Multiple second messenger routes enhance two high-voltage-activated calcium currents in molluscan neuroendocrine cells

Dreijer, A.M.C.; Kits, Karel S.

doi:10.1016/0306-4522(94)00446-c

Cited by 22 publications

(18 citation statements)

References 40 publications

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“…These results are consistent with previous findings that stimulation of PKA, PKC or cGMP-dependent protein kinase enhanced the sustained calcium current in CDCs (Dreijer and Kits, 1995). Moreover, neither specific inhibitors of PKA and PKC, nor the broad spectrum protein kinase inhibitor H-7, that prevent phosphorylation of the calcium channels in CDCs by PKA, PKC or cGMP-dependent protein kinase, caused suppression of the calcium currents (Dreijer and Kits, 1995).…”

Section: Signal Transduction Of the Fmrfa-induced Inhibitionsupporting

confidence: 93%

“…Next we investigated whether cAMP, PKC or cGMP were involved in the FMRFa-induced inhibition. Previous experiments have shown that stimulation of one of these intracellular messengers causes augmentation of both HVA calcium currents (Dreijer and Kits, 1995). Bath application of 8-cpt-cAMP (0.5 raM), a membrane-permeable analog of cAMP, did not interfere with the FMRFa-effect.…”

Section: Suppression Of the Calcium Currents (Measured As Peak Currmentioning

confidence: 76%

“…Control currents consisted of a transient and a sustained calcium current ( Fig. 2A) (Dreijer and Kits, 1995; see also Materials and Methods). The inhibitory effect of FMRFa became apparent at a membrane potential of -10 mV and increased with further depolarization.…”

Section: Resultsmentioning

confidence: 99%

“…The CDCs display two types of dihydropyridine-sensitive, high-voltage-activated (HVA) calcium currents, which differ in voltage-dependence of activation and inactivation and steady-state inactivation properties (Dreijer and Kits, 1995). The currents were characterized as: (1) a rapidly inactivating or transient current ('ginact = -10-25 ms), which activates at membrane potentials of > -40 mV and has a bell-shaped voltagedependence of inactivation; half-maximal steady-state inactivation occurs at about -22 mV; (2) a slowly inactivating or sustained current ('[inact ----100--300 ms), which activates at more depolarized potentials (> -10 mV) and inactivates voltage-dependently; its midpoint of steady-state inactivation is about +8 mV.…”

Section: Introductionmentioning

confidence: 99%

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Inhibition of a slowly inactivating high-voltage-activated calcium current by the neuropeptide FMRFa in molluscan neuroendocrine cells

Dreijer

Verheule

Kits

1995

Invertebrate Neuroscience

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Using the whole-cell voltage-clamp technique, the effects of the neuropeptide Phe-Met-Arg-Phe-NH 2 (FMRFa) on two types of dihydropyridine-sensitive, high-voltage-activated calcium currents were investigated in isolated neuroendocrine caudo-dorsal cells (CDCs), which control egg-laying in the mollusc Lymnaea stagnalis. These currents are: (1) a transient current ('~inact = -10-25 ms) with an activation threshold of-40 mV and maximal amplitude at + 10 mV and (2) a sustained current ('Cinac t = -100-300 ms) with a threshold of -10 mV and a peak at +30 mV.FMRFa caused a partial block of the calcium current that was rapid, reversible and dose-dependent (ED50 = 4.3 nM). The FMRFa-sensitive and insensitive currents differed in voltage-dependence of activation and inactivation, steadystate inactivation characteristics and time course of recovery from inactivation, all indicating that FMRFa selectively suppressed the sustained calcium current.Internal perfusion of CDCs with GTP-?-S or GDP-[3-S depressed the FMRFa response, suggesting the involvement of G-proteins. Experiments aimed at elucidation of the signal transduction pathway between the FMRFa receptor and the calcium channel revealed no involvement of second messengers and protein kinases. The FMRFa-induced inhibition of the sustained calcium current probably results from a direct interaction between a G-protein, activated by the FMRFa receptor, and the calcium channel.The selective inhibition of this calcium current is likely to decrease the influx of calcium during the action potential, which will reduce the release of autoexcitatory CDC-peptides and contribute to a suppression of excitability.

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Section: Signal Transduction Of the Fmrfa-induced Inhibitionsupporting

confidence: 93%

Section: Suppression Of the Calcium Currents (Measured As Peak Currmentioning

confidence: 76%

Section: Resultsmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

See 2 more Smart Citations

Inhibition of a slowly inactivating high-voltage-activated calcium current by the neuropeptide FMRFa in molluscan neuroendocrine cells

Dreijer

Verheule

Kits

1995

Invertebrate Neuroscience

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“…However, the mechanisms of signal transduction in this synaptic enhancement have not yet been determined. In general, the studies of the second-messenger system in L. stagnalis have not been advanced very far (Dreijer and Kits, 1995). Only the work by McCrohan and Gillette (1988) suggested that cyclic AMP (cAMP) is a candidate of the second messenger in the CGC by demonstrating the appearance of Na + current by the cAMP injection.…”

Section: Introductionmentioning

confidence: 99%

PKA-Dependent Regulation of Synaptic Enhancement between a Buccal Motor Neuron and Its Regulatory Interneuron in Lymnaea stagnalis

Nakamura¹,

Kobayashi²,

Kojima³

et al. 1999

Zoological Science

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ABSTRACT-The cerebral giant cell (CGC) is known to play a crucial role in the regulation of feeding response in the pond snail, Lymnaea stagnalis. However, the mechanisms of signal transduction from the CGC to the following buccal motor neurons are not clear. In the present study, we examined whether cyclic AMP (cAMP)-dependent protein kinase (PKA) contributes to enhancement of a monosynaptic connection between the presynaptic CGC and the postsynaptic buccal motor neuron 1 (B1 cell). Injection of cAMP into the CGC or inhibition of phosphodiesterase by isobutylmethylxanthine in the CGC increased the amplitude of excitatory postsynaptic potential (EPSP) in the B1 cell, whereas no changes were detected in the electrical properties of the CGC. The synaptic enhancement in the B1 cell was completely blocked by inhibition of PKA in the CGC but did not require a de novo protein synthesis due to a PKA phosphorylation. The increase in the EPSP amplitude of B1 cell was associated with the increase in the amount of serotonin release from the CGC. These results hence provided the physiological evidence of the direct regulation of a synaptic enhancement by PKA in the CNS of L. stagnalis, indicating the completely different mechanism from that in the well-studied siphon-and gill-withdrawal reflex in Aplysia.

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Electrically induced changes in Ca2+ inHelisoma neurons: Regional and neuron-specific differences and implications for neurite outgrowth

Torreano

Cohan

1997

J. Neurobiol.

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Multiple second messenger routes enhance two high-voltage-activated calcium currents in molluscan neuroendocrine cells

Cited by 22 publications

References 40 publications

Inhibition of a slowly inactivating high-voltage-activated calcium current by the neuropeptide FMRFa in molluscan neuroendocrine cells

Inhibition of a slowly inactivating high-voltage-activated calcium current by the neuropeptide FMRFa in molluscan neuroendocrine cells

PKA-Dependent Regulation of Synaptic Enhancement between a Buccal Motor Neuron and Its Regulatory Interneuron in Lymnaea stagnalis

Electrically induced changes in Ca2+ inHelisoma neurons: Regional and neuron-specific differences and implications for neurite outgrowth

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