all classes of pyloric neurons. Since these agents differ both in structure and site of action in the cAMP pathway, their physiological effects on the motor pattern probably result from increased cAMP levels in pyloric neurons. 3. When forskolin was applied to synaptically isolated neurons, it caused a strong activation or enhancement of activity of all pyloric cells. However, it induced different types of activity in different cells, including the induction of bursting pacemaker potentials in one cell type, activation of plateau potentials in another, and depolarization with activation or enhancement of tonic spike activity in the remaining cells. Thus there is no single physiological response to cAMP elevation in the pyloric circuit; its effects can be quite diverse, mediating several activity states, in different cells. 4. Radioimmunoassays were performed on whole stomatogastric ganglia to determine whether known neuromodulators can affect cAMP concentrations. Both forskolin and octopamine increased cAMP levels, whereas dopamine, serotonin, proctolin, and FMRFamide did not appreciably affect cAMP levels. The physiological effects of octopamine and forskolin are similar in most, but not all, pyloric cells. Octopamine is thus a candidate neuromodulator whose actions may be mediated, at least in part, by increased cAMP in some pyloric cells; however, forskolin does not completely mimic the physiological effects of octopamine on all pyloric neurons, suggesting that octopamine can also act by other biochemical mechanisms.
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PMID:cAMP elevation modulates physiological activity of pyloric neurons in the lobster stomatogastric ganglion. 244 16

We investigated efferent neurotransmission in the Limulus lateral eye by studying the action of pharmacological agents on responses of photoreceptor cells in vitro. We recorded transmembrane potentials from single cells in slices of retina that were excised during the day and maintained for several days in a culture medium. Potentials recorded in the absence of pharmacological agents resemble those recorded from cells in vivo during the day. Octopamine, a putative efferent neurotransmitter, induced changes in photoreceptor potentials that mimicked in part those generated at night by a circadian clock located in the brain. Specifically, octopamine (100 to 500 microM) decreased the frequency of occurrence of quantum bumps in the dark and increased the amplitude of photoreceptor responses to intermediate and high light intensities. Similar actions were produced by naphazoline (25 to 100 microM, potent agonist of octopamine), forskolin (8 to 400 microM, activator of adenylate cyclase), IBMX (1 mM, inhibitor of phosphodiesterase), and 8-bromo-cAMP (500 microM, analogue of cAMP). 8-bromo-cGMP (500 microM, analogue of cGMP) decreased the rate of spontaneous quantum bumps only. Our results support the hypothesis that (1) octopamine is an efferent neurotransmitter of circadian rhythms in the Limulus eye and that (2) it activates adenylate cyclase to increase levels of the second messenger, cAMP, in photoreceptor cells. Circadian changes in photoreceptor responses to moderate intensities may be a specific action of cAMP, since cGMP has no effect. Circadian changes in the rate of spontaneous quantum bumps may involve a less specific intermediate, since both cAMP and cGMP reduce bump rate. Characteristics of the retinal slice preparation precluded a detailed study of the effects of pharmacological agents on retinal morphology.
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PMID:Efferent neurotransmission of circadian rhythms in Limulus lateral eye. II. Intracellular recordings in vitro. 246 93

Efferent fibers from a central circadian clock innervate photoreceptors along the ventral nerve of Limulus and release octopamine when active. We have recorded ERG-like responses from the ventral eye in vivo over several day periods. We have also used intracellular microelectrodes to study changes in ventral photoreceptor function during exogenous applications of octopamine (the putative efferent neurotransmitter), IBMX (a phosphodiesterase inhibitor), and forskolin (an adenylate cyclase activator): (1) Responses to light measured at night from ventral photoreceptors in vivo are greater in amplitude than those recorded during the day; (2) Octopamine and agents that increase intracellular levels of cAMP in ventral photoreceptors decrease the rate of spontaneous (dark) bumps, increase photoreceptor response to light without changing threshold, and often increase the bump duration; and (3) These changes in function of ventral photoreceptors are similar to those that have been observed in the photoreceptor of the lateral eye during circadian clock activity at night, and in vitro in the presence of those same pharmacological agents.
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PMID:Circadian change in function of Limulus ventral photoreceptors. 248 47

Octopamine exerts its effects in insects through interaction with at least two classes of receptors, designated octopamine-1 and octopamine-2. Octopamine-2 receptors are positively coupled to adenylate cyclase, while octopamine-1 receptors are not coupled to this enzyme system. Ceratitis capitata brain appears to have octopamine receptors as unique aminergic receptors coupled to adenylate cyclase. These receptors show some pharmacological analogies with respect to octopamine-2 receptors, however they should constitute a new class of octopamine receptors. C. capitata brain octopamine receptors have also been characterized by [3H]octopamine-binding studies, exhibiting similar regulatory mechanisms to other receptors coupled to adenylate cyclase activation.
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PMID:A possible new class of octopamine receptors coupled to adenylate cyclase in the brain of the dipterous Ceratitis capitata. Pharmacological characterization and regulation of 3H-octopamine binding. 250 8

Insecticidal Bacillus thuringiensis (Bt) delta-endotoxins are cytolytic to a range of insect cell lines in vitro. Addition of Bt var. aizawai or var. israelensis toxins to Mamestra brassicae (cabbage moth) cells in vitro increased intracellular cyclic AMP, which was paralleled by activation of adenylate cyclase in isolated membranes. Var. kurstaki toxin, which does not lyse M. brassicae cells, had no effect on cyclic AMP concentrations in intact cells, but was able to stimulate adenylate cyclase in membrane preparations. In contrast, the bee-venom toxin melittin, which is also cytolytic, increased intracellular cyclic AMP in whole cells, but inhibited adenylate cyclase in isolated membranes. Octopamine and forskolin also increased cyclic AMP in cells, but were not cytolytic. When added to cells at concentrations exceeding their LC90 (concentration causing 90% cell death), melittin and var. israelensis toxins caused cell lysis without a concomitant increase in intracellular cyclic AMP. Taken together, these results suggest that activation of adenylate cyclase by cytolytic toxins is a secondary effect (related perhaps to interactions of these toxins with membrane lipids) and is neither necessary nor sufficient for cytolysis.
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PMID:Activation of insect cell adenylate cyclase by Bacillus thuringiensis delta-endotoxins and melittin. Toxicity is independent of cyclic AMP. 284 67

The effect of octopamine on intestinal smooth muscle of rabbit isolated jejunum has been studied. Octopamine induced a dose-dependent decrease of muscle tone and this reproducible relaxation was not modified by tetrodotoxin or by agents that acted on adrenergic nerve terminals. Adrenoceptor antagonists, at concentrations sufficient to block each adrenoceptor type, did not reduce the actions of octopamine. On the other hand, octopamine-induced relaxations were affected by agents that have the ability to change cyclic AMP (cAMP) content; such as alloxan (an adenylate cyclase inhibitor), imidazole (a stimulator of phosphodiesterase), and isobutyl methylxanthine (an inhibitor of phosphodiesterase). Direct stimulation of adenylate cyclase by octopamine was demonstrated using radioimmunoassay of cAMP. Furthermore, haloperidol and perphenazine at concentration required to block dopamine receptor sites attenuated both smooth muscle relaxation and the formation of cAMP induced by octopamine. The effect of octopamine was totally blocked by SCH 23390, an antagonist of dopamine D-1 receptors. The lack of effect of domperidone and sulpiride, antagonists of dopamine D-2 receptors, on the actions of octopamine excludes the involvement of dopamine D-2 receptors. These results suggest that octopamine acts on intestinal dopamine D-1 receptor sites to produce relaxation of rabbit jejunum through an increase of cAMP.
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PMID:Octopamine relaxes rabbit jejunal smooth muscle by selective activation of dopamine D1 receptors. 285 5


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