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PubMed1978

Neuronal generation of the leech swimming movement.

The swimming movement of the leech is produced by an ensemble of bilaterally symmetric, rhythmically active pairs of motor neurons present in each segmental ganglion of the ventral nerve cord. These motor neurons innervate the longitudinal muscles in dorsal or ventral sectors of the segmental body wall. Their duty cycles are phase-locked in a manner such that the dorsal and ventral body wall sectors of any given segment undergo an antiphasic contractile rhythm and that the contractile rhythms of different segments form a rostrocaudal phase progression. This activity rhythm is imposed on the motor neurons by a central swim oscillator, of which four bilaterally symmetric pairs of interneurons present in each segmental ganglion appear to constitute the major component. These interneurons are linked intra- and intersegmentally via inhibitory connections to form a segmentally iterated and inter-segmentally concatenated cyclic neuronal network. The network appears to owe its oscillatory activity pattern to the mechanism of recurrent cyclic inhibition.

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PubMed1982

Synapses between neurons regenerate accurately after destruction of ensheathing glial cells in the leech.

Individual glial cells that ensheathe axons in the central nervous system of the leech were destroyed by intracellular injection of protease. The axons were then severed, and regeneration by particular neurons was studied physiologically and morphologically. Although certain axons sprouted more in the absence of the glial cell, functional synapses were accurately regenerated with normal frequency.

Animals↗

PubMed2000

Ingested blood contributes to the specificity of the symbiosis of Aeromonas veronii biovar sobria and Hirudo medicinalis, the medicinal leech.

Hirudo medicinalis, the medicinal leech, usually carries in its digestive tract a pure culture of Aeromonas veronii bv. sobria. Such specificity is unusual for digestive tracts that are normally colonized by a complex microbial consortium. Important questions for the symbiotic interaction and for the medical application after microvascular surgery are whether other bacteria can proliferate or at least persist in the digestive tract of H. medicinalis and what factors contribute to the reported specificity. Using a colonization assay, we were able to compare experimentally the ability of clinical isolates and of a symbiotic strain to colonize H. medicinalis. The symbiotic A. veronii bv. sobria strain proliferated well and persisted for at least 7 days inside the digestive tract. In contrast, the proliferation of Pseudomonas aeruginosa and Staphylococcus aureus was inhibited inside the animal compared to growth in the in vitro control, indicating that the ingested blood was modified within the digestive tract. However, both strains were able to persist in the digestive tract for at least 7 days. For an Escherichia coli strain, the viable counts decreased approximately 1, 000-fold within 42 h. The decrease of viable E. coli could be prevented by interfering with the activation of the membrane-attack complex of the complement system that is present in blood. This suggests that the membrane-attack complex remained active inside H. medicinalis and prevented the proliferation of sensitive bacteria. Thus, antimicrobial properties of the ingested vertebrate blood contribute to the specificity of the A. veronii-H. medicinalis symbiosis, in addition to modifications of the blood inside the digestive tract of H. medicinalis.

Aeromonas↗

PubMed2006

Endogenous and half-center bursting in morphologically inspired models of leech heart interneurons.

Based on a detailed morphology "Full Model" of a leech heart interneuron, we previously developed a computationally efficient, morphologically inspired "Reduced Model" to expedite tuning the model to produce endogenous bursting and alternating bursting when configured as a half-center oscillator (paired with reciprocally inhibitory synapses). To find conductance density distributions that produce endogenous bursting, we implemented a genetic algorithm automated parameter search. With multiple searches, we found eight parameter sets that produced endogenous bursting in the Reduced Model. When these parameter sets were applied to the Full Model, all produced endogenous bursting, although when the simulation time was extended from 80 to 300 s, only four parameter sets produced sustained bursting in the Reduced Models. All parameter sets produced alternating half-center bursting in the Reduced and Full Models throughout the entire 300 s. When conductance amplitudes were systematically varied for each of the four sustained burster sets, the effects on bursting activity differed, both for the same parameter set in the Reduced and Full Models and for different parameter sets with the same level of morphological detail. This implies that morphological detail can affect burst activity and that these parameter sets may represent different mechanisms for burst generation and/or regulation. We also tested the models with parameter variations that correspond to experimental manipulations. We conclude that, whereas similar output can be achieved with multiple different parameter sets, perturbations such as conductance variations can highlight differences. Additionally, this work demonstrates both the utility and limitations of using simplified models to represent more morphologically accurate models.

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PubMed2006

Creation and reduction of a morphologically detailed model of a leech heart interneuron.

Conductance-based neuron models aid in understanding the role intrinsic and synaptic currents play in producing neuronal activity. Incorporating morphological detail into a model allows for additional analysis of nonhomogeneous distributions of active and synaptic conductances, as well as spatial segregation of electrical events. We developed a morphologically detailed "Full Model" of a leech heart interneuron that replicates reasonably well intracellular recordings from these interneurons. However, it constitutes hundreds of compartments, each increasing parameter space and simulation time. To reduce the number of compartments of the Full Model, while preserving conductance densities and distributions, its compartments were grouped into functional groups that each share identical conductance densities. Each functional group was sequentially reduced to one or two compartments, preserving surface area, conductance densities, and its contribution to input resistance. As a result, the input resistance and membrane time constant were preserved. The axial resistances of several compartments were rescaled to match the amplitude of synaptic currents and low-threshold calcium currents and the shape of action potentials to those in the Full Model. This reduced model, with intrinsic conductances, matched the activity of the Full Model for a variety of simulated current-clamp and voltage-clamp data. Because surface area and conductance distribution of the functional groups of the Full Model were maintained, parameter changes introduced into the reduced model can be directly translated to the Full Model. Thus our computationally efficient reduced morphology model can be used as a tool for exploring the parameter space of the Full Model and in network simulations.

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PubMed2005

Serotonin modulates axo-axonal coupling between neurons critical for learning in the leech.

S cells form a chain of electrically coupled neurons that extends the length of the leech CNS and plays a critical role in sensitization during whole-body shortening. This process requires serotonin, which acts in part by altering the pattern of activity in the S-cell network. Serotonin-containing axons and varicosities were observed in Faivre's nerve where the S-to-S-cell electrical synapses are located. To determine whether serotonin modulates these synapses, S-cell action-potential (AP) propagation was studied in a two-ganglion chain containing one electrical synapse. Suction electrodes were placed on the cut ends of the connectives to stimulate one S cell while recording the other, coupled S cell's APs. A third electrode, placed en passant, recorded the APs near the electrical synapse before they propagated through it. Low concentrations of the gap junction inhibitor octanol increased AP latency across the two-ganglion chain, and this effect was localized to the region of axon containing the electrical synapse. At higher concentrations, APs failed to propagate across the synapse. Serotonin also increased AP latency across the electrical synapse, suggesting that serotonin reduced coupling between S cells. This effect was independent of the direction of propagation and increased with the number of electrical synapses in progressively longer chains. Furthermore, serotonin modulated instantaneous AP frequency when APs were initiated in separate S cells and in a computational model of S-cell activity after mechanosensory input. Thus serotonergic modulation of S-cell electrical synapses may contribute to changes in the pattern of activity in the S-cell network.

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PubMed2002

Phase relationships between segmentally organized oscillators in the leech heartbeat pattern generating network.

Motor pattern generating networks that produce segmentally distributed motor outflow are often portrayed as a series of coupled segmental oscillators that produce a regular progression (constant phase differences) in their rhythmic activity. The leech heartbeat central pattern generator is paced by a core timing network, which consists of two coupled segmental oscillators in segmental ganglia 3 and 4. The segmental oscillators comprise paired mutually inhibitory oscillator interneurons and the processes of intersegmental coordinating interneurons. As a first step in understanding the coordination of segmental motor outflow by this pattern generator, we describe the functional synaptic interactions, and activity and phase relationships of the heart interneurons of the timing network, in isolated nerve cord preparations. In the timing network, most (approximately 75%) of the coordinating interneuron action potentials were generated at a primary spike initiation site located in ganglion 4 (G4). A secondary spike initiation site in ganglion 3 (G3) became active in the absence of activity at the primary site. Generally, the secondary site was characterized by a reluctance to burst and a lower spike frequency, when compared with the primary site. Oscillator interneurons in G3 inhibited spike activity at both initiation sites, whereas oscillator interneurons in G4 inhibited spike activity only at the primary initiation site. This asymmetry in the control of spike activity in the coordinating interneurons may account for the observation that the phase of the coordinating interneurons is more tightly linked to the G3 than G4 oscillator interneurons. The cycle period of the timing network and the phase difference between the ipsilateral G3 and G4 oscillator interneurons were regular within individual preparations, but varied among preparations. This variation in phase differences observed across preparations implies that modulated intrinsic membrane and synaptic properties, rather than the pattern of synaptic connections, are instrumental in determining phase within the timing network.

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PubMed2002

Model of intersegmental coordination in the leech heartbeat neuronal network.

We have created a computational model of the timing network that paces the heartbeat of the medicinal leech, Hirudo medicinalis. The rhythmic activity of this network originates from two segmental oscillators located in the third and fourth midbody ganglia. In the intact nerve cord, these segmental oscillators are mutually entrained to the same cycle period. Although experiments have shown that the segmental oscillators are coupled by inhibitory coordinating interneurons, the underlying mechanisms of intersegmental coordination have not yet been elucidated. To help understand this coordination, we have created a simple computational model with two variants: symmetric and asymmetric. In the symmetric model, neurons within each segmental oscillator called oscillator interneurons, inhibit the coordinating interneurons. In contrast, in the asymmetric model only the oscillator interneurons of one segmental oscillator inhibit the coordinating interneurons. In the symmetric model, when two segmental oscillators with different inherent periods are coupled, the faster one leads in phase, and the period of the coupled system is equal to the period of the faster oscillator. This behavior arises because, during each oscillation cycle, the oscillator interneurons of the faster segmental oscillator begin to burst before those of the slower oscillator, thereby terminating spike activity in the coordinating interneurons. Thus there is a brief period of time in each cycle when the oscillator interneurons of the slower segmental oscillator are relieved of inhibition from the coordinating interneurons. This "removal of synaptic inhibition" allows, within certain limits, the slower segmental oscillator to be sped to the period of the faster one. Thus the symmetric model demonstrates a plausible biophysical mechanism by which one segmental oscillator can entrain the other. In general the asymmetric model, in which only one segmental oscillator has the ability to inhibit the coordinating interneurons, behaves similarly, except only one segmental oscillator can control the period of the system. In addition, we simulated physiological experiments in which a "driving" stimulus, consisting of alternating positive and negative current steps, was used to control a single oscillator interneuron and thereby entrain the activity of the entire timing network.

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PubMed2005

Myomodulin increases Ih and inhibits the NA/K pump to modulate bursting in leech heart interneurons.

In the medicinal leech, a rhythmically active 14-interneuron network composes the central pattern generator for heartbeat. In two segmental ganglia, bilateral pairs of reciprocally inhibitory heart interneurons (oscillator interneurons) produce a rhythm of alternating bursts of action potentials that paces activity in the pattern-generating network. The neuropeptide myomodulin decreases the period of this bursting and increases the intraburst spike frequency when applied to isolated ganglia containing these oscillator interneurons. Myomodulin also decreases period, increases spike frequency, and increases the robustness of endogenous bursting in synaptically isolated (with bicuculline) oscillator interneurons. In voltage-clamp experiments using hyperpolarizing ramps, we identify an increase in membrane conductance elicited by myomodulin with the properties of a hyperpolarization-activated current. Voltage steps confirm that myomodulin indeed increases the maximum conductance of the hyperpolarization-activated current I(h). In similar experiments using Cs(+) to block I(h), we demonstrate that myomodulin also causes a steady offset in the ramp current that is not associated with an increase in conductance. This current offset is blocked by ouabain, indicating that myomodulin inhibits the Na/K pump. In current-clamp experiments, when I(h) is blocked with Cs(+), myomodulin decreases period and increases spike frequency of alternating bursting in synaptically connected oscillator interneurons, suggesting that inhibiting the Na/K pump modulates these burst characteristics. These observations indicate that myomodulin decreases period and increases spike frequency of endogenous bursting in synaptically isolated oscillator heart interneurons and alternating bursting of reciprocally inhibitory pairs of interneurons, at least in part, by increasing I(h) and by decreasing the Na/K pump.

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PubMed2006

Hybrid systems analysis of the control of burst duration by low-voltage-activated calcium current in leech heart interneurons.

The leech heartbeat CPG is paced by the alternating bursting of pairs of mutually inhibitory heart interneurons that form elemental half-center oscillators. We explore the control of burst duration in heart interneurons using a hybrid system, where a living, pharmacologically isolated, heart interneuron is connected with artificial synapses to a model heart interneuron running in real-time, by focusing on a low-voltage-activated (LVA) calcium current I(CaS). The transition from silence to bursting in this half-center oscillator occurs when the spike frequency of the bursting interneuron declines to a critical level, f(Final), at which the inhibited interneuron escapes owing to a build-up of the hyperpolarization-activated cation current, I(h). We varied I(CaS) inactivation time constant either in the living heart interneuron or in the model heart interneuron. In both cases, varying I(CaS) inactivation time constant did not affect f(Final) of either interneuron, but in the varied interneuron, the time constant of decline of spike frequency during bursts to f(Final) and thus the burst duration varied directly and nearly linearly with I(CaS) inactivation time constant. Bursts of the opposite, nonvaried interneuron did not change. We show also that control of burst duration by I(CaS) inactivation does not require synaptic interaction by reconstituting autonomous bursting in synaptically isolated living interneurons with injected I(CaS). Therefore inactivation of LVA calcium current is critically important for setting burst duration and thus period in a heart interneuron half-center oscillator and is potentially a general intrinsic mechanism for regulating burst duration in neurons.

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PubMed2003

Detailed model of intersegmental coordination in the timing network of the leech heartbeat central pattern generator.

To address the general problem of intersegmental coordination of oscillatory neuronal networks, we have studied the leech heartbeat central pattern generator. The core of this pattern generator is a timing network that consists of two segmental oscillators, each of which comprises two identified, reciprocally inhibitory oscillator interneurons. Intersegmental coordination between the segmental oscillators is mediated by synaptic interactions between the oscillator interneurons and identified coordinating interneurons. The small number of neurons (8) and the distributed structure of the timing network have made the experimental analysis of the segmental oscillators as discrete, independent units possible. On the basis of this experimental work, we have made conductance-based models to explore how intersegmental phase and cycle period are determined. We show that although a previous simple model, which ignored many details of the living system, replicated some essential features of the living system, the incorporation of specific cellular and network properties is necessary to capture the behavior of the system seen under different experimental conditions. For example, spike frequency adaptation in the coordinating interneurons and details of asymmetries in intersegmental connectivity are necessary for replicating driving experiments in which one segmental oscillator was injected with periodic current pulses to entrain the activity of the entire network. Nevertheless, the basic mechanisms of phase and period control demonstrated here appear to be very general and could be used by other networks that produce coordinated segmental motor outflow.

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PubMed2004

Selective serotonin reuptake inhibitors induce spontaneous interneuronal activity in the leech nervous system.

Serotonin [5-hydroxytryptamine (5-HT)] is a conspicuous neuromodulator of sensory-motor networks that affects a variety of neurons at different levels of the network hierarchy. Because of its many possible targets, it has been difficult to obtain a comprehensive picture of how 5-HT achieves its final modulatory output on any given network. Our hypothesis is that the profile of 5-HT actions is dictated by its pattern of release from endogenous sites. We tested this hypothesis in the leech nervous system by means of a selective serotonin reuptake blocker (SSRI), fluoxetine. Fluoxetine evoked barrages of synaptic potentials in identified sensory, motor, and interneurons. This effect was mimicked by the tricyclic antidepressants imipramine and clomipramine, and by the SSRI citalopram, with relative efficacies that matched their known relative selectivities for the 5-HT transporter. The synaptic responses evoked by fluoxetine in different neurons were temporally correlated, suggesting that they had a common origin. The profile of the synaptic responses matched that expected from the activation of the mechanosensory pressure cells, known to act by polysynaptic pathways. The results suggest that endogenous 5-HT acted on cord spanning interneurons. On the other hand, bath-applied 5-HT evoked an effect different from that of the SSRI. Taken together, the results evidenced that the pattern of action of the monoamine is dictated by the spatial distribution of the 5-HT release sites.

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PubMed2004

Modulation of mechanosensory responses by motoneurons that regulate skin surface topology in the leech.

Central regulation of somatosensory signals has been extensively studied, but little is known about their regulation in the periphery. Given the widespread exposure of the skin sensory terminals to the environment, it is of interest to explore how somatosensory sensitivity is affected by changes in properties of the skin. In the leech, the annuli that subdivide the skin can be erected under the control of the annulus erector (AE) motoneurons. To analyze whether this surface change influences mechanosensory sensitivity, we studied the responses of low threshold mechanosensory T cells to mechanical stimulation of the skin as AE motoneurons were activated. In segments of the body wall connected to the corresponding ganglion and submerged in an aqueous environment, T cells responded to localized bubbling on the skin and to water flow parallel to its surface. Excitation of AE motoneurons diminished these responses in a way that depended on the motoneuron firing frequency. Video recordings established that the range of AE firing frequencies that produced effective annulus erection coincided with that influencing T cell responses. In isolated ganglia, AE firing had no effect on T cell excitability, suggesting that annulus erection diminished T cell responsiveness to mechanical input. Counteracting this effect, mechanosensory inputs inhibited AE motoneurons. However, because depolarization of AE cells caused a decrease in their input resistance, the more active the motoneuron, the less sensitive it became to inhibitory signals. Thus when brought to fire, AE motoneurons would stay "committed" to a high activity level, and this would limit sensory responsiveness to incoming mechanical signals.

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PubMed1979

Voltage-modulated membrane resistance in coupled leech neurons.

1. Resistive interactions have been studied between two pairs of large identifiable neurons in ganglion 6 of the leech CNS, called the lateral and rostral cells. Both are motor neurons causing penile eversion. 2. Lateral and rostral neurons have different membrane resistance properties. Input resistances of lateral neurons are virtually constant. By contrast, membrane resistances of rostral neurons are highly voltage dependent. When depolarized from resting potential to firing level, a rostral neuron's input resistance can increase 10-fold, from 30 to 300 Momega. 3. Voltage-dependent membrane characteristics of rostral neurons cause resistive interactions with lateral neurons to be nonlinear. DC potentials evoked in lateral cells are transmitted to rostral cells with an efficiency varying over a 10-fold range. Hyperpolarizing coupling is weak, with coupling factors of about 0.03. Depolarizing coupling factors increase progressively with increasing lateral neuron depolarization, reaching values of up to 0.3. 4. Membrane resistance changes in rostral neurons accompany lateral to rostral cell interactions. Input resistances increase during depolarizing and decrease during hyperpolarizing coupling potentials. The lateral to rostral cell junctional resistance is high and invariant, as evidenced by uniformly weak coupling in the reverse direction, from rostral to lateral neurons. 5. In conclusion, asymmetries in lateral to rostral cell interaction are based on postsynaptic rather than junctional resistance changes. The impact of the lateral onto the rostral cell's excitability contains a nonlinear component besides the usual linear additive one. As in conventional resistive coupling, depolarizing coupling potentials raise the rostral neuron closer to its voltage threshold. But more significantly, depolarizing coupling potentials lower the rostral neuron's current threshold because increases in resistance proportionately reduce the amount of excitatory current needed to reach firing level. Thus, the resistance change acts to amplify the input signal efficiency. In addition to the static changes in current threshold, the reostral neuron also changes dynamically. Membrane resistance increases lead to increases in space constant shrinking the neuron's electrical lenght. 6. Other properties of the network have been analyzed. The pair of lateral neurons is strongly coupled, whereas the pair of rostral neurons is weakly coupled, the coupling factors are 0.3 and 0.05, respectively. Hyperpolarizing membrane time constants for the lateral and rostral neurons are estimated to be between 100 and 200 ms. Time constants of depolarized rostral neurons are significantly larger.

Animals↗

PubMed1980

Control of multiple impulse-initiation sites in a leech interneuron.

1. Several heart interneurons (HN cells) of the leech nerve cord have impulse-initiation sites in every segmental ganglion through which their single axons pass. All these initiation sites are capable of producing rhythmic impulse bursts. However, under normal conditions a dominant primary initiation site in the ganglion where the cell body is located suppresses the activity of the other secondary sites. 2. Hyperpolarization of the primary initiation site by injected current permits immediate expression of rhythmic activity by a secondary site, usually the one located in the next posterior ganglion. 3. The free-running impulse burst rhythm of the primary site is stronger than that of the secondary site, having a greater burst duration and a tendency toward a higher burst frequency. 4. Bursts of primary-site impulses intercalated into the secondary-site impulse burst rhythm have a twofold effect. First, early to midway through the secondary-site's burst cycle, they phase delay its impulse burst rhythm. Second, early in the secondary-site's burst cycle, they tend to suppress ongoing impulse bursts, and late in the secondary-site's burst cycle, they tend to suppress the next expected impulse burst. The amount of burst suppression seen early and late in the secondary-site burst cycle depends on the burst duration and intraburst impulse frequency of the intercalated burst. 5. The ability of a train of primary-site impulse bursts to completely suppress secondary-site activity depends on burst duration, intraburst impulse frequency, and burst period. 6. Primary-site impulse trains with burst parameters close to those of naturally occurring primary-site bursts completely suppress secondary-site activity. 7. These results are consistent with the notion that the primary-site impulse burst rhythm of an HN cell suppresses the activity of its secondary site because, cycle by cycle, it delays and/or suppresses the next secondary-site burst so that no secondary-site bursts are produced. Dominance of the primary site over the secondary site is ensured by virtue of the primary-site's stronger impulse burst rhythm.

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PubMed1982

Dynamic analysis of a rhythmic neural circuit in the leech Hirudo medicinalis.

1. The results of perturbation experiments demonstrate the functional diversity of the interneurons (HN cells) that generate heartbeat in the medicinal leech. 2. HN cells were individually stimulated by single current pulses. The induced activity of HN cells in the first four ganglia (cell pairs HN(1)-HN(4)) reset the rhythm of the interneuron network; induced activity of those in the fifth through seventh ganglia (cell pairs HN(5)-HN(7)) did not. 3. Cells HN(1)-HN(4) can entrain every other interneuron of the network; cells HN(5)-HN(7) cannot. 4. Thus the HN interneuron network includes two distinct subsets: cells HN(1)-HN(4) form the network's timing oscillator; cells HN(5)-HN(7), driven by the timing oscillator, force one of the two coordination states on the heart motor neurons. 5. In general the dynamic behavior of the heart interneuron network was predictable given the web of identified synapses between HN cells. Nevertheless, the unexpected capacity of cells HN(3) and HN(4) to entrain the network shows that there are functional connections still to be found. Burst termination experiments suggest that cells HN(3) and HN(4) inhibit directly the more rostral HN cells. 6. The timing oscillation seems to arise from a balance between the endogenous polarization rhythms of interneurons HN(1)-HN(4) and selective reciprocal inhibition between these same cells.

Animals↗

PubMed1983

Generation and coordination of heartbeat timing oscillation in the medicinal leech. II. Intersegmental coordination.

1. A network of four pairs of interneurons, HN(1)-HN(4), times the heartbeat of the medicinal leech. The following model accounts for the stable phase relationships in the network and the network's response to perturbation, entrainment, and stimulation. 2. There are two centers of oscillation, one the HN(3) pair in the third ganglion, the other the HN(4) pair in the fourth ganglion. 3. The two other pairs, HN(1) and HN(2), couple the oscillation of the HN(3) pair with that of the HN(4) pair, thereby guaranteeing that a coherent time signal is sent to the rest of the heartbeat system. 4. The HN(1) and HN(2) pairs can play this coupling role because they have impulse-initiation sites in the third and fourth ganglia and have input and output connections with the HN(3) and HN(4) pairs. 5. In the context of the network, the intrinsic frequency of the HN(4) pair appears to be higher than that of the HN(3) pair. Coupled, the two pairs strike a stable compromise in which the HN(4) pair leads the HN(3) pair.

Animals↗

PubMed1984

Potassium distribution and membrane potential of sensory neurons in the leech nervous system.

The intracellular K activity (aKi) and membrane potential of sensory neurons in the leech central nervous system were measured in normal and altered external K+ concentrations, [K+]o, using double-barreled, liquid ion-exchanger microelectrodes. In control experiments membrane potential measurements were made using potassium chloride-filled single-barreled microelectrodes. All values are means +/- SD. At the normal [K+]o (4 mM) the mean aKi of all cells tested was 72.6 +/- 10.6 mM (n = 40) and the average membrane potential was -47.3 +/- 5.2 mM (n = 40). When measured with single-barreled microelectrodes, the membrane potential averaged -45.3 +/- 2.9 mV (n = 12). Assuming an intracellular K+ activity coefficient of 0.75, the intracellular K+ concentration of sensory neurons would be 96.8 +/- 14.1 mM). With an extracellular K+ concentration of 5.8 mM in the intact ganglion compared to the K+ concentration of 4 mM in the bath, the K+ equilibrium potential was -71.5 mV. When the ganglion capsule was opened, the extracellular K+ concentrations in the ganglion were similar to that of the bathing medium and the calculated K+ equilibrium potential was -81 mV. The membrane of sensory neurons depolarized following the changes to elevated [K+]o (greater than or equal to 10-100 mM), whereas aKi changed only little or not at all. At very low [K+]o (0.2, 0 mM) aKi and membrane potential showed little short-term (less than 3 min) effect but began to change after longer exposure (greater than 3 min). Reduction of [K+]o from 4 to 0.2 mM (or 0 mM) produced first a slow, and then a more rapid decrease of aKi and membrane resistance, accompanied by a slow membrane hyperpolarization. Following readdition of normal [K+]o, the membrane first depolarized and then transiently hyperpolarized, eventually returning slowly to the normal membrane potential.(ABSTRACT TRUNCATED AT 400 WORDS)

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