Cholinergic activation of the lobster cardiac ganglion

SUMMARYIn insects, a family of peptides with sequence homology to the vertebrate calcitonins has been implicated in the control of diuresis, a process that includes mixing of the hemolymph. Here, we show that a member of the insect calcitonin-like diuretic hormone (CLDH) family is present in the American lobster, Homarus americanus, serving, at least in part, as a powerful modulator of cardiac output. Specifically, during an ongoing EST project, a transcript encoding a putative H. americanus CLDH precursor was identified; a full-length cDNA was subsequently cloned. In silico analyses of the deduced prepro-hormone predicted the mature structure of the encoded CLDH to be GLDLGLGRGFSGSQAAKHLMGLAAANFAGGPamide (Homam-CLDH), which is identical to a known Tribolium castaneum peptide. RT-PCR tissue profiling suggests that Homam-CLDH is broadly distributed within the lobster nervous system, including the cardiac ganglion (CG), which controls the movement of the neurogenic heart. RT-PCR analysis conducted on pacemaker neuron-and motor neuron-specific cDNAs suggests that the motor neurons are the source of the CLDH message in the CG. Perfusion of Homam-CLDH through the isolated lobster heart produced dose-dependent increases in both contraction frequency and amplitude and a dose-dependent decrease in contraction duration, with threshold concentrations for all parameters in the range 10 -11 to 10 -10 moll -1 or less, among the lowest for any peptide on this system. This report is the first documentation of a decapod CLDH, the first demonstration of CLDH bioactivity outside the Insecta, and the first detection of an intrinsic neuropeptide transcript in the crustacean CG.

Section: Cldh Is a Powerful Cardioactive Peptide In H Americanusmentioning

confidence: 99%

Identification of a calcitonin-like diuretic hormone that functions as an intrinsic modulator of the American lobster,Homarus americanus, cardiac neuromuscular system

Christie

Stevens

Bowers

et al. 2010

“…Actions of cholinergic agonists and GABA on the cardiac ganglion Acetylcholine (ACh) is thought to be the neurotransmitter that is released from one of the acceleratory fibers projecting from the CNS to the CG to increase cardiac activity (Cooke, 2002), and the sensitivity of the CG to ACh and muscarinic cholinergic agonists has been described in other species (Freschi, 1991;Freschi and Livengood, 1989;Sullivan and Miller, 1990). Fig.·7A shows extracellular recordings in control (top trace) and in the presence of 10 -5 ·mol·l -1 pilocarpine, the muscarinic ACh receptor agonist (bottom trace).…”

Section: Effects Of Amines On the Cardiac Ganglionmentioning

confidence: 99%

“…It is known that the CG is modulated by substances released locally from regulatory nerve fibers and by hormones released from endocrine sites such as the pericardial organs (POs) (Alexandrowicz and Carlisle, 1953;Christie et al, 1995;Cooke, 2002;Cooke and Hartline, 1975;Li et al, 2003;Li et al, 2002;Pulver and Marder, 2002;Skiebe, 2001). The isolated CG is sensitive to biogenic amines (Benson, 1984;Berlind, 2001;Cooke and Hartline, 1975;Fort et al, 2004;Hashemzadeh-Gargari and Freschi, 1992b;Miller et al, 1984;Saver et al, 1999), GABA (Kerrison and Freschi, 1992), glutamate (Hashemzadeh-Gargari and Freschi, 1992a), cholinergic agonists (Freschi, 1991;Freschi and Livengood, 1989;Sullivan and Miller, 1990), proctolin (Freschi, 1989;Miller and Sullivan, 1981;Saver et al, 1999;Sullivan and Miller, 1984), crustacean cardioactive peptide (CCAP) (Saver et al, 1999), FMRFamide-like peptides (FLPs) (CruzBermúdez et al, 2006;Saver et al, 1999) and nitric oxide (Mahadevan et al, 2004).…”

Section: Introductionmentioning

confidence: 99%

Multiple modulators act on the cardiac ganglion of the crab,Cancer borealis

Cruz-Bermúdez

Marder

2007

crustacean cardioactive peptide (CCAP), a number of extended FLRFamide peptides, and cholinergic agonists increased the activity of the CG, GABA inhibited the CG, while other substances had little or no significant effect on the CG motor pattern. These results demonstrate, in one species, that the CG is multiply modulated. We suggest that multiple modulators may be important to regulate and coordinate the activity of the heart and other organs in response to external stimuli or the endogenous physiological state.

“…The transcript for this peptide hormone, which strongly activates cardiac activity, is present within the motor neurons of the CG. It has also been suggested that acetylcholine may act as an intrinsic modulator (reviewed in Cooke, 2002), since the ganglion can synthesize this transmitter (Sullivan and Miller, 1990) and is sensitive to it (Freschi and Livengood, 1989). In addition, the CG is thought to receive sensory feedback from the heart musculature through stretch-sensitive dendrites on the neurons of the ganglion itself (Cooke, 2002).…”

Section: Introductionmentioning

confidence: 99%

The peptide hormone pQDLDHVFLRFamide (crustacean myosuppressin) modulates theHomarus americanuscardiac neuromuscular system at multiple sites

Stevens

Cashman

Smith

et al. 2009

SUMMARY pQDLDHVFLRFamide is a highly conserved crustacean neuropeptide with a structure that places it within the myosuppressin subfamily of the FMRFamide-like peptides. Despite its apparent ubiquitous conservation in decapod crustaceans, the paracrine and/or endocrine roles played by pQDLDHVFLRFamide remain largely unknown. We have examined the actions of this peptide on the cardiac neuromuscular system of the American lobster Homarus americanus using four preparations: the intact animal, the heart in vitro, the isolated cardiac ganglion (CG), and a stimulated heart muscle preparation. In the intact animal, injection of myosuppressin caused a decrease in heartbeat frequency. Perfusion of the in vitro heart with pQDLDHVFLRFamide elicited a decrease in the frequency and an increase in the amplitude of heart contractions. In the isolated CG, myosuppressin induced a hyperpolarization of the resting membrane potential of cardiac motor neurons and a decrease in the cycle frequency of their bursting. In the stimulated heart muscle preparation, pQDLDHVFLRFamide increased the amplitude of the induced contractions, suggesting that myosuppressin modulates not only the CG, but also peripheral sites. For at least the in vitro heart and the isolated CG, the effects of myosuppressin were dose-dependent (10 -9 to 10 ) consistent with the peptide serving as a circulating hormone. Although cycle frequency, a parameter directly determined by the CG, consistently decreased when pQDLDHVFLRFamide was applied to all preparation types, the magnitudes of this decrease differed, suggesting the possibility that, because myosuppressin modulates the CG and the periphery, it also alters peripheral feedback to the CG.