Separation of neuronal sites of driver potential and impulse generation by ligaturing in the cardiac ganglion of the lobster,Homarus americanus

1983 ◽  
Vol 151 (3) ◽  
pp. 329-346 ◽  
Author(s):  
Kenro Tazaki ◽  
Ian M. Cooke
1990 ◽  
Vol 63 (2) ◽  
pp. 370-384 ◽  
Author(s):  
K. Tazaki ◽  
I. M. Cooke

1. The anterior motorneurons of the cardiac ganglion of Homarus americanus were ligated less than 300 microns from the soma. This removes impulse-generating membrane and sites of synaptic input while preserving the ability of the soma to generate the burst-forming potentials termed "driver potentials" regenerative, slow (250-ms duration) depolarizations (to -20 mV) in response to brief, depolarizing stimuli. At stimulus intervals corresponding to rates of bursting observed in spontaneously active, intact ganglia (0.3-1.2/s), driver potential amplitude increases with increasing stimulus interval. 2. A two-electrode voltage clamp was used to characterize inward current observable from the ligated neurons in tetrodotoxin (TTX)-tetraethylammonium (TEA)-containing salines. The amplitude of inward current shows a hyperbolic relation to [Ca]o that is well fitted by a form of the Michaelis-Menten equation. Inward current is maintained but not augmented when Ca2+ is replaced by Ba2+ or Sr2+. It is concluded that the inward current, to be referred to as ICa, is mediated by voltage-dependent Ca channels. 3. Contamination of ICa by early outward current (IA) was evaluated by addition of 4-aminopyridine (4-AP, 4 mM). In the presence of 4-AP, the net inward current is increased and the potential at which maximum ICa occurs is shifted 10 mV more positive. 4. Subtraction of outward currents recorded in Mn2(+)-containing saline from overall currents in the absence of Mn2+ provided another means to separate inward from outward current. I-V curves from such "Mn-subtracted" records show ICa approaches a saturating value for steps to -5 mV and more depolarized. The time to peak ICa is voltage dependent. The largest inward currents (up to 240 nA) and minimal time to peak (4 ms) are observed for steps from holding potentials of -50 to -60 mV. 5. Decline of ICa during depolarized steps observed in Mn-subtracted records represents inactivation rather than development of competing outward current. Inactivation is slow and incomplete; the rate and fractional amount of inactivation are not directly voltage dependent. Nonsubtracted responses to 500-ms depolarizations to potentials evoking little outward current show that an initial rapid decline of ICa (tau approximately 40 ms) is followed at approximately 80 ms by a slower phase of decline (tau approximately 180 ms). With repetitive clamps, the early phase proved labile.(ABSTRACT TRUNCATED AT 400 WORDS)


1967 ◽  
Vol 47 (2) ◽  
pp. 327-341
Author(s):  
DANIEL K. HARTLINE

1. Simultaneous recording from several pairs of electrodes placed along the ganglion and certain efferent nerves, during stimulation of other efferents, allows the course of antidromic impulses in each stimulated axon to be mapped. 2. These impulses disappear as they approach their somata, being incapable of invading them, a fact which permits identification of a particular efferent axon with a particular soma. 3. By these means the courses of all such efferent axons, and their corresponding somata, have been determined. These all belong to the five large cells. 4. The impulses from each such axon occurring during the spontaneous burst can be identified, as can impulses from each small cell. 5. Each large-cell axon appears to be inexcitable until it is a few mm from the soma. 6. If the axon branches within this inexcitable region, the branches tend to fire impulses independently. 7. The technique of cell identification opens the way to a more complete analysis of the ganglion's activity and the synaptic interactions which produce it.


1975 ◽  
Vol 63 (1) ◽  
pp. 33-52
Author(s):  
I. M. Cooke ◽  
D. K. Hartline

The spontaneous burst discharges of isolated lobster (Homarus americanus) cardiac ganglia were recorded with a spaced array of electrodes. Small regions (less than 1 mm) of the ganglion were exposed to the cardioexcitor neurohormone in extracts of pericardial organs (XPO) or to 10(−5) M 5-hydroxytryptamine (5HT). All axons were excited (increased mean firing frequency, f) by both substances, but only by applications in the region between the soma (but excluding it) and proximal site of impulse initiation. Units not so exposed changed their f relatively little despite f increases of as much as threefold in exposed units and changes in burst rate and overall length. Regularity and grouping of all impulse activity into bursts was never disturbed. 5HT increases burst rate at any point of application. The increases are larger if small cells are affected than if only large cells are exposed. Burst length decreases except when the pacemaker is affected. In contrast, XPO affects neither burst rate or length unless small cells are affected. Length is increased if non-pacemaker small cells are affected; both rate and length increase if the pacemaker is affected. The pacemaker usually exhibits an f of intermediate value. Rate changes are not simply related to its f. A small cell can “burst” in the absence of impulses from any other cells. XPO may enhance endogenous “driver potentials,” while 5HT may excite by depolarizing at limited sites.


2020 ◽  
Vol 124 (4) ◽  
pp. 1241-1256
Author(s):  
Emily R. Oleisky ◽  
Meredith E. Stanhope ◽  
J. Joe Hull ◽  
Andrew E. Christie ◽  
Patsy S. Dickinson

Premotor and motor neurons of the Homarus americanus cardiac ganglion (CG) are normally electrically and chemically coupled, and generate rhythmic bursting that drives cardiac contractions; we show that they can establish independent bursting patterns when physically decoupled by a ligature. The neuropeptide myosuppressin modulates different aspects of the bursting pattern in these neuron types to determine the overall modulation of the intact CG. Differential distribution of myosuppressin receptors may underlie the observed responses to myosuppressin.


1973 ◽  
Vol 62 (4) ◽  
pp. 448-472 ◽  
Author(s):  
Earl Mayeri

External recording and stimulation, techniques were used to determine which neurons and interactions are essential for production of the periodic burst discharge in the lobster cardiac ganglion. Burst activity can be modulated by brief single shocks applied to the four small cells, but not by similar stimulation of the five large cells, suggesting that normally one or more small cells primarily determine burst rate and duration. Repetitive electrical stimulation of large cells initiates spike activity in small cells, probably via excitatory synaptic and/or electrotonic connections which may normally act to prolong bursts and decrease burst rate. Transection of the ganglion can result in burst activity in small cells in the partial or complete absence of large cell spike activity, but large cells isolated from small cell excitatory synaptic input by transection or by application of dinitrophenol do not burst. Generally, transections which decrease excitatory feedback to small cells are accompanied by an increase in burst rate, but mean spike frequency over an entire burst cycle stabilizes at the original level within 10–30 min for various groups of cells whose spike-initiating sites are still intact. These and previous results suggest that the system is two layered: one or more small cells generate the burst pattern and impose it on the large cells which are the system's motorneurons.


2000 ◽  
Vol 203 (9) ◽  
pp. 1447-1457 ◽  
Author(s):  
A. Sakurai ◽  
H. Yamagishi

We present several lines of evidence for the occurrence of graded synaptic transmission in addition to impulse-mediated transmission at the neuromuscular junction between cardiac ganglion (CG) neurones and the myocardium in the isopod crustacean Ligia exotica. In the heart of adult Ligia exotica, the CG acts as a primary pacemaker for the heartbeat by generating periodic bursts of impulses and entrains the myogenicity of the myocardium via impulse-mediated excitatory junctional potentials. When impulse generation was blocked by tetrodotoxin (TTX; 50 nmol l(−)(1)), the CG neurones and the myocardium periodically exhibited synchronized slow depolarizing potentials. The association between the slow depolarizing potentials in the neurone and the myocardium was eliminated by application of Joro spider toxin (JSTX), a specific glutamate antagonist. When the CG neurone was made quiescent by a higher dose of TTX (1.0 micromol l(−)(1)), sinusoidal current injected into the CG neurone induced similar sinusoidal membrane potential responses in the myocardium. The sinusoidal muscle responses were eliminated by application of either JSTX or low-Ca(2+) saline. Under voltage-clamp conditions, the myocardium exhibited periodic inward current responses to sinusoidal current stimuli applied to the CG neurone. The reversal potential for the current response of the myocardium was similar to that of the impulse-mediated excitatory junctional current (EJC). Extracellular macropatch recordings of EJCs made at the neuromuscular junctional site revealed the spontaneous appearance of miniature EJCs asynchronous with the CG spikes in addition to large spike-evoked EJCs. The miniature EJCs were present in saline containing TTX, and their frequency was strongly affected by the slow membrane potential change in the CG neurone. These results suggest that the CG neurones drive the myocardium by graded neuromuscular transmission in addition to impulse-mediated transmission in the heart of Ligia exotica.


1980 ◽  
Vol 87 (1) ◽  
pp. 285-313
Author(s):  
J. A. Benson

1. The five large and four small neurones in the cardiac ganglion of the crab, Portunus, are electrotonically coupled and behave as a single relaxation oscillator, exhibiting periodic bursting activity in vitro. Recorded from the large neurone somata, this activity consists of 200-400 ms slow depolarizations called ‘driver potentials’ (Tazaki & Cooke, 1979a), accompanied by attenuated action potentials and EPSP's from small neurone input. 2. There is a strong positive correlation between the duration of the driver potential and the duration of the following interburst interval in the spontaneously active ganglion. This correlation is preserved during prolonged depolarization and hyperpolarization. 3. When a driver potential is prematurely terminated by an injected current pulse, the following interburst interval is shortened in direct proportion to the decrease in driver potential duration. 4. When a driver potential or a burst of high-frequency action potential activity is evoked by a depolarizing current pulse, the cardiac oscillator resets to the point of maximum hyperpolarization of the burst cycle, and the following interburst interval is of normal duration. Resetting following an evoked driver potential is complete. Partial resetting occurs only after short, evoked action potential bursts in the absence of a driver potential. 5. Reset of the oscillator causes phase shifts in the subsequent cycles of activity, which vary with the phase of application and duration of the injected current pulse. Response curves have been constructed for a comprehensive range of durations and intensities of hyperpolarizing and depolarizing current pulses applied at all phases of the oscillator cycle. 6. The phase shifts are composed of contributions from the duration of the current pulse, from the premature initiation of the slow depolarizing pacemaker potential due to early termination of the burst, and from the change in interburst interval correlated with truncation of the driver potential. 7. Considering the cardiac ganglion as a relaxation oscillator, frequencey control by entrainment to periodically applied current pulses was quantitatively predicted from the phase-response curves and experimentally confirmed. 8. A high concentration (10(−5) M) of octopamine can inhibit driver potential activity in the large neurones. This was used to examine possible frequency modulating effects of electrotonic feedback from the large neurone driver potentials onto the small neurone pacemaker activity. 9. The observations are discussed in relation to the ionic model for driver potentials and slow pacemaker potential activity in the cardiac ganglion, as proposed by Tazaki & Cooke (1979a, b).


1984 ◽  
Vol 108 (1) ◽  
pp. 97-118 ◽  
Author(s):  
MARK W. MILLER ◽  
JACK A. BENSON ◽  
ALLAN BERLIND

1. Dopamine, a cardioexcitor in decapod crustaceans, increased the frequency and/or duration of bursts of action potentials in the semi-isolated cardiac ganglia of two species of crabs. The number of motoneurone action potentials in each burst was increased, which in the intact heart would increase the force and amplitude of heart contraction. 2. The effects were concentration-dependent, with a threshold concentration of 10−8M or lower when dopamine was applied by continuous perfusion. At 5×10−6M, dopamine increased burst frequency by 200%. 3. The main site of dopamine action was the group of four posterior small interneurones which normally function as the pacemaker for the cardiac ganglion system. Effects on the five large motoneurones occurred at higher concentrations. This regional difference in sensitivity was demonstrated by selective applications of dopamine to different parts of the cardiac ganglion and by the use of preparations in which the two ends of the ganglion had been functionally separated by a ligature around the ganglionic trunk. 4. In the small neurones, dopamine was found to stimulate the slow tetrodotoxin-resistant regenerative depolarizations known as driver potentials. The effects on driver potential frequency and train duration were concentration dependent. In one of the two species of crabs, in which electrotonic connections between small and large neurones are strong, large neurone driver potentials were indirectly induced by dopamine. 5. In the tetrodotoxin-treated large motoneurones, dopamine, at a concentration about ten-fold higher than needed to activate the small neurones, decreased the threshold for current-induced driver potentials, and slightly reduced membrane resistance. 6. We suggest that the excitatory action of dopamine on the untreated cardiac ganglion can in large part be accounted for by its action on driver potential production in the small neurones.


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