Fort, Timothy J., Vladimir Brezina, and Mark W. Miller. Modulation of an integrated central pattern generator-effector system: dopaminergic regulation of cardiac activity in the blue crab Callinectes sapidus. J Neurophysiol 92: 3455-3470, 2004; doi:10.1152/ jn.00550.2004. Theoretical studies have suggested that the output of a central pattern generator (CPG) must be matched to the properties of its peripheral effector system to ensure production of functional behavior. One way that such matching could be achieved is through coordinated central and peripheral modulation. In this study, morphological and physiological methods were used to examine the sources and actions of dopaminergic modulation in the cardiac system of the blue crab, Callinectes sapidus. Immunohistochemical localization of tyrosine hydroxylase (TH) revealed a prominent neuron in the commissural ganglion, the L-cell, that projected a large-diameter axon to the pericardial organ (PO) by an indirect and circuitous route. Within the PO, the L-cell axon gave rise to fine varicose fibers, suggesting that it releases dopamine in a neurohormonal fashion onto the heart musculature. In addition, one branch of the axon continued beyond the PO to the heart, where it innervated the anterior motor neurons and the posterior pacemaker region of the cardiac ganglion (CG). In physiological experiments, exogenous dopamine produced multiple effects on contraction and motor neuron burst parameters that corresponded to the dual central-peripheral modulation suggested by the L-cell morphology. Interestingly, parameters of the ganglionic motor output were modulated differently in the isolated CG and in a novel semiintact system where the CG remained embedded within the heart musculature. These observations suggest a critical role of feedback from the periphery to the CG and underscore the requirement for integration of peripheral (neurohormonal) actions and direct ganglionic modulation in the regulation of this exceptionally simple system.
In regulating neurophysiological systems, neuromodulators exert multiple actions at multiple sites in such a way as to control the activity in an integrated manner. We are studying how this happens in a simple central pattern generator (CPG)-effector system, the heart of the blue crab Callinectes sapidus. The rhythmic contractions of this heart are neurogenic, driven by rhythmic motor patterns generated by the cardiac ganglion (CG). In this study, we used anatomical and physiological methods to examine the sources and actions on the system of crustacean cardioactive peptide (CCAP). Immunohistochemical localization revealed a plexus of CCAP-immunoreactive fibers in the pericardial organs (POs), neurohemal structures from which blood-borne neurohormones reach the heart. Combined backfill and immunohistochemical experiments indicated that the CCAP in the POs originated from a large contralateral neuron in each thoracic neuromere. In physiological experiments, we examined the actions of exogenous CCAP on the intact working heart, on the semi-intact heart in which we could record the motor patterns as well as the muscle contractions, and on the isolated CG. CCAP had strong positive inotropic and chronotropic effects. Dissection of these effects in terms of dose dependency, time course, and the preparation type in which they occurred suggested that they were produced by the interaction of three primary actions of CCAP exerted both on the heart muscle and on the CG. We conclude that CCAP released from the POs as a neurohormone regulates the crab heart by multiple actions on both the central and peripheral components of this model CPG-effector system.
Fort TJ, Brezina V, Miller MW. Regulation of the crab heartbeat by FMRFamide-like peptides: multiple interacting effects on center and periphery.
The neurogenic heart of decapod crustaceans is a very simple, self-contained, model central pattern generator (CPG)-effector system. The CPG, the nine-neuron cardiac ganglion (CG), is embedded in the myocardium itself; it generates bursts of spikes that are transmitted by the CG's five motor neurons to the periphery of the system, the myocardium, to produce its contractions. Considerable evidence suggests that a CPG-peripheral loop is completed by a return feedback pathway through which the contractions modify, in turn, the CG motor pattern. One likely pathway is provided by dendrites, presumably mechanosensitive, that the CG neurons project into the adjacent myocardial muscle. Here we have tested the role of this pathway in the heart of the blue crab, Callinectes sapidus. We performed "de-efferentation" experiments in which we cut the motor neuron axons to the myocardium and "de-afferentation" experiments in which we cut or ligated the dendrites. In the isolated CG, these manipulations had no effect on the CG motor pattern. When the CG remained embedded in the myocardium, however, these manipulations, interrupting either the efferent or afferent limb of the CPG-peripheral loop, decreased contraction amplitude, increased the frequency of the CG motor neuron spike bursts, and decreased the number of spikes per burst and burst duration. Finally, passive stretches of the myocardium likewise modulated the spike bursts, an effect that disappeared when the dendrites were cut. We conclude that feedback through the dendrites indeed operates in this system and suggest that it completes a loop through which the system self-regulates its activity.
When modulators of neuromuscular function alter the motor neuron spike patterns that elicit muscle contractions, it is predicted that they will also retune correspondingly the connecting processes of the neuromuscular transform. Here we confirm this prediction by analyzing data from the cardiac neuromuscular system of the blue crab. We apply a method that decodes the contraction response to the spike pattern in terms of three elementary building-block functions that completely characterize the neuromuscular transform. This method allows us to dissociate modulator-induced changes in the neuromuscular transform from changes in the spike pattern in the normally operating, essentially unperturbed neuromuscular system.
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