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J L Wilkens

Publications and source records attributed to J L Wilkens.

At least 19 recordsLinked to original sources

Regulation of blood pressure in the land crab Cardisoma guanhumi.

We examined the cardiovascular responses to acute and chronic changes in blood volume (BV) in the land crab Cardisoma guanhumi. Acute reduction in BV caused an increase in activity in the dorsoventral muscles (DVMs) and to a lesser extent in the epimeral attractor muscles (EAMs). Contraction of the DVMs and EAMs will decrease the volume of the dorsal sinus and the thorax as a whole, respectively. BV reduction also caused bradycardia with frequent periods of cardiac arrest. There was a small drop in hemolymph pressure. BV expansion had the reciprocal effect on DVM and EAM activity but had no effect on heart rate (fH). After the cardioregulatory nerves were cut, acute hypovolemia had no effect on fH but still caused a moderate increase in DVM activity. After dehydration-induced BV reduction, DVM activity increased, whereas hemolymph pressure, fH, and EAM activity were maintained close to control levels.

Animals↗

Sites and modes of action of proctolin and the FLP F2 on lobster cardiac muscle.

At the threshold concentration (1-10 pmol l(-1)), the neuropeptide hormones proctolin (PR) and the FLRFamide-like peptide (FLP) F(2) cause an increase in amplitude of electrically evoked contractions (each contraction is a brief tetanus) of lobster heart ostial muscle. At higher concentrations each peptide also induces an increase in tonus (contracture). The PR-induced contracture and augmentation of tetani are proportional to increases in [Ca2+]i. The rate of onset and recovery of peptide-induced effects on both tetani and contracture appeared to reduced by Ca2+ storage by the sarcoplasmic reticulum (SR). Enhanced tetani following a contracture may be due to enhanced voltage-gated Ca2+ current and sarcoplasmic reticular (SR) Ca2+ loading. The SR Ca2+ loading appears to be specific for PR and F2, since glutamic-acid-induced contractures are not followed by increased tetani. The prolonged elevation of [Ca2+]i during contracture causes a right-ward shift in the force-pCa curve indicating a decrease in myofibrillar sensitivity to Ca2+. Blocking voltage-gated Ca2+ channels with Cd2+, nifedipine or verapamil, while reducing tetani, does not prevent peptide-induced contracture and enhanced tetani. Opening SR Ca2+ channels and depleting SR Ca2+ with either caffeine or ryanodine blocked tetani but permitted accelerated peptide-induced contractures. We conclude that PR and F2 at low concentration enhance voltage-dependent Ca2+ induced Ca2+ release from the SR, while higher hormone levels directly gate Ca2+ entry across the sarcolemma.

Animals↗

The steady-state force-Ca2+ relationship in intact lobster (Homarus americanus) cardiac muscle.

The heart of the decapod crustacean is activated by regular impulse bursts from the cardiac ganglion. The cardiac pump function depends on ganglionic burst frequency, burst duration, and burst impulse frequency. Here, we activated isolated lobster cardiac ostial muscle (Orbicularis ostii muscle, OOM) by stimulus trains in vitro in order to characterize the response of the contractile apparatus to [Ca2+]i. We employed stimulus trains that generate a steady state between the [Ca2+]i and force in order to estimate the Ca2+ sensitivity of myofilaments. Force and [Ca2+]i transients were simultaneously recorded using a silicon strain gauge and the fluorescence of iontophoretically microinjected fura-2 salt. We examined the effects of tetanus duration (TD), the interval between trains, and 6 microM cyclopiazonic acid, an inhibitor of the SR Ca2+ pump, on the steady-state force-[Ca2+]i relationship. The instantaneous force-[Ca2+]i relationships appeared sigmoidal (EC50 and Hill coefficient, 98.8+/-32.7 nM and 2.47+/-0.20, mean +/- SD, respectively), as did the curves superimposed after 500 ms following the start of stimulation, indicating that the force-[Ca2+]i relationship had reached a steady state at that time. Also, the maximum activated force (Fmax) was estimated using the steady-state force-[Ca2+]i relationship. Prolonged stimulus trains, decreasing the interval between recurrent trains from 5 to 2.5 s, and cyclopiazonic acid each increased the measured EC50 without changing Fmax. The EC50 correlated strongly with averaged [Ca2+]i over time. We conclude that the steady-state force-[Ca2+]i relationships in the OOM indicate cooperation between force generation and Ca2+ binding by the myofilaments. Our data also suggest the existence of a novel Ca2+-dependent mechanism which reduces Ca2+ sensitivity and accelerates relaxation of lobster cardiac muscle myofilaments.

Animals↗

The control of vascular resistance in the southern rock lobster, Jasus edwardsii (Decapoda: Palinuridae).

In Jasus edwardsii (Hutton) the vascular resistance of each of the seven major arterial systems leaving the heart was increased in response to several of the following neurotransmitters and neurohormones: acetylcholine, adrenalin, serotonin, dopamine, octopamine and peptides proctolin and FLRFamide-related peptide F(1). The resistance to flow through the infrabranchial sinus (IBS), part of the venous system, was also sensitive to these drugs. Unexpectedly, the responses of the IBS continued after removal of the gills. Differences in the profiles of responses of the arteries to individual hormones and in the magnitudes and the time courses of back pressure changes, eliminate a common downstream location such as the venous sinuses or gills, as the source of the arterial responses. Vasoactive drugs were effective when applied either via the lumen or, with longer delay, to the basal side of an artery via the IBS. It is concluded that the resistance of each of these sections of the vascular system is independently controllable by hormones.

Animals↗

Excitation-contraction coupling in cardiac muscle of lobster (Homarus americanus); the role of the sarcolemma and sarcoplasmic reticulum.

The T-tubules and sarcoplasmic reticulum (SR) serving excitation-contraction (EC) coupling in lobster (Homarus americanus) cardiac muscle are similar to those in mammalian myocardium. Tetanic contraction is elicited by a burst of action potentials from the cardiac ganglion. In this study we evaluated the roles of the sarcolemma and SR in EC coupling of the ostial valve muscle (orbicularis ostii m. or OOM) of lobster heart. The OOM was mounted in a bath with saline on a microscope stage; force was measured by strain gauge. [Ca2+]i was measured using iontophoretically micro-injected fura-2 salt. Peak [Ca+]i, peak tetanic force and time to peak [Ca2+]i increased with that of stimulus train duration (TD), to a maximum at a TD of 500 ms. Force increased with [Ca2+]. Cd2+ reduced force by 90%; ryanodine and caffeine reduced tetanic [Ca2+]i transients by 80% and 70%, and force by 90% and 80%, respectively. Ryanodine, caffeine and cyclopiazonic acid slowed the decline of [Ca2+]i and force during relaxation. Relaxation required [Na+]o. The rate of decline of [Ca2+]i appeared to be a sigmoidal function of the [Ca2+]i and increased for any [Ca2+]i with TD. Inactivity slowed relaxation of force; stimulation accelerated relaxation. These data suggest important contributions of Ca2+ transport both across the sarcolemma and across the SR membrane during EC-coupling of lobster cardiac muscle, while average cytosolic [Ca2+]i regulates the rate of [Ca2+]i elimination during relaxation.

Animals↗

Physiology and excitation-contraction coupling in the intestinal muscle of the crayfish Procambarus clarkii.

The intestinal muscles of Procambarus clarkii are striated and yet they are specialized to produce slow peristaltic waves of contraction, not unlike those seen in vertebrate visceral smooth muscle. These muscles cannot be tetanized either by repetitive stimulation or by elevated potassium saline. The excitation-contraction (E-C) coupling mechanism was explored and compared with that known in crustacean skeletal muscle. Contraction is dependent on external Ca2+ which triggers the release of intracellular calcium from the sarcoplasmic reticulum (SR) via calcium-induced calcium release (CICR). Whereas contraction force is proportional to [Ca2+]o up to that in normal saline (13.4 mM), higher levels of Ca2+ reduce force. Ryanodine, which blocks calcium release from the SR, abolishes electrically stimulated contractions and CICR. Relaxation is achieved by removal of calcium from the cytosol in at least two ways, first by the re-loading of calcium into the SR by Ca2+-ATPases and second by the movement of calcium out of the cell by extruding it across the sarcolemma via Na+/Ca2+-exchangers. It is hypothesized that the inability of this muscle to show tetanus arises from inactivation of the voltage-gated calcium channels by high calcium. This is supported by the result that caffeine application causes an increase in tonus and size of phasic contractions by circumventing the sarcolemma and dumping SR calcium stores.

Anesthetics, Local↗

In situ and in vitro identification and characterization of cardiac ganglion neurons in the crab, Carcinus maenas.

The aim of this study was to investigate the intrinsic membrane properties and hormonal responses of individual central pattern generating neurons in the cardiac ganglion of the shore crab Carcinus maenas. Because the cardiac ganglion in this crustacean species is buried within the heart musculature and is therefore inaccessible for direct morphological and electrophysiological analysis, we developed two novel in vitro preparations. First, to make the ganglion accessible, we established a brief enzymatic treatment procedure that enabled us to isolate the entire cardiac ganglion, in the absence of muscle tissue. Second, a cell culture procedure was developed to isolate individual neurons in vitro. With the use of both isolated ganglionic and neuronal cell culture techniques, this study provides the first direct account of the neuroanatomy of the cardiac ganglion in shore crabs. We demonstrate that cultured neurons not only survived the isolation procedures, but that they also maintained their intrinsic membrane and transmitter response properties, similar to those seen in the intact ganglion. Specifically, we tested the peptides proctolin, crustacean cardioactive peptide, the FLRFamide-related peptide F2, and an amine (serotonin) on both isolated ganglion and in vitro culture neurons. We measured changes in neuronal burst rate, burst amplitude, pacemaker slope, and membrane potential oscillation amplitude in response to the above four hormones. Each hormone either increased neuronal activity in spontaneously bursting neurons, or induced a bursting pattern in quiescent cells. The in vitro cell culture system developed here now provides us with an excellent opportunity to elucidate cellular, synaptic and hormonal mechanisms by which cardiac activity is generated in shore crabs.

Animals↗

Crustacean cardioexcitatory peptides may inhibit the heart in vivo.

Peptide neurohormones exist as functionally similar analogues in a wide variety of invertebrate and vertebrate phyla, and many have been implicated as cardiovascular regulators. In decapod crustaceans, these include the pentapeptide proctolin, crustacean cardioactive peptide (CCAP) and the FMRF amide-related peptides F1 and F2, all of which are found in the pericardial organs located immediately upstream of the heart. Cardioexcitatory activity has been demonstrated by these four peptides in both isolated and semi-isolated arthropod hearts; CCAP, however, has minimal effects on the heart of Cancer magister. In the present study, we determined the effects of proctolin, F1 and F2 on the heart of the crab C. magister in both in vitro (semi-isolated heart) and in vivo (whole animal) preparations. In semi-isolated hearts, infusion of each peptide caused cardioexcitation, increasing the rate and stroke volume of the heart. In whole crabs, the peptides were cardioinhibitory; the strongest effects were observed with F1 and F2, which dramatically decreased heart rate, cardiac stroke volume and cardiac output. These results cast doubt on current perceptions of the functional role of cardioactive peptides in the regulation of invertebrate cardiovascular performance in vivo.

Animals↗

Effects of scaphognathite nerve stimulation on the acutely deafferented crab ventilatory central pattern generator.

1. Sensory axons from crab (Carcinus maenas) scaphognathites enter the thoracic ganglion primarily via the LNb branch of the levator nerve. The LNa branch of the levator nerve and the depressor nerve each contain relatively few sensory axons. 2. Acutely deafferented ventilatory central pattern generators show a free running burst rate which is lower than that observed in intact crabs. Electrical stimulation of the levator nerve, or of its LNb branch, increases the burst rate in a frequency dependent manner. Stimulation at high enough intensity to recruit afferents will restart a paused motor rhythm. Stimulation of the levator nerve with short pulse trains phase resets and can entrain the rhythm. 3. In addition to increasing the burst rate, LNb stimulation also causes a progressive elimination of motor neurons from the bursts as the stimulating frequency increases, probably due to depolarization of the 3 oval organ 'giant' afferent axons in this branch. Intracellular depolarization of single oval organ afferents will also inhibit some motor neurons as well as slow or stop the rhythm. 4. Continuous stimulation of the depressor nerve does not affect the ganglionic burst rate and this nerve contains only a few small diameter afferent axons; however, brief trains of stimuli can reset the rhythm in a phase-dependent manner.

Animals↗

Cardiac performance in semi-isolated heart of the crab Carcinus maenas.

A semi-isolated, in situ heart preparation of the shore crab, Carcinus maenas, supported by its alary ligaments, pumps vigorously for hours at a mean heart rate of 49.7 beats/min and cardiac output of 30 ml.kg-1.min-1. These hearts show no adaptive responses to changes in pericardial sinus pressure, outflow resistance, or afterload. Direct perfusion-induced stretch of the heart wall causes increases in contractile force but minimal changes in heart rate. Stroke work and power are lower than comparable values for animals with myogenic hearts and closed circulatory systems. The values for heart rate and cardiac output are lower than in vivo values and may in part reflect the technique used as well as intrinsic performance of the heart without neural and neurohormonal inputs. Morphometrically the heart represents 0.2% of whole body weight, and the mean stroke volume of 0.35-0.45 ml/kg represents an ejection fraction of 27-34% of ventricular volume (1.4 ml/kg).

Animals↗

Dopamine and nicotine, but not serotonin, modulate the crustacean ventilatory pattern generator.

Dopamine (DA) causes a dose-dependent increase in the frequency of motor neuron bursts [virtual ventilation (fR)] produced by deafferented crab ventilatory pattern generators (CPGv). Domperidone, a D2-specific DA antagonist, by itself reversibly depresses fR and also blocks the stimulatory effects of DA. Serotonin (5HT) has no direct effects on this CPGv. Nicotine also causes dramatic dose-dependent increases in the frequency of motor bursts from the CPGv. The action is triphasic, beginning with an initial reversal of burst pattern typical of reversed-mode ventilation, followed by a 2- to 3-min period of depression and then a long period of elevated burst rate. Acetylcholine chloride (ACh) alone is ineffective, but in the presence of eserine is moderately stimulatory. The inhibitory effects of nicotine are only partially blocked by curare. The excitatory action of nicotine is blocked by prior perfusion of domperidone, but not by SKF-83566.HCl, a D1-specific DA antagonist. SKF-83566 had no effects on the ongoing pattern of firing. These observations support the hypothesis that dopaminergic pathways are involved in the maintenance of the CPGv rhythm and that the acceleratory effects of nicotine may involve release of DA either directly or via stimulation of atypical ACh receptors at intraganglionic sites.

2,3,4,5-Tetrahydro-7,8-dihydroxy-1-phenyl-1H-3-ben↗

Modulatory effects of proctolin on a crab ventilatory muscle.

Proctolin enhances nerve-evoked, phasic contractions of a selected respiratory muscle of the shore crab, Carcinus maenas, but has no effect on muscle tonus. Proctolin also increases the work and power output of this muscle. These effects are functionally appropriate in view of previous reports that proctolin stimulates the ventilatory rhythm. They also suggest that proctolin exerts coordinated modulatory control at the central and peripheral levels of the gill ventilatory system. In contrast, serotonin, dopamine and octopamine have no effect on this muscle.

Animals↗

Neuronal control of respiration in decapod crustacea.

Respiratory exchange in decapod crustacea requires the coordinated activity of the heart and the scaphognathites, appendages which ventilate the gills. There is common central nervous system neuronal modulation of both autogenically active systems as well as direct neuronal communication between both systems. The heart and scaphognathites also respond directly to oxygen tension. The neuronal control of the scaphognathites also respond directly to oxygen tension. The neuronal control of the scaphognathites is analyzed at several levels. Particular attention is directed toward the means by which the innately organized and stereotyped motor pattern for forward beating can be altered to produce reversed beating. The importance of sensory feedback in maintaining normal rates of scaphognathite beating is noted. And the phenomenon of bilateral coordination between the morphologically independent scaphognathites is described. Several different models of parts of the over-all scaphognathite neuronal circuitry are presented for heuristic purposes.

Animals↗

Patterns and bilateral coordination of scaphognathite rhythms in the lobster Homarus americanus.

The bilateral patterns of forward and reversed scaphognathite (SG) pumping are described for the American lobster. During forward pumping the two SGs usually function synchronously, but may also function independently. The nine muscles of one SG are arranged into four functional groups which are sequentially active during forward pumping. During reversed beats, motor neurones to one group of muscles are inactive while bursts to another are either delayed or missing. Reversal beats do not appear to alter the phasing of the central oscillators that generate the basic SG rhythm. Phase analysis of bilateral SG beating demonstrates two types of relationship: phase coupling or phase drifting with a tendency to couple. An animal may remain in one state for long periods of time or may alternate between states. Coupling can occur at more than one phase indicating phase multistability. The coupled state may remain constant at markedly different frequencies of beating, indicating phase rather than latency coupling between SGs. During the drifting state each SG tends to assume its "intrinsic" rate of oscillation. The drift state reflects the inherent asymmetry of the two SG systems. The influence of several parameters of sensory stimulation on phase and frequency of SG beating are analyzed.

Action Potentials↗