Regulation of calcium influx into buccal muscles of <i>Aplysia</i> by acetylcholine and serotonin

Ram, Jeffrey L.; Parti, Rajesh

doi:10.1002/neu.480160106

Cited by 13 publications

(5 citation statements)

References 17 publications

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“…This is unlike the invertebrate muscle systems that were studied such as the buccal musculature of Aplysia where ACh is the primary transmitter in several types of motor neurons (Cohen et al 1978). In the Aplysia accessory radula closer (ARC) system, ACh causes contraction by depolarizing the muscle and causing Ca 2ϩ influx (Brezina and Weiss 1993;Ram and Parti 1985), but in Lymnaea FMRFamide a peptidergic rather than a classical, low molecular weight transmitter causes Ca 2ϩ influx by activating a membrane Ca 2ϩ channel. In the Lymnaea heart ACh inhibits the heartbeat and is the transmitter of a completely different motor neuron type (Buckett et al 1990b).…”

Section: Comparison With Other Systemsmentioning

confidence: 99%

FMRFamide-Activated Ca²⁺Channels inLymnaeaHeart Cells Are Modulated by “SEEPLY,” a Neuropeptide Encoded on the Same Gene

Brezden

Yeoman

Gardner

et al. 1999

Journal of Neurophysiology

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The cell-attached, patch-clamp technique was used to investigate the modulatory role of the neuropeptide SEQPDVDDYLRDVVLQSEEPLY ("SEEPLY") on FMRFamide-activated Ca2+ channels in isolated Lymnaea heart ventricular cells. Both SEEPLY and FMRFamide are encoded on the same neuropeptide gene and are coexpressed in a pair of excitatory motor neurons that innervate the heart. FMRFamide applied alone was capable of significantly increasing the P(open) time of a Ca2+ channel in isolated heart muscle cells. However, SEEPLY applied alone did not significantly alter the basal level of Ca2+ channel activity in the same cells. Repeated applications of FMRFamide (15 s every min) resulted in a progressive reduction in the number of Ca2+ channel openings and the overall P(open) time of the channel. The fifth successive 15-s application of FMRFamide failed to cause the Ca2+ channels to open in the majority of cells tested. When FMRFamide and SEEPLY were repeatedly applied together (2-min applications every 4 min) the FMRFamide-activated Ca2+ channels continued to respond after the fifth application of the two peptides. Indeed channel activity was seen to continue after repeated 2-min applications of FMRFamide and SEEPLY for as long as the patch lasted (

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Section: Comparison With Other Systemsmentioning

confidence: 99%

FMRFamide-Activated Ca²⁺Channels inLymnaeaHeart Cells Are Modulated by “SEEPLY,” a Neuropeptide Encoded on the Same Gene

Brezden

Yeoman

Gardner

et al. 1999

Journal of Neurophysiology

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“…ACh increases 45Ca2+ influx into the muscle (Ram and Parti, 1985) and our preliminary experiments (Bi-ezina and Weiss, 1993) have shown that ACh-induced contractions of the dissociated fibers are completely blocked when extracellular Ca2+ is removed or nifedipine added at about the concentrations at which it blocks the "L''-type Ca current. Furthermore, when the AChinduced depolarization is clamped below the activation threshold of the Ca current, no contraction occurs.…”

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confidence: 94%

Enhancement of Ca current in the accessory radula closer muscle of Aplysia californica by neuromodulators that potentiate its contractions

1994

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A major goal of neuroscience is to identify the neural and cellular mechanisms of behavior and its plasticity. Progress toward this goal has come particularly from work with a small number of tractable model preparations. One of these is the simple neuromuscular circuit consisting of the accessory radula closer (ARC) muscle of the mollusk Aplysia californica and its innervating motor and modulatory neurons. Contraction of the ARC muscle underlies a component of Aplysia feeding behavior, and plasticity of the behavior is in large part due to modulation of the amplitude and duration of the contractions of the muscle by a variety of modulatory neurotransmitters and peptide cotransmitters, among them the small cardioactive peptides (SCPs), myomodulins (MMs), and serotonin (5-HT). We have studied single dissociated ARC muscle fibers in order to determine whether modulation of membrane ion currents in the muscle might underlie these effects. First, we confirmed that the dissociated fibers were functionally intact: just as with the whole ARC muscle, their contractions were potentiated by 5-HT and SCPB and potentiated as well as depressed by MMA, and their cAMP content was greatly elevated by 5-HT, SCPA and SCPB, and to a lesser extent by MMA and MMB. Next, using voltage-clamp techniques, we found that two ion currents present in the fibers were indeed modulated. The fibers possess a dihydropyridine-sensitive, high- threshold “L”-type Ca current. This current was enhanced by the modulators that potentiate ARC-muscle contractions--5-HT, SCPA and SCPB, and MMA and MMB--but not by buccalinA, a modulator that does not act directly on the ARC muscle. All of the potentiating modulators, as well as elevation of cAMP in the fibers by forskolin or a cAMP analog, maximally enhanced the current about twofold and mutually occluded each other's effects. Since the Ca current supplies Ca2+ necessary for contraction of the muscle, the enhancement of the current is a good candidate to be a major mechanism of the potentiation of the contractions. In the following article we report that the modulators also, to different degrees, activate a distinctive K current and thereby depress the contractions. Net potentiation or depression then depends on the balance between the relative strengths of the modulation of the two ion currents.

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“…Studies on the influx of calcium-45 in response to ACh have been used to determine whether calcium dependence of contraction involves physical movement of calcium into the cell. ACh stimulates influx of calcium-45 into Aplysia buccal muscles El and 15 (Ram and Parti, 1985;Gole el ai. 1987); however, ACh does not significantly increase calcium-45 influx into ABRM (Tameyasu and Sugi.…”

Section: Discussionmentioning

confidence: 99%

“…Although previous experiments on mechanisms mediating the modulatory effect of 5-HT on buccal muscles have suggested roles for cyclic AMP (Mandelbaum, 1980: Rametal.. 1983) and calcium ( Ram etal.. 1984b;Ram and Parti. 1985), the cellular targets of these mediators have not been determined.…”

Section: Introductionmentioning

confidence: 98%

Contraction, Serotonin-Elicited Modulation, and Membrane Currents of Dissociated Fibers of Aplysia Buccal Muscle

Ram¹,

Zhang²,

Liu³

1991

The Biological Bulletin

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Feeding muscles of the buccal mass of Aplysia are innervated by cholinergic and serotonergic neurons. Buccal muscle 15 contracts in response to acetylcholine (ACh). During feeding arousal, ACh-elicited contraction of muscle 15 is potentiated by serotonin (5-HT). This paper demonstrates a dissociated cell preparation of muscle 15 in which cellular mechanisms regulating contraction can be investigated. Dissociated muscle fibers contracted in response to both KCl and ACh. Serotonin (10-6 M) significantly potentiated the shortening caused by both KCl and ACh. Potentiation lasted at least 4 min, similar to potentiation in intact muscles. Four types of currents recorded by patch clamp methods are illustrated. With 540 mM KCl in the patch electrode, stretch-activated channels having a chord conductance of 150 pS are observed in on-cell patches. In whole cell configuration, ACh elicits inward current at a holding potential of -60 mV. With high potassium in the electrode, depolarization elicits an outward current. The voltage-dependent outward current is blocked with cesium in the electrode and 4-aminopyridine and tetraethylammonium outside the cells. The remaining voltage-dependent inward current is calcium dependent. The voltage-dependent inward and outward currents are activated within the range of depolarization produced by ACh and may therefore play roles in regulating contractile responses elicited by ACh.

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Regulation of calcium influx into buccal muscles of Aplysia by acetylcholine and serotonin

Cited by 13 publications

References 17 publications

FMRFamide-Activated Ca²⁺Channels inLymnaeaHeart Cells Are Modulated by “SEEPLY,” a Neuropeptide Encoded on the Same Gene

FMRFamide-Activated Ca²⁺Channels inLymnaeaHeart Cells Are Modulated by “SEEPLY,” a Neuropeptide Encoded on the Same Gene

Enhancement of Ca current in the accessory radula closer muscle of Aplysia californica by neuromodulators that potentiate its contractions

Contraction, Serotonin-Elicited Modulation, and Membrane Currents of Dissociated Fibers of Aplysia Buccal Muscle

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Regulation of calcium influx into buccal muscles of Aplysia by acetylcholine and serotonin

Cited by 13 publications

References 17 publications

FMRFamide-Activated Ca2+Channels inLymnaeaHeart Cells Are Modulated by “SEEPLY,” a Neuropeptide Encoded on the Same Gene

FMRFamide-Activated Ca2+Channels inLymnaeaHeart Cells Are Modulated by “SEEPLY,” a Neuropeptide Encoded on the Same Gene

Enhancement of Ca current in the accessory radula closer muscle of Aplysia californica by neuromodulators that potentiate its contractions

Contraction, Serotonin-Elicited Modulation, and Membrane Currents of Dissociated Fibers of Aplysia Buccal Muscle

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Product

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FMRFamide-Activated Ca²⁺Channels inLymnaeaHeart Cells Are Modulated by “SEEPLY,” a Neuropeptide Encoded on the Same Gene

FMRFamide-Activated Ca²⁺Channels inLymnaeaHeart Cells Are Modulated by “SEEPLY,” a Neuropeptide Encoded on the Same Gene