The role of cGMP in the extinction of the reactions of identified neurons of the edible snail in response to acetylcholine

Pivovarov, A. S.; Drozdova, E. I.; Kotlyar, B. I.

doi:10.1007/bf01236326

Cited by 3 publications

(7 citation statements)

References 17 publications

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“…It also suggests that electrophysiological identification of specific NO-sensitive neurons is likely to be quite straightforward. Although our understanding of the function of the NO/cyclic GMP pathway in invertebrate nervous systems is in its infancy, several potential roles have been established, including modulation of synaptic efficacy (Pivovarov et al, 1990(Pivovarov et al, , 1995Mothet et al, 1996), sensory integration (Gelperin, 1994;Muller and Hildebrandt, 1995;Elphick et al, 1996), central pattern generation (Moroz et al, 1993;Elphick et al, 1995), higher information processing (Muller, 1996), and control over neural development (Scholz et al, 1995;Kuzin et al, 1996;Truman et al, 1996). The large sizes and reproducible locations of the NO-sensitive cells in the lobster nervous system offer the prospect of further evaluating the properties of this important second messenger pathway in a relatively simple and well-studied set of neuronal networks.…”

Section: Discussionmentioning

confidence: 99%

“…NO-induced guanylate cyclase activity has also been demonstrated in the nervous systems of moths (Morton, 1996), grasshoppers , crabs (Scholz et al, 1996), and lobsters (Scholz et al, 1995), using immunocytochemical methods to detect the cyclic GMP formed when these tissues are exposed to NO. Preliminary studies suggest that, as in vertebrates, this NO-sensitive cyclase may play a role both in neurodevelopment (Scholz et al, 1995;Kuzin et al, 1996;Truman et al, 1996) and in neurotransmitter-dependent modulation of synaptic strength (Pivovarov et al, 1990(Pivovarov et al, , 1995Mothet et al, 1996).…”

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confidence: 99%

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Identification of Nitric Oxide‐Sensitive and ‐Insensitive Forms of Cytoplasmic Guanylate Cyclase

Prabhakar

Short

Scholz

et al. 1997

Journal of Neurochemistry

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Cytoplasmic, nitric oxide-activated guanylate cyclases are expressed in many regions of the mammaian brain and are thought to participate in functions as diverse as synaptogenesis and long-term potentiation. In this study, we have characterized cytoplasmic guanylate cyclases in the nervous system of an invertebrate, the American lobster. Cytoplasmic cyclase specific activity is higher in lobster nerve cord than in any other lobster tissue tested, and considerably higher than in typical rat tissues (cerebellum, lung, and liver). However, nitric oxide donors have minimal effects on lobster nerve cord cyclic GMP production, when applied either to intact tissue or to cytoplasmic extracts. Parallel immunocytochemical studies, using an anti-cyclic GMP antibody, reveal that only a small subset of lobster neurons responds to nitric oxide with a significant elevation of cyclic GMP levels. HPLC analysis of nerve cord cytoplasm reveals two chromatographically separable cyclases, a minor nitric oxide-sensitive form whose retention time is identical to that of the conventional mammalian enzyme and a more abundant nitric oxide-insensitive form that appears to be novel. The physiological function and phylogenetic distribution of this nitric oxide-insensitive enzyme, and the signaling mechanisms that regulate its activity, are not known.

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Section: Discussionmentioning

confidence: 99%

mentioning

confidence: 99%

Identification of Nitric Oxide‐Sensitive and ‐Insensitive Forms of Cytoplasmic Guanylate Cyclase

Prabhakar

Short

Scholz

et al. 1997

Journal of Neurochemistry

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“…Activators of guanylate cyclase, the nitrogen-containing compounds Na nitroprusside (0.5-1 mM) and Na azide (0.5-1 mM) that increases [sic] the content of cGMP in the cell, intensify the extinction of the ACh-reactions [1,8,10,33]. In the RPa4 neuron the nitrogen-containing compounds increase the rate and depth of extinction, while not altering the duration of the spontaneous recovery of the extinguished response.…”

Section: Regulation Of the Plasticity Of The Cholinoreceptors By Secomentioning

confidence: 99%

“…The pharmacological effects on the adenylate cyclase system of the cell have no influence on the extinction of the ACh-reaction [1,7,8]. Neither forskolin (20-60 ~M), an activator of adenylate cyclase, which increases the content of cAMP, nor imidazole (5 mM), a phosphodiesterase activator that decreases the basal level of cAMP, alter extinction.…”

Section: Regulation Of the Plasticity Of The Cholinoreceptors By Secomentioning

confidence: 99%

“…The local application of acetylcholine (ACh) to the soma of RPa4, RPa3, and LPa3 neurons induces depolarization, which in the RPa4 neuron is succeeded by hyperpolarization [7,19]. ACh may induce these reactions by binding either with specific cholinoreceptors (CR), or with some nonspecific low-affinity membrane centers; therefore, the identification of ACh binding sites on the somatic membrane of these identified neurons was carried out.…”

Section: Identification Of Cholinoreceptorsmentioning

confidence: 99%

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Cholinoreceptor neurons of the snail: Identification, plasticity, and its regulation by opioids and second messengers

Pivovarov

1994

Neurosci Behav Physiol

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A review of the author's own data on the cholinoreceptors of identified neurons of the snail and the regulation of their plasticity. The following sections are presented: the identification of the cholinoreceptors; the coupling of the cholinoreceptors with ion channels; the identification of the opioid receptors; the modulation by opioids of the activity of the cholinoreceptors; the plasticity of the cholinoreceptors; the regulation of the plasticity of the cholinoreceptors by opioids; the regulation of the plasticity of the cholinoreceptors by second messengers; the second messengers involved in the regulation of the plasticity of the cholinoreceptors by the opiate kappa agonist, bremazocine.

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Effect of nitric oxide and cyclic guanosine monophosphate on the desensitization of choline receptors in snail neurons

Pivovarov

Drozdova

1996

Bull Exp Biol Med

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Desensitization of choline receptors is studied after pharmacological effects on the intracellular level of nitric oxide and cyclic guanosine monophosphate in snail neurons. It is shown that inhibitors of NO synthase do not alter desensitization, whereas an activator of guanylate cyclase as well as intracellular injection of guanosine monophosphate boost it.Key Words: nitric oxide; cyclic 3',5"guanosine monophosphate, desensitization of choline receptors; snail neuronsThe recently discovered second messenger nitric oxide (NO) [4,5] is an intermediate link between the transmitter receptor and soluble guanylate cyclase. Binding to the heme group of the enzyme, NO activates it and stimulates the synthesis of cyclic 3',5'-guanosine monophosphate (cGMP) [4,5].As was previously shown by us, cGMP is involved in desensitization of the choline receptors of the identified RPa3 and LPa3 neurons of the snail when sodium nitroprusside, an activator of guanilate cyclase, is used [1]. Stimulation of soluble guanylate cyclase by endogenous NO points to its role in the activation of cGMP synthesis in neurons and its involvement in the regulation of choline receptor desensitization. In this connection this study was devoted to an investigation of the influence of NO synthase inhibitors, cGMP, and guanylate cyclase modulators on desensitization of choline receptors of snail neurons. MATERIALS AND METHODS Experiments were carried out on the identified RPa3 and LPa3 neurons Of the edible snail (Helix lucorum)in a preparation of isolated ganglia. Transmembrane ion currents were recorded using the technique of the double-electrode voltage-clamp on the membrane.Desensitization of the choline receptors was assessed according to the suppression of the amplitude of the acetylcholine (AC)-induced inward current (AC current) during a series of 11-13 local rhythmic AC applications. To lower the amplitude of the AC current the first 10 stimuli were applied at a constant interval, the duration of which was 45-240 sec in series on different neurons. The next 1-3 stimuli were delivered at 10-rain intervals for estimation of the extent and rate of restoration of the diminished reaction.The following substances were used: inhibitors of NO synthase No-methyl-L-arginine acetate (L-NMMA, Fluka), the hydrochloride of the methyl ether of N-nitro-L-arginine (L-NAME, Sigma); the NO donor S-nitroso-N-acetylpenicillamine (SNAP, RBI); the inhibitor of soluble guanylate cyclase LY-

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The role of cGMP in the extinction of the reactions of identified neurons of the edible snail in response to acetylcholine

Cited by 3 publications

References 17 publications

Identification of Nitric Oxide‐Sensitive and ‐Insensitive Forms of Cytoplasmic Guanylate Cyclase

Identification of Nitric Oxide‐Sensitive and ‐Insensitive Forms of Cytoplasmic Guanylate Cyclase

Cholinoreceptor neurons of the snail: Identification, plasticity, and its regulation by opioids and second messengers

Effect of nitric oxide and cyclic guanosine monophosphate on the desensitization of choline receptors in snail neurons

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