Matrix of neuromodulators in neurosecretory structures of the crab Cancer borealis.

1995 ◽  
Vol 198 (12) ◽  
pp. 2431-2439 ◽  
Author(s):  
A E Christie ◽  
P Skiebe ◽  
E Marder
Keyword(s):  
Ophthalmic Artery ◽  
Neural Circuit ◽  
Stomatogastric Ganglion ◽  
Red Pigment ◽  
Cancer Borealis ◽  
Double Labeling ◽  
Neuroactive Compounds ◽  
Crustacean Cardioactive Peptide ◽  
Other Substances ◽  
Neurohemal Organs

The crustacean stomatogastric ganglion, which is situated in the ophthalmic artery, can be modulated by both intrinsically released molecules and hormones. In the crab Cancer borealis, over a dozen neuroactive compounds have been identified in the input axons that project into the stomatogastric neuropil. However, little is known about the modulator content of the two major neurohemal organs, the sinus glands and the pericardial organs, in this crab. We now report the results of a series of immunocytochemical experiments designed to identify putative neurohormones in these tissues. We find that the majority of modulators present in the input axons of the stomatogastric ganglion are also present in at least one of the neurohemal organs. Specifically, allatostatin-like, buccalin-like, cholecystokinin-like, FLRFamide-like, GABA-like, locustatachykinin-like, myomodulin-like, proctolin-like, red pigment concentrating hormone-like and serotonin-like immunoreactivities are all present in both the stomatogastric neuropil and at least one of the neurohemal organs. Thus, these substances are likely to serve a dual role as both local and hormonal modulators of the stomatogastric network. Two other substances, beta-pigment dispersing hormone and crustacean cardioactive peptide, are not present in the stomatogastric neuropil, but beta-pigment dispersing hormone immunoreactivity is present in the sinus glands and crustacean cardioactive peptide immunoreactivity is present in the pericardial organs. It is likely that crustacean cardioactive peptide exerts its influence on the stomatogastric neural circuit via hormonal pathways. Double-labeling experiments show that the patterns of modulator co-localization present in the stomatogastric neuropil are different from those in the neurosecretory organs, suggesting that few rules of colocalization hold across these tissues.

Peptidergic modulation of a multioscillator system in the lobster. I. Activation of the cardiac sac motor pattern by the neuropeptides proctolin and red pigment-concentrating hormone

1989 ◽  
Vol 61 (4) ◽  
pp. 833-844 ◽  
Author(s):  
P. S. Dickinson ◽  
E. Marder
Keyword(s):  
Nervous System ◽  
Motor Neurons ◽  
Motor Pattern ◽  
Stomatogastric Ganglion ◽  
Red Pigment ◽  
Stomatogastric Nervous System ◽  
Two Phase ◽  
Motor Patterns ◽  
Neuronal Element

1. The cardiac sac motor pattern consists of slow and irregular impulse bursts in the motor neurons [cardiac sac dilator 1 and 2 (CD1 and CD2)] that innervate the dilator muscles of the cardiac sac region of the crustacean foregut. 2. The effects of the peptides, proctolin and red pigment-concentrating hormone (RPCH), on the cardiac sac motor patterns produced by in vitro preparations of the combined stomatogastric nervous system [the stomatogastric ganglion (STG), the paired commissural ganglia (CGs), and the oesophageal ganglion (OG)] were studied. 3. Bath applications of either RPCH or proctolin activated the cardiac sac motor pattern when this motor pattern was not already active and increased the frequency of the cardiac sac motor pattern in slowly active preparations. 4. The somata of CD1 and CD2 are located in the esophageal and stomatogastric ganglia, respectively. Both neurons project to all four of the ganglia of the stomatogastric nervous system. RPCH elicited cardiac sac motor patterns when applied to any region of the stomatogastric nervous system, suggesting a distributed pattern generating network with multiple sites of modulation. 5. The anterior median (AM) neuron innervates the constrictor muscles of the cardiac sac. The AM usually functions as a part of the gastric mill pattern generator. However, when the cardiac sac is activated by RPCH applied to the stomatogastric ganglion, the AM neuron becomes active in antiphase with the cardiac sac dilator bursts. This converts the cardiac sac motor pattern from a one-phase rhythm to a two-phase rhythm. 6. These data show that a neuropeptide can cause a neuronal element to switch from being solely a component of one neuronal circuit to functioning in a second one as well. This example shows that peptidergic "reconfiguration" of neuronal networks can produce substantial changes in the behavior of associated neurons.

scholarly journals Episodic Bouts of Activity Accompany Recovery of Rhythmic Output By a Neuromodulator- and Activity-Deprived Adult Neural Network

2003 ◽  
Vol 90 (4) ◽  
pp. 2720-2730 ◽  
Author(s):  
Jason A. Luther ◽  
Alice A. Robie ◽  
John Yarotsky ◽  
Christopher Reina ◽  
Eve Marder ◽  
...  
Keyword(s):  
Neural Network ◽  
Neuronal Network ◽  
Recovery Process ◽  
Stomatogastric Ganglion ◽  
Cancer Borealis ◽  
Pyloric Network ◽  
Underlying Mechanisms ◽  
Over Time ◽  
Phase Relationships ◽  
Pyloric Rhythm

The pyloric rhythm of the stomatogastric ganglion of the crab, Cancer borealis, slows or stops when descending modulatory inputs are acutely removed. However, the rhythm spontaneously resumes after one or more days in the absence of neuromodulatory input. We recorded continuously for days to characterize quantitatively this recovery process. Activity bouts lasting 40–900 s began several hours after removal of neuromodulatory input and were followed by stable rhythm recovery after 1–4 days. Bout duration was not related to the intervals (0.3–800 min) between bouts. During an individual bout, the frequency rapidly increased and then decreased more slowly. Photoablation of back-filled neuromodulatory terminals in the stomatogastric ganglion (STG) neuropil had no effect on activity bouts or recovery, suggesting that these processes are intrinsic to the STG neuronal network. After removal of neuromodulatory input, the phase relationships of the components of the triphasic pyloric rhythm were altered, and then over time the phase relationships moved toward their control values. Although at low pyloric rhythm frequency the phase relationships among pyloric network neurons depended on frequency, the changes in frequency during recovery did not completely account for the change in phase seen after rhythm recovery. We suggest that activity bouts represent underlying mechanisms controlling the restructuring of the pyloric network to allow resumption of an appropriate output after removal of neuromodulatory input.

scholarly journals Electrical coupling and innexin expression in the stomatogastric ganglion of the crabCancer borealis

2014 ◽  
Vol 112 (11) ◽  
pp. 2946-2958 ◽  
Author(s):  
Sonal Shruti ◽  
David J. Schulz ◽  
Kawasi M. Lett ◽  
Eve Marder
Keyword(s):  
Sequence Similarity ◽  
Electrical Coupling ◽  
Homarus Americanus ◽  
Stomatogastric Ganglion ◽  
Electrical Synapse ◽  
Coupling Coefficients ◽  
Cancer Borealis ◽  
Electrophysiological Recordings ◽  
Pyloric Dilator ◽  
Lateral Posterior

Gap junctions are intercellular channels that allow for the movement of small molecules and ions between the cytoplasm of adjacent cells and form electrical synapses between neurons. In invertebrates, the gap junction proteins are coded for by the innexin family of genes. The stomatogastric ganglion (STG) in the crab Cancer borealis contains a small number of identified and electrically coupled neurons. We identified Innexin 1 ( Inx1), Innexin 2 (Inx2), Innexin 3 (Inx3), Innexin 4 ( Inx4), Innexin 5 (Inx5), and Innexin 6 ( Inx6) members of the C. borealis innexin family. We also identified six members of the innexin family from the lobster Homarus americanus transcriptome. These innexins show significant sequence similarity to other arthropod innexins. Using in situ hybridization and reverse transcriptase-quantitative PCR (RT-qPCR), we determined that all the cells in the crab STG express multiple innexin genes. Electrophysiological recordings of coupling coefficients between identified pairs of pyloric dilator (PD) cells and PD-lateral posterior gastric (LPG) neurons show that the PD-PD electrical synapse is nonrectifying while the PD-LPG synapse is apparently strongly rectifying.

Calcium-dependent plateau potentials in a crab stomatogastric ganglion motor neuron. I. Calcium current and its modulation by serotonin

1995 ◽  
Vol 74 (5) ◽  
pp. 1929-1937 ◽  
Author(s):  
B. Zhang ◽  
R. M. Harris-Warrick
Keyword(s):  
Motor Neuron ◽  
Voltage Clamp ◽  
Physiological Role ◽  
Input Resistance ◽  
Stomatogastric Ganglion ◽  
Channel Blockers ◽  
Plateau Potentials ◽  
Cancer Borealis ◽  
Calcium Dependent ◽  
Voltage Dependent

1. Using current- and voltage-clamp techniques, we examined the biophysical properties of a voltage-dependent Ca2+ current and its physiological role in plateau potential generation in the dorsal gastric (DG) motor neuron of the stomatogastric ganglion in the crab, Cancer borealis. 2. Stimulation of one of a set of identified serotonergic/cholinergic mechanosensory cells, the gastropyloric receptor (GPR) cells, induced plateau potentials in DG. A brief pressure application of serotonin (5-HT) closely mimicked the effect of the GPR cells. The 5-HT-evoked plateau in DG was not blocked by the sodium channel blocker, tetrodotoxin (TTX), or a combination of TTX with potassium channel blockers, including tetraethylammonium (TEA) and 4-aminopyridine (4-AP), and the Ih blocker, CsCl. The 5-HT-evoked plateau was eliminated by the Ca2+ channel blockers Co2+ and Cd2+, suggesting that Ca2+ entry is essential for plateau potentials in DG. During the plateau, we observed a 30% decrease in input resistance. 3. When sodium and potassium currents were blocked pharmacologically, injection of suprathreshold depolarizing current evoked all-or-none plateau-like responses lasting several seconds, even in the absence of 5-HT. This response was blocked by Ca2+ channel blockers, further supporting a role for Ca2+ in plateau generation. 5-HT significantly prolonged the duration of this plateau. 4. We isolated a voltage-dependent Ca2+ current in voltage-clamped DG neurons. This current was analyzed with the use of either Ca2+ or Ba2+ as the charge carrier after other currents had been maximally blocked with extracellular TTX, TEA, 4-AP, and CsCl and intracellular loading with Cs+ and ethylene glycol-bis(beta-aminoethyl ether)-N,N,N',N'-tetraacetic acid (EGTA). The Ca2+ current was detectable at -45 mV, peaked at -15 mV, and was estimated to reverse at +45 mV. Co2+ and Cd2+ effectively blocked the Ca2+ current. 5. The voltage dependence of activation of the Ca2+ current was quantantitively analyzed by fitting the voltage-conductance relation with a third power Boltzmann relation. The maximum conductance (gA), half-activation voltage (VA) for individual gating steps, and the slope steepness (k) were 0.19 +/- 0.02 (SE) microS, -36.5 +/- 2.0 mV, and 4.4 +/- 1.4 mV/e-fold, respectively. 6. 5-HT significantly potentiated the gA by approximately 42% without affecting VA and k. 7. We conclude from our current- and voltage-clamp results that a voltage-dependent Ca2+ current plays an important role in generating plateau potentials in the DG neuron. Enhancement of the voltage-dependent Ca2+ current by 5-HT is one of the mechanisms for 5-HT-evoked plateau potentials.

scholarly journals Rapid adaptation to elevated extracellular potassium in the pyloric circuit of the crab, Cancer borealis

2020 ◽  
Vol 123 (5) ◽  
pp. 2075-2089 ◽  
Author(s):  
Lily S. He ◽  
Mara C.P. Rue ◽  
Ekaterina O. Morozova ◽  
Daniel J. Powell ◽  
Eric J. James ◽  
...  
Keyword(s):  
Potassium Concentration ◽  
Fold Increase ◽  
Stomatogastric Ganglion ◽  
Extracellular Potassium ◽  
Rapid Adaptation ◽  
Cancer Borealis ◽  
High Potassium ◽  
Transient Loss ◽  
High Potassium Concentration ◽  
Nonstationary Effects

Solutions with elevated extracellular potassium are commonly used as a depolarizing stimulus. We studied the effects of high potassium concentration ([K+]) on the pyloric circuit of the crab stomatogastric ganglion. A 2.5-fold increase in extracellular [K+] caused a transient loss of activity that was not due to depolarization block, followed by a rapid increase in excitability and recovery of spiking within minutes. This suggests that changing extracellular potassium can have complex and nonstationary effects on neuronal circuits.

Restoration of descending inputs fails to rescue activity following deafferentation of a motor network

2012 ◽  
Vol 108 (3) ◽  
pp. 871-881 ◽  
Author(s):  
Jebun Nahar ◽  
Kawasi M. Lett ◽  
David J. Schulz
Keyword(s):  
Time Course ◽  
Critical Role ◽  
Stomatogastric Ganglion ◽  
Homeostatic Plasticity ◽  
Projection Neurons ◽  
Cancer Borealis ◽  
Compensatory Response ◽  
Pyloric Network ◽  
Motor Network ◽  
Network Output

Motor networks such as the pyloric network of the stomatogastric ganglion often require descending neuromodulatory inputs to initiate, regulate, and modulate their activity and their synaptic connectivity to manifest physiologically appropriate output. Prolonged removal of these descending inputs often results in a compensatory response that alters the inputs themselves, their targets, or both. Using the pyloric network of the crab, Cancer borealis, we investigated whether isolation of motor networks would result in alterations that change the responses of these networks to restored modulatory input. We used a reversible block with isotonic sucrose to transiently alter descending inputs into the pyloric network of the crab stomatogastric ganglion. Using this method, we found that blocking neuromodulatory inputs caused a reduced ability for subsequently restored modulatory projections to appropriately generate network output. Our results suggest that this could be due to changes in activity of descending projection neurons as well as changes in sensitivity to neuromodulators of the target neurons that develop over the time course of the blockade. These findings suggest that although homeostatic plasticity may play a critical role in recovery of functional output in a deafferented motor network, the results of these compensatory changes may alter the network such that restored inputs no longer function appropriately.

Feeding State-Dependent Modulation of Feeding-Related Motor Patterns

2021 ◽  
Author(s):  
Aaron P. Cook ◽  
Michael P. Nusbaum
Keyword(s):  
Neural Circuit ◽  
Projection Neuron ◽  
Neuron Activity ◽  
Gastric Mill ◽  
Stomatogastric Nervous System ◽  
Cancer Borealis ◽  
Motor Patterns ◽  
State Dependent ◽  
Reduced Activity ◽  
Time Point

Studies elucidating modulation of microcircuit activity in isolated nervous systems have revealed numerous insights regarding neural circuit flexibility, but this approach limits the link between experimental results and behavioral context. To bridge this gap, we studied feeding behavior-linked modulation of microcircuit activity in the isolated stomatogastric nervous system (STNS) of male Cancer borealis crabs. Specifically, we removed hemolymph from a crab that was unfed for ≥24 h ('unfed' hemolymph) or fed 15 min - 2 h before hemolymph removal ('fed' hemolymph). After feeding, the first significant foregut emptying occurred >1 h later and complete emptying required ≥6 h. We applied the unfed or fed hemolymph to the stomatogastric ganglion (STG) in an isolated STNS preparation from a separate, unfed crab to determine its influence on the VCN (ventral cardiac neuron)-triggered gastric mill (chewing)- and pyloric (filtering of chewed food) rhythms. Unfed hemolymph had little influence on these rhythms, but fed hemolymph from each examined time-point (15 min, 1- or 2 h post-feeding) slowed one or both rhythms without weakening circuit neuron activity. There were also distinct parameter changes associated with each time-point. One change unique to the 1 h time-point (i.e. reduced activity of one circuit neuron during the transition from the gastric mill retraction to protraction phase) suggested the fed hemolymph also enhanced the influence of a projection neuron which innervates the STG from a ganglion isolated from the applied hemolymph. Hemolymph thus provides a feeding state-dependent modulation of the two feeding-related motor patterns in the C. borealis STG.

GABA and responses to GABA in the stomatogastric ganglion of the crab Cancer borealis

2000 ◽  
Vol 203 (14) ◽  
pp. 2075-2092 ◽  
Author(s):  
A.M. Swensen ◽  
J. Golowasch ◽  
A.E. Christie ◽  
M.J. Coleman ◽  
M.P. Nusbaum ◽  
...  
Keyword(s):  
Nervous System ◽  
Gaba Receptors ◽  
Reversal Potential ◽  
Stomatogastric Ganglion ◽  
Projection Neurons ◽  
Gamma Aminobutyric Acid ◽  
Stomatogastric Nervous System ◽  
Cancer Borealis ◽  
Excitatory Response ◽  
Commissural Neuron

The multifunctional neural circuits in the crustacean stomatogastric ganglion (STG) are influenced by many small-molecule transmitters and neuropeptides that are co-localized in identified projection neurons to the STG. We describe the pattern of gamma-aminobutyric acid (GABA) immunoreactivity in the stomatogastric nervous system of the crab Cancer borealis and demonstrate biochemically the presence of authentic GABA in C. borealis. No STG somata show GABA immunoreactivity but, within the stomatogastric nervous system, GABA immunoreactivity co-localizes with several neuropeptides in two identified projection neurons, the modulatory proctolin neuron (MPN) and modulatory commissural neuron 1 (MCN1). To determine which actions of these neurons are evoked by GABA, it is necessary to determine the physiological actions of GABA on STG neurons. We therefore characterized the response of each type of STG neuron to focally applied GABA. All STG neurons responded to GABA. In some neurons, GABA evoked a picrotoxin-sensitive depolarizing, excitatory response with a reversal potential of approximately −40 mV. This response was also activated by muscimol. In many STG neurons, GABA evoked inhibitory responses with both K(+)- and Cl(−)-dependent components. Muscimol and beta-guanidinopropionic acid weakly activated the inhibitory responses, but many other drugs, including bicuculline and phaclofen, that act on vertebrate GABA receptors were not effective. In summary, GABA is found in projection neurons to the crab STG and can evoke both excitatory and inhibitory actions on STG neurons.

Buccalin-like and myomodulin-like peptides in the stomatogastric ganglion of the crab Cancer borealis.

1994 ◽  
Vol 193 (1) ◽  
pp. 337-343 ◽  
Author(s):  
A E Christie ◽  
C Hall ◽  
M Oshinsky ◽  
E Marder
Keyword(s):  
Stomatogastric Ganglion ◽  
Cancer Borealis

Serotonergic/cholinergic muscle receptor cells in the crab stomatogastric nervous system. II. Rapid nicotinic and prolonged modulatory effects on neurons in the stomatogastric ganglion

1989 ◽  
Vol 62 (2) ◽  
pp. 571-581 ◽  
Author(s):  
P. S. Katz ◽  
R. M. Harris-Warrick
Keyword(s):  
Motor Neurons ◽  
Preceding Paper ◽  
Stomatogastric Ganglion ◽  
Cell Group ◽  
Muscarinic Antagonists ◽  
Gastric Mill ◽  
Stomatogastric Nervous System ◽  
Cancer Borealis ◽  
Mechanical Coupling ◽  
Plateau Potential

1. The gastropyloric receptor (GPR) cells, which are described in the preceding paper, are a set of proprioceptive cells in the crabs Cancer borealis and Cancer irroratus that contain serotonin (5-hydroxytryptamine, 5-HT) and choline acetyltransferase. These cells have a variety of synaptic effects on cells in the stomatogastric ganglion (STG). We used pharmacologic methods to distinguish the effects that were due to acetylcholine (ACh) from those that could be due to serotonin. 2. The GPR cells evoke excitatory postsynaptic potentials (EPSPs) in two gastric mill motor neurons [lateral and dorsal gastric (LG and DG)] in the stomatogastric ganglion. The EPSPs exhibit nicotinic pharmacology, indicating that they may be due to the release of ACh from the GPR cells. 3. A train of GPR action potentials induces plateau potential properties in the DG motor neuron. This plateau potential induction is not blocked by nicotinic or muscarinic antagonists, suggesting it might be due to serotonin released from the GPR cells. Bath-applied serotonin induces a tonic depolarization of DG with high-intensity spiking. 4. In the accompanying paper, it is shown that DG-evoked muscle contraction leads to the excitation of GPR2 through mechanical coupling of the muscles. Because GPR2 also excites DG, a positive feedback loop exists between GPR2 and DG. This reflex loop may be involved in the control of the medial tooth of the gastric mill. 5. GPR stimulation initiates or enhances rhythmic pyloric cycling. This is due at least in part to a direct enhancement of bursting in the pyloric dilator/anterior burster (PD/AB) pacemaker cell group and can outlast the period of GPR stimulation by up to 1 min. GPR-induced PD burst enhancement continues in the presence of nicotinic and muscarinic antagonists, indicating that the effect is probably not due to the release of ACh. Bath application of serotonin mimicks the neuromodulatory effect of GPR stimulation on the PD/AB group by inducing or enhancing bursting. 6. Thus the GPR cells elicit at least three different synaptic actions in the stomatogastric ganglion: 1) classical, fast nicotinic cholinergic EPSPs that may be important for reflex functions in the gastric mill; 2) noncholinergic, cycle-by-cycle plateau potential induction that might be critical for the timing and operation of the gastric mill, and 3) prolonged, noncholinergic burst enhancement in pyloric neurons that is mimicked by serotonin, lasts many cycles, and may act to assure that the pyloric central pattern generator (CPG) is activated and cycling strongly.

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