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R M Harris-Warrick

Publications and source records attributed to R M Harris-Warrick.

At least 55 records · Page 3Linked to original sources
PubMed1993

Mapping the dynamics of a bursting neuron.

The anterior burster (AB) neuron of the lobster stomatogastric ganglion displays varied rhythmic behavior when treated with neuromodulators and channel-blocking toxins. We introduce a channel-based model for this neuron and show how bifurcation analysis can be used to investigate the response of this model to changes of its parameters. Two dimensional maps of the parameter space of the model were constructed using computational tools based on the theory of nonlinear dynamical systems. Changes in the intrinsic firing and oscillatory properties of the model AB neuron were correlated with the boundaries of Hopf and saddle-node bifurcations on these maps. Complex rhythmic patterns were observed, with a bounded region of the parameter plane producing bursting behavior of the model neuron. Experiments were performed by treating an isolated AB cell with 4-aminopyridine which selectively reduces gA, the conductance of the transient potassium channel. The model accurately predicts the qualitative changes in the neuronal voltage oscillations that are observed over a range of reduction of gA in the neuron. These results demonstrate the efficacy of dynamical systems theory as a means of determining the varied oscillatory behaviors inherent in a channel-based neural model. Further, the maps of bifurcations provide a useful tool for determining how these behaviors depend upon model parameters and comparing the model to a real neuron.

4-Aminopyridine↗
PubMed1993

Amine modulation of electrical coupling in the pyloric network of the lobster stomatogastric ganglion.

1. The neurons of the pyloric network of the lobster (Panulirus interruptus) stomatogastric ganglion organize their rhythmic motor output using both chemical and electrical synapses. The 6 electrical synapses within this network help set the firing phases of the pyloric neurons during each rhythmic cycle. We examined the modulatory effects of the amines dopamine (DA), serotonin (5HT) and octopamine (Oct) on coupling at all the electrical synapses of the pyloric network. 2. Electrical coupling within the pacemaker group [anterior burster (AB) to pyloric dilator (PD), and PD-PD] was non-rectifying, while coupling at the other electrical synapses [AB to ventral dilator (VD), PD-VD, lateral pyloric (LP) to pyloric (PY), and PY-PY] was rectifying. 3. Dopamine decreased or increased the coupling strength of all the pyloric electrical synapses: the sign of the effect depended upon which neuron was the target of current injection. For example, DA decreased AB-->PD coupling (i.e., when current was injected into the AB) but increased coupling in the other direction, PD-->AB. Dopamine decreased AB to VD coupling when current was injected into either neuron. Serotonin also had mixed effects; it enhanced PD-->AB coupling but decreased AB to VD and PD to VD coupling in both directions. Octopamine's only effect was to reduce PD-->VD coupling. 4. Dopamine increased the input resistance of the AB neuron but decreased the input resistance of the PD and VD neurons. Serotonin reduced the input resistance of the VD and PY neurons, while Oct did not significantly change the input resistance of any pyloric neuron. 5. The characteristic modulation of electrical coupling by each amine may contribute to the unique motor pattern that DA, 5HT and Oct each elicit from the pyloric motor network.

Amines↗
PubMed1993

Pattern generation.

Significant advances have been made in understanding the cellular mechanisms for pattern generation in both invertebrate and vertebrate preparations. In a number of preparations, slow neuromodulators have been shown not only to modify network function, but to be intimately involved in development and/or normal function of the neural network and its associated behavior. The mechanisms underlying coordination between multiple pattern-generating networks, including switching of neurons from one network to another, are now being studied. Several new quantitative models of network function have been developed, and modeling is now an important component of research in this field.

Animals↗
PubMed1992

Elevated temperature alters the ionic dependence of amine-induced pacemaker activity in a conditional burster neuron.

The anterior burster neuron of the lobster (Panulirus interruptus) stomatogastric ganglion is a conditional burster that functions as the primary pacemaker for the pyloric motor network. When modulatory inputs to this cell are blocked, it loses its bursting properties and becomes quiescent. Applications of the monoamines, dopamine, octopamine or serotonin restore rhythmic bursting in this cell (Flamm and Harris-Warrick 1986). At 15 degrees C, serotonin- and octopamine-induced oscillations depend critically upon sodium entry (blocked by low sodium saline or tetrodotoxin); dopamine-induced oscillations depend upon calcium entry (blocked by reduced extracellular calcium; Harris-Warrick and Flamm 1987). We show here that the ionic dependence of amine-induced oscillations in the anterior burster cell differs at 15 and 21 degrees C. At 21 degrees C, all amines have the potential to induce rhythmic oscillations in saline containing tetrodotoxin. At the elevated temperature and in tetrodotoxin, both calcium and sodium currents are essential for the maintenance of dopamine-induced oscillations; serotonin-induced oscillations do not depend upon either calcium or sodium alone; octopamine-induced oscillations do not depend upon calcium and show a variable dependence upon sodium. Thus, multiple ionic mechanisms, which vary with both the modulator and the ambient temperature, can be recruited to support rhythmic activity in a conditional burster neuron.

Animals↗
PubMed1992

Physiological role of the transient potassium current in the pyloric circuit of the lobster stomatogastric ganglion.

1. Our experiments were performed to assess the quantitative role of the transient potassium current, IA, in determining the cycle frequency and phasing of neurons in the network generating the pyloric motor rhythm in the stomatogastric ganglion of the spiny lobster, Panulirus interruptus. We used 4-aminopyridine (4-AP) to reduce IA and recorded the effects of this treatment on cell activity. 2. In the intact circuit with an actively cycling pyloric rhythm, 4-AP had three major effects on the rhythm. First, the cycle period was decreased approximately 20%. Second, 4-AP enhanced the activity of all cells, causing increases in spikes/burst and spike frequency within bursts. Third, 4-AP altered the phasing of follower cells relative to the onset of the pacemaker (AB/PD) bursts. The lateral pyloric (LP) and pylorics (PYs) were phase advanced by 4-AP, whereas the ventral dilator (VD) was phase delayed. 3. Voltage-clamp studies indicated that pyloric cells differed in the amount of IA they expressed on or near the soma. IA was largest in pyloric dilator (PD) and PY cells, smaller in the anterior burster (AB), LP, and inferior cardiac (IC) cells, and undetectable in the VD cell. When cells were isolated from synaptic input, however, all were excited by 4-AP, suggesting that all possess functionally significant IA. In VD cells, IA-like currents probably occur primarily in nonsomatic cell regions. 4. We measured postinhibitory rebound by determining the delay to the first spike after a series of 200-ms hyperpolarizing prepulses in the PD, PY, LP, VD, and IC cells. In all five cell types, the delay was progressively increased as the potential of the hyperpolarizing prepulse became more negative. This increased delay reflected the removal of IA inactivation. The delay was greatest in the PY cell and least in the IC. In four cells (the PD, PY, LP, and VD) 4-AP decreased the delay to the first spike at all prepulse potentials. In the IC the delay to the first spike was unaffected by 4-AP, suggesting that IA was not responsible for the relatively short delay after hyperpolarizing prepulses. 5. In all five cell types, 4-AP increased the spike frequency for the duration of a 1-s depolarization. The 4-AP-sensitive current responsible for this behavior appears to have very rapid kinetics and may represent a distinct channel subtype. Functionally, this current may act to dampen cell excitability and to reduce spike frequency during bursts.

4-Aminopyridine↗
PubMed1992

Serotonergic stretch receptors induce plateau properties in a crustacean motor neuron by a dual-conductance mechanism.

1. The mechanisms for induction of bistable plateau potential properties by a set of serotonergic/cholinergic peripheral stretch receptor cells [gastropyloric receptor (GPR) cells] were examined in the crab stomatogastric ganglion (STG) with the use of intracellular recording techniques. 2. GPR cell stimulation evoked nicotinic excitatory postsynaptic potentials (EPSPs) and induced plateau potential capability in the dorsal gastric (DG) motor neuron. The plateau potential could be triggered during a GPR train either by the summating nicotinic EPSPs or by brief intracellular current injection. After pharmacological blockade of nicotinic and muscarinic receptors, a slow depolarization in response to GPR stimulation was revealed. Prolonged plateau potentials could still be evoked after this treatment. Local application of serotonin (5-HT; 10 microM to 1 mM) mimicked the noncholinergic plateau inducing effects of GPR stimulation in the DG motor neuron. 3. The synergistic action of acetylcholine (ACh) and 5-HT was examined by stimulating the GPR cells at different frequencies (1-20 Hz). The plateau induction was present down to 2 Hz. The time to onset for triggering a plateau during a GPR train was determined by the co-released ACh. 4. The 5-HT-evoked slow depolarization persisted in tetrodotoxin (TTX; 0.1-1 microM), and the DG motor neuron could still produce a plateau potential on brief depolarization in the absence of the spike-generating mechanism. 5. In normal TTX-containing saline, the 5-HT-evoked depolarization was accompanied by a weak and variable decrease in apparent input conductance. After substituting one-half of the extracellular sodium with either Trisma-HCl or choline, the decrease in apparent input conductance became more pronounced. This decrease was converted to an increase in apparent input conductance when extracellular Ca2+ was replaced with Mg2+. 6. Under voltage-clamp conditions, local application of 5-HT caused a slow inward current of prolonged duration in DG. The current versus voltage relationship had an inverted U-shape with no apparent reversal potential in the entire voltage range investigated (-90 to -5 mV). The 5-HT-induced changes in input conductance showed a complex voltage dependence, with a conductance decrease from moderately depolarized voltages. 7. Extracellular Cs+ (2-4 mM) caused the DG to hyperpolarize 2-4 mV from rest, whereas lowering extracellular Ca2+ caused it to depolarize 7-15 mV. The combined action of low extracellular Ca2+ and 2-4 mM Cs+ caused an almost complete block of the slow 5-HT-evoked depolarization.(ABSTRACT TRUNCATED AT 400 WORDS)

Acetylcholine↗
PubMed1992

5-HT modulation of hyperpolarization-activated inward current and calcium-dependent outward current in a crustacean motor neuron.

1. Serotonergic modulation of a hyperpolarization-activated inward current, Ih, and a calcium-dependent outward current, Io(Ca), was examined in the dorsal gastric (DG) motor neuron, with the use of intracellular recording techniques in an isolated preparation of the crab stomatogastric ganglion (STG). 2. Hyperpolarization of the membrane from rest with maintained current pulses resulted in a slow time-dependent relaxation back toward rest and a depolarizing overshoot after termination of the current pulse. In voltage clamp, hyperpolarizing commands negative to approximately -70 mV caused a slowly developing inward current, Ih, which showed no inactivation. Repolarization back to the holding potential of -50 mV revealed a slow inward tail current. 3. The reversal potential for Ih was approximately -35 mV. Raising extracellular K+ concentration ([K+]o) from 11 to 22 mM enhanced, whereas decreasing extracellular Na+ concentration ([Na+]o) reduced the amplitude of Ih. These results indicate that Ih in DG is carried by both K+ and Na+ ions. 4. Bath application of serotonin (5-HT; 10 microM) caused a marked increase in the amplitude of Ih through its active voltage ranges. 5. The time course of activation of Ih was well fitted by a single exponential function and strongly voltage dependent. 5-HT increased the rate of activation of Ih. 5-HT also slowed the rate of deactivation of the Ih tail on repolarization to -50 mV. 6. The activation curve for the conductance (Gh) underlying Ih was obtained by analyzing tail currents. 5-HT shifted the half activation for Gh from approximately -105 mV in control to -95 mV, resulting in an increase in the amplitude of Gh active at rest. 7. Two to 4 mM Cs+ abolished Ih, whereas barium (200 microM to 2 mM) had only weak suppressing effects on Ih. Concomitantly, Cs+ also blocked the 5-HT-induced inward current and conductance increase seen at voltages negative to rest. In current clamp, Cs+ caused DG to hyperpolarize 3-4 mV from rest, suggesting that Ih is partially active at rest and contributes to the resting membrane potential. 8. Depolarizing voltage commands from a holding potential of -50 mV resulted in a total outward current (Io) with an initial transient component and a sustained steady-state component. Application of 5-HT reduced both the transient and sustained components of Io. 9. Io was reduced by 10-20 mM tetraethylammonium (TEA), suggesting that it is primarily a K+ current.(ABSTRACT TRUNCATED AT 400 WORDS)

Animals↗
PubMed1991

Recruitment of crab gastric mill neurons into the pyloric motor pattern by mechanosensory afferent stimulation.

1. The gastropyloric receptor (GPR) cells are stretch-sensitive muscle receptors in the crab stomatogastric nervous system that use both 5-hydroxytryptamine (serotonin) and acetylcholine as cotransmitters. Brief stimulation of these afferent neurons causes two gastric mill neurons to be recruited into the pyloric motor pattern. 2. The GPR cells evoke complex synaptic potentials in the lateral gastric (LG) and medial gastric (MG) motor neurons, two component neurons of the gastric mill central pattern generator. When the gastric mill is quiescent (as often happens in vivo), GPR stimulation transiently inhibits LG and MG. After this transient inhibition, these cells undergo a prolonged excitation during which they fire bursts of action potentials at a constant phase relation to the pyloric motor pattern. 3. To determine the causes for this effect, we examined the effects of GPR stimulation on these two cells and on the inferior cardiac motor neuron, which is electrically coupled to them. When GPR is stimulated, all three cells receive rapid biphasic synaptic potentials that are blocked by nicotinic antagonists, followed by a slow, prolonged depolarizing potential. 4. The slow, prolonged depolarizing potential is not blocked by nicotinic or muscarinic cholinergic antagonists but is mimicked and occluded by exogenously applied serotonin. 5. The prolonged excitation, mediated at least in part by serotonin, may be responsible for the recruitment of the gastric mill neurons into the pyloric motor pattern. Thus sensory input can directly exert prolonged modulatory effects that change the functional cellular composition of pattern-generating circuits.

Acetylcholine↗
PubMed1991

Temperature sensitivity of graded synaptic transmission in the lobster stomatogastric ganglion.

We examined the temperature sensitivity of graded chemical synaptic strength within the pyloric circuit of the spiny lobster stomatogastric ganglion. Cooling from 20.4 degrees C to 11.3 degrees C reduced the graded synaptic potential (GSP) amplitude at all six pyloric synapses tested. Cooling appeared to reduce the slope of the linear part of the input-output curve at three of these synapses, and did not significantly alter the threshold for transmitter release at any synapses. Pairs of neurons with a presynaptic pyloric dilator (PD) cell showed reductions in graded synaptic strength at 16.5 degrees C but those with presynaptic lateral pyloric (LP) or ventral dilator (VD) cells did not. A generalized decrease in input resistance is not responsible for the reduced GSP amplitude upon cooling, as determined by input resistance, action potential amplitude and electrical coupling measurements. We conclude that cooling reduces graded chemical strength by a direct synaptic action. Since the PD and VD cells use the same transmitter and act on some of the same postsynaptic cells, their differential sensitivity to cooling further suggests a presynaptic site of action. The temperature range used in our experiments encompasses the range that the animal normally encounters in nature. Thus, the relative importance of graded synaptic interactions in generating the pyloric motor rhythm may vary with transient changes in temperature.

Action Potentials↗
PubMed1990

Actions of identified neuromodulatory neurons in a simple motor system.

Recent work on neurons that release slow neuromodulators has revealed important generalities about the roles played by neuromodulation in motor systems. Activity of these cells can affect the cellular and synaptic properties of central pattern generating circuits, orchestrating new variations of motor patterns and sometimes coordinating their outputs with other motor patterns. Many modulatory neurons use multiple transmitters to evoke both fast and slow synaptic responses of various types in different target cells. Some modulatory cells can have a mediating as well as a modulating role, simultaneously acting as sensory neurons or components of another pattern generating circuit.

Animals↗
PubMed1990

Aminergic modulation of graded synaptic transmission in the lobster stomatogastric ganglion.

Graded chemical synaptic transmission is important for establishing the motor patterns produced by the pyloric central pattern generator (CPG) circuit of the lobster stomatogastric ganglion (Raper, 1979; Anderson and Barker, 1981; Graubard et al., 1983). We examined the modulatory effects of the amines dopamine (DA), serotonin (5-HT), and octopamine (Oct) on graded synaptic transmission at all the central chemical synapses made by the pyloric dilator (PD) neuron onto its follower cells, using synaptic input-output curves measured from cell somata. DA strongly reduced the graded synaptic strength at all the PD synapses. DA reduction of chemical synaptic strength from PD onto the inferior cardiac (IC) neuron could change the sign of synaptic interaction between these 2 cells from inhibitory to excitatory by uncovering a weak electrical connection. 5-HT had weaker and more variable effects, reducing graded synaptic strength from the PD onto the lateral pyloric and pyloric neurons and enhancing the weak synapse from the PD to the IC cell. Oct strongly enhanced the graded synaptic strength at all the PD central synapses. Oct enhancement of graded synaptic strength between the PD and IC cells could also change the sign of the interaction: weak, excitatory electrical coupling, which was sometimes dominant before Oct, was masked by the enhanced chemical inhibitory interaction during Oct application. Measurements of electrical coupling between 2 PD cells and between 2 postsynaptic cells suggest that Oct does not change the input resistance of these cells and may act directly at the PD synapses. The effects of DA and 5-HT are most easily explained by their general reductions in pre- and postsynaptic input resistance. DA, 5-HT, and Oct each produce a distinct pyloric motor pattern (Flamm and Harris-Warrick, 1986a). These amine-induced motor patterns may be explained by the unique actions of each amine on the intrinsic membrane properties of different pyloric CPG neurons (Flamm and Harris-Warrick, 1986b) and by modulation of graded synaptic transmission between the pyloric neurons.

Action Potentials↗
PubMed1990

Neuromodulation of the crab pyloric central pattern generator by serotonergic/cholinergic proprioceptive afferents.

In the stomatogastric nervous system of the crab, Cancer borealis, a set of 4 serotonergic/cholinergic proprioceptive neurons, called gastropyloric receptor (GPR) cells, have effects on the pyloric motor pattern. In a semi-intact foregut preparation, the GPR cells are not activated by movements of the pyloric filter; instead they respond to the slower movements of the gastric mill (Katz et al., 1989). Thus, their activity is not synchronized to the pyloric motor pattern. However, when the GPR cells are stimulated in an in vitro preparation in a manner that resembles their normal firing pattern, they produce dramatic effects on the pyloric motor pattern. These effects include: (1) a prolonged increase in the pyloric cycle frequency, (2) a momentary pause in the motor pattern, (3) transient inhibition of some motor neurons, (4) strong excitation of other motor neurons, and (5) altered phase relationships of the different components of the motor pattern. These changes in the motor pattern are due to direct effects of the GPR cells on neurons in the pyloric central pattern generator (CPG). All of the cells in the pyloric circuit appear to receive GPR input. However, only 2 neurons receive detectable rapid nicotinic synaptic potentials. The other neurons receive only slower neuromodulatory input from GPR stimulation. The neuromodulatory effects include burst enhancement, plateau potential enhancement, excitation, and inhibition. These modulatory effects are largely mimicked by bath-applied serotonin (5-HT). Thus, primary sensory neurons can alter the production of motor patterns by a CPG through a phase-independent mechanism; these proprioceptors do not need to fire at a precise time in the cycle to be effective because their effects are mediated through the slower actions of the neuromodulator 5-HT.

Animals↗
PubMed1989

Forskolin reduces a transient potassium current in lobster neurons by a cAMP-independent mechanism.

Forskolin decreases the transient potassium current, IA, in voltage-clamped somata of identified neurons in the stomatogastric ganglion of the spiny lobster, Panulirus interruptus. The diterpene reduces the peak outward current and accelerates the rate of inactivation of IA. Forskolin has no detectable effects on two other identifiable potassium currents in these cells, IK(Ca) and IK(V). Three identified stomatogastric neuron types (PD, PY, AB) have marked amounts of IA which are affected by forskolin; three other cell types (LP, IC, VD) have little or no IA, and forskolin has no effect on their outward currents. Bath application of 8-bromo-cAMP, N,N-dibutyryl-cAMP and IBMX do not affect IA. In addition, the forskolin analog, 1,9-dideoxyforskolin, which does not activate adenylate cyclase, mimics forskolin's effects on IA. Thus, the effects of forskolin on IA are not mediated by cAMP elevation.

Animals↗
PubMed1989

Serotonergic/cholinergic muscle receptor cells in the crab stomatogastric nervous system. I. Identification and characterization of the gastropyloric receptor cells.

1. Serotonin (5-hydroxytryptamine) immunohistochemistry was used to locate and anatomically describe a set of four muscle receptor cells in the stomatogastric nervous system of the crabs Cancer borealis and Cancer irroratus. We found that these sensory cells, which we named gastropyloric receptor (GPR) cells, are the sole source of serotonergic inputs to the stomatogastric ganglion (STG) in these species. Thus any endogenous serotonergic modulation of the central pattern generators (CPGs) in the STG must be afferent and not descending from other ganglia. 2. There are two bilateral pairs of GPR cells. Each pair consists of two cell types (GPR1 and GPR2) based on differences in muscle innervation and physiological response characteristics. GPR2 responds in a mostly tonic fashion to increases in muscle tension caused by passive stretch or motor neuron-evoked contraction, whereas GPR1 responds more phasically and adapts more rapidly. Both GPR cell types project to the midline STG and terminate in each of the bilaterally paired commissural ganglia (COGs). 3. The GPR cells have sensory endings unlike any described for other muscle receptor cells: the terminals enter invaginations of the muscle surface and end near the z-bands of the muscle. These novel structures may be involved in the sensory transduction process. 4. The GPR cells may contain acetylcholine in addition to serotonin, as indicated by the presence of choline acetyltransferase (ChAT) in GPR2 (Table 1) and probably GPR1 as well. 5. The GPR cells have no direct effect on muscle properties or neuromuscular transmission: excitatory junctional potential (EJP) amplitude and motor neuron-evoked tension are unaffected by GPR stimulation. However, very low concentrations of exogenously applied serotonin do cause an increase in motor neuron-evoked muscle tension, probably reflecting a hormonal action of the amine. 6. The activity of GPR2 was monitored in a semi-intact preparation. GPR2 is active in phase with normal movements of the gastric mill. GPR2 is also capable of endogenous rhythmic activity. This indicates that even in the absence of mechanical stimulation, the GPR cells may still provide patterned input to the CPGs in the STG. 7. The GPR cells are proprioceptive cells that use serotonin and acetylcholine as cotransmitters. It is important to characterize these cells to understand the role of serotonergic modulation in the production of motor programs by stomatogastric CPGs.

Acetylcholine↗
PubMed1989

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

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.

Animals↗
PubMed1988

An alpha 40 subunit of a GTP-binding protein immunologically related to Go mediates a dopamine-induced decrease of Ca2+ current in snail neurons.

Dopamine induces a decrease in voltage-dependent Ca2+ current in identified neurons of the snail H. aspersa. This effect is blocked by intracellular injection of activated B. pertussis toxin and of an affinity-purified antibody against the alpha subunit of bovine Go protein. The dopamine effect is mimicked by intracellular injection of mammalian alpha o. In snail nervous tissue, pertussis toxin ADP-ribosylates a single protein band on SDS gels, and this band is recognized in immunoblots by the anti-alpha o antibody. We propose that this is a 40 kd alpha subunit of a molluscan G protein immunologically related to alpha o and that it mediates the effect of dopamine on Ca2+ currents in identified snail neurons.

Animals↗
PubMed1987

Potassium channel blockade induces rhythmic activity in a conditional burster neuron.

In the lobster stomatogastric ganglion the Anterior Burster (AB) neuron loses its rhythmic bursting capabilities when isolated from all synaptic input. Here we report that compounds which reduce the current through several different types of potassium channels induce bursting in isolated AB neurons. These results suggest that when quiescent, this neuron has all the conductances necessary to support bursting, but bursting is actively inhibited by tonic potassium conductances.

4-Aminopyridine↗