Functional Uncoupling between the Receptor and G-Protein as the Result of PKC Activation, Observed in Aplysia Neurons.

Sasaki, Kazuhiko; Kawasaki, Satoshi; Kimura, Shuichi; Fujita, Reiko; Takashima, Koichiro; Matsumoto, Marissa L.; Sato, Moritoshi

doi:10.2170/jjphysiol.47.241

Cited by 7 publications

(6 citation statements)

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“…Earlier we described that members of the MIP family elicit an outward current in D-neurons of Helix pomatia (Kiss et al, 1999). The peptide-elicited outward current could be blocked by Ba 2+ , Cs 2+ , TEA + and 4AP, and in this respect was similar to the K-current evoked by dopamine, histamine, FMRFa and APGWa in Planorbarius, Lymnaea and Aplysia Brezina, 1988;Bolshakov et al, 1993;Sasaki et al, 1997;Tol-Steye et al, 1997). Furthermore, dopamine, histamine, serotonin, acetylcholine, FMRFa and APWGa receptors are all G-protein coupled and all converge onto a single type of K-channel (Ascher & Chesnoy-Marchais, 1982;Brezina, 1988;Bolshakov et al, 1993;Tol-Steye et al, 1997).…”

Section: Discussionsupporting

confidence: 52%

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G‐protein coupled activation of potassium channels by endogenous neuropeptides in snail neurons

Kiss

2005

Eur J of Neuroscience

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Members of the mytilus inhibitory peptide (MIP) family play an important role in the modulation of many physiological processes in molluscs. The signal transduction pathways affected by the MIP effect have not, however, been elucidated. Application of guanosine 5'-[gamma-thio]triphosphate tetralithium salt (GTPgammaS), guanosine 5'-[beta-thio]diphosphate trilithium salt (GDPbetaS), the G-protein inhibitor suramin and pertussis toxin (PTX) demonstrated the involvement of the PTX-insensitive G-protein in the signal transduction pathway mediating MIP effects. Both G-protein alpha(i) and betagamma subunits were identified in D-neurons of Helix pomatia by immunoblotting. Their role in signal transduction was shown in electrophysiological experiments, which supported the notion that, in addition to the Galpha subunit, the betagamma dimer also participates in the neuropeptide-induced activation of K-channels in snail neurons. Finally, neuropeptide-activated responses were inhibited by the activation of adenylyl cyclase and by blockers of the phospholipase pathway. We suggest that bifurcation of the signal transduction takes place at the level of G-protein subunits. The alpha subunit may have a direct effect on adenylyl cyclase, while the betagamma subunit may have a direct effect on phospholipase enzymes.

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Section: Discussionsupporting

confidence: 52%

“…The indirect interaction of G‐proteins with the channels also has been documented in molluscs (Sasaki et al ., 1997). It was reported that the lipoxygenase metabolites of arachidonic acid are involved in the signal transduction route of the K (s) ‐channels (Belardetti et al ., 1989; Buttner et al ., 1989; Bahls et al ., 1992).…”

Section: Introductionmentioning

confidence: 99%

G‐protein coupled activation of potassium channels by endogenous neuropeptides in snail neurons

Kiss

2005

Eur J of Neuroscience

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“…An endogenous PTX‐sensitive G i ‐coupled receptor, potentially a D 2 ‐like receptor, was previously described. Upon DA stimulation, it was shown to induce a K + ‐current response in Aplysia sensory neurons (Sasaki et al . 1997).…”

Section: Resultsmentioning

confidence: 99%

“…An endogenous PTX-sensitive G i -coupled receptor, potentially a D 2 -like receptor, was previously described. Upon DA stimulation, it was shown to induce a K + -current response in Aplysia sensory neurons (Sasaki et al 1997). When injected with plasmid coding for the Ap dop1 receptor, sensory neurons still showed an inhibitory response following DA application at concentrations sufficient to induce maximal response of the Ap dop1 receptor (Fig.…”

Section: Expression Of the Ap Dop1 Receptor In Aplysia Sensory Neuronsmentioning

confidence: 92%

An aplysia dopamine₁‐like receptor: molecular and functional characterization

Barbas

Zappulla

Angers

et al. 2005

Journal of Neurochemistry

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In Aplysia, the neurotransmitter dopamine is involved in the regulation of various physiological processes and motor functions, like feeding behaviour, and in the siphon-gill withdrawal reflex. In this paper, we report the characterization of the first Aplysia D1-like dopamine receptor (Apdop1) mainly expressed in the CNS, heart and buccal mass. Following expression of the Apdop1 receptor in HEK293 cells, a higher level of cAMP was observed in the absence of the receptor ligand, showing that Apdop1 is constitutively active. This activity was blocked by the inverse agonist flupentixol. Application of dopamine (EC50 of 35 nm) or serotonin (EC50 of 36 microm) to Apdop1-transfected HEK293 cells further increased the level of cAMP, suggesting that the receptor is linked to the stimulatory Gs protein pathway. When expressed in cultured sensory neurons, Apdop1 immunoreactivity was observed in the cell body and neurites. Control sensory neurons responded to dopamine with a decrease in excitability mediated by a pertusis toxin-sensitive G protein. Expression of Apdop1 produced an increase in hyperpolarization in the absence of agonist and an increase in membrane excitability following stimulation by dopamine. In the presence of pertussis toxin to inhibit the Gi protein inhibitory pathway responsible for decrease in excitability mechanism, Stimulation of membrane excitability was observed. Apdop1 sensitivity to dopamine makes it a potential modulator of operant conditioning procedure.

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“…PDBu has been used previously in Aplysia to activate PKC (Sacktor and Schwartz, 1990;Critz and Byrne, 1992;Wu et al, 1995;Sasaki et al, 1997;Manseau et al, 1998) and has been shown to induce long-term increases in sensory neuron excitability in Aplysia (Manseau et al, 1998). Treatment of cultures with 1.5 hr PDBu (0.25 M) produced no change in glutamate uptake (1 Ϯ 14%; t ϭ 0.08; n ϭ 8; p Ͼ 0.9) measured 24 hr after treatment (Fig.…”

Section: Pkc Is Not Involved In the Long-term Increase In Glutamate Umentioning

confidence: 83%

Coregulation of Glutamate Uptake and Long-Term Sensitization inAplysia

Khabour¹,

Levenson²,

Lyons³

et al. 2004

J. Neurosci.

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In Aplysia, long-term facilitation (LTF) at sensorimotor synapses of the pleural-pedal ganglia is mediated by an increase in the release of a neurotransmitter, which appears to be glutamate. Glutamate uptake also is increased in sensory neurons 24 hr after the induction of long-term sensitization (Levenson et al., 2000b). The present study investigated whether the same signaling pathways were involved in the long-term increase in glutamate uptake as in the induction of LTF. Thus, roles for cAMP, PKA (cAMP-dependent protein kinase), MAPK (mitogen-activated protein kinase), and tyrosine kinase in the regulation of glutamate uptake were tested. We found that 5-HT increased cAMP and activated PKA in sensory neurons. Exposure of pleural-pedal ganglia to analogs of cAMP or forskolin increased glutamate uptake 24 hr after treatments. Inhibitors of PKA (KT5720), MAPK (U0126 and PD98059), and tyrosine kinase (genistein) blocked the long-term increase in glutamate uptake produced by 5-HT. In addition, bpV, a tyrosine phosphatase inhibitor, facilitated the ability of subthreshold levels of 5-HT to increase glutamate uptake. Inhibition of PKC, which is not involved in LTF, had no effect on the long-term increase in glutamate uptake produced by 5-HT. Furthermore, activation of PKC by phorbol-12,13-dibutyrate did not produce long-term changes in glutamate uptake. The results demonstrate that the same constellation of second messengers and kinases is involved in the long-term regulation of both glutamate release and glutamate uptake. These similarities in signaling pathways suggest that regulation of glutamate release and uptake during formation of long-term memory are coordinated through coregulation of these two processes.

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Functional Uncoupling between the Receptor and G-Protein as the Result of PKC Activation, Observed in Aplysia Neurons.

Cited by 7 publications

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G‐protein coupled activation of potassium channels by endogenous neuropeptides in snail neurons

G‐protein coupled activation of potassium channels by endogenous neuropeptides in snail neurons

An aplysia dopamine₁‐like receptor: molecular and functional characterization

Coregulation of Glutamate Uptake and Long-Term Sensitization inAplysia

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Functional Uncoupling between the Receptor and G-Protein as the Result of PKC Activation, Observed in Aplysia Neurons.

Cited by 7 publications

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G‐protein coupled activation of potassium channels by endogenous neuropeptides in snail neurons

G‐protein coupled activation of potassium channels by endogenous neuropeptides in snail neurons

An aplysia dopamine1‐like receptor: molecular and functional characterization

Coregulation of Glutamate Uptake and Long-Term Sensitization inAplysia

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An aplysia dopamine₁‐like receptor: molecular and functional characterization