Modulation of Membrane Potential in Mesothoracic Moto- and Interneurons During Stick Insect Front-Leg Walking

2005 ◽  
Vol 94 (4) ◽  
pp. 2772-2784 ◽  
Author(s):  
Björn Ch. Ludwar ◽  
Sandra Westmark ◽  
Ansgar Büschges ◽  
Joachim Schmidt
Keyword(s):  
Membrane Potential ◽  
Spike Activity ◽  
Membrane Resistance ◽  
Stick Insect ◽  
Signal Transfer ◽  
Motoneuron Pool ◽  
Current Pulses ◽  
Nonspiking Interneurons ◽  
Resistance Decrease ◽  
Synaptic Drive

During walking, maintenance and coordination of activity in leg motoneurons requires intersegmental signal transfer. In a semi-intact preparation of the stick insect, we studied membrane potential modulations in mesothoracic (middle leg) motoneurons and local premotor nonspiking interneurons that were induced by stepping of a front leg on a treadmill. The activity in motoneurons ipsi- and contralateral to the stepping front leg was recorded from neuropilar processes. Motoneurons usually exhibited a tonic depolarization of ≤5 mV throughout stepping sequences. This tonic depolarization depended on membrane potential and was found to reverse in the range of −32 to −47 mV. It was accompanied by a mean membrane resistance decrease of ∼12%. During front-leg stepping, an increased spike activity to depolarizing current pulses was observed in 73% of contralateral flexor motoneurons that were tested. Motoneurons ipsilateral to the walking front leg exhibited phasic membrane potential modulations coupled to steps in accordance with previously published results. Coupling patterns were typical for a given motoneuron pool. Local nonspiking mesothoracic interneurons that provide synaptic drive to tibial motoneurons also contribute to the modulation of membrane potential of tibial motoneurons during front-leg walking. We hypothesize that the tonic depolarization of motoneurons during walking is a cellular correlate of arousal that usually increases effectiveness of phasic excitation in supporting motoneuron firing.

Sustained membrane potential change of uropod motor neurons during the fictive abdominal posture movement in crayfish

1986 ◽  
Vol 56 (3) ◽  
pp. 702-717 ◽  
Author(s):  
M. Takahata ◽  
M. Hisada
Keyword(s):  
Membrane Potential ◽  
Motor Neurons ◽  
Membrane Resistance ◽  
Potential Change ◽  
Quiescent State ◽  
Membrane Potential Change ◽  
Synaptic Potentials ◽  
Nonspiking Interneurons ◽  
Body Rolling ◽  
Dendritic Branches

The occurrence of the uropod steering response as one of the equilibrium reflexes to body rolling in crayfish is significantly facilitated if the stimulus is given while the animal is performing the abdominal posture movement. This facilitation of the descending statocyst pathway by the abdominal posture system takes place between the uropod motor neurons and the statocyst interneurons, which directly project from the brain to the terminal abdominal ganglion where the motor neurons originate. To elucidate the synaptic mechanisms underlying the postural facilitation of the steering response, we analyzed in this study the activity of an identified set of uropod motor neurons during the fictive abdominal extension movement in the whole-animal preparation. Intracellular recordings from the dendritic branches of uropod motor neurons revealed that they were continuously excited during the fictive abdominal extension. The large fast motor neurons usually showed a sustained depolarization of the subthreshold magnitude. The small slow ones showed a suprathreshold sustained depolarization with spikes superimposed. Putative inhibitory motor neurons, on the other hand, showed a sustained hyperpolarization with their spontaneous spike discharge suppressed. The discrete synaptic potentials could hardly be distinguished and, instead, small fluctuations of the membrane potential were observed during the sustained depolarization of both the fast and slow motor neurons. Occasionally, large discrete synaptic potentials could be observed to be superimposed on the sustained depolarization. The occurring frequency of these synaptic potentials showed, however, no significant increase associated with the sustained depolarization. It hence seemed unlikely that these potentials were responsible for producing the sustained depolarization. Their amplitude during the sustained depolarization was smaller than that observed during the quiescent state. The sustained membrane potential change during the fictive abdominal movement was also observed in many neurons other than motor neurons, including local nonspiking interneurons and mechanosensory spiking interneurons. Both motor neurons and interneurons showed a decrease in their membrane resistance during the sustained membrane potential change. We concluded that the sustained depolarization of uropod motor neurons during the fictive abdominal extension was produced by the summation of small chemically transmitted postsynaptic potentials.(ABSTRACT TRUNCATED AT 400 WORDS)

Effects of bethanechol and the octapeptide of cholecystokinin on colonic smooth muscle in the cat

1987 ◽  
Vol 252 (5) ◽  
pp. G654-G661
Author(s):  
W. J. Snape ◽  
S. T. Tan ◽  
H. W. Kao
Keyword(s):  
Smooth Muscle ◽  
Membrane Potential ◽  
Slow Wave ◽  
Spike Activity ◽  
Membrane Resistance ◽  
Wave Pattern ◽  
Isometric Tension ◽  
Muscle Membrane ◽  
Maximum Effect ◽  
Smooth Muscle Membrane

The aim of this study is to compare the action of the cholinergic agonist, bethanechol, with the action of the octapeptide of cholecystokinin (CCK-OP) on feline circular colonic smooth muscle membrane potential and isometric tension, using the double sucrose gap. Depolarization of the membrane greater than 10 mV by K+ or bethanechol increased tension and spontaneous spike activity. CCK-OP (10(-9) M) depolarized the membrane (6.1 +/- 1.3 mV) without an increase in tension or spike activity. Depolarization of the membrane by increasing [K+]o was associated with a decrease in the membrane resistance. The slow-wave duration (2.3 +/- 0.2 s) was unchanged by administration of K+ or bethanechol but was prolonged after increasing concentrations of CCK-OP. The maximum effect occurred at a 10(-10) M concentration of CCK-OP (4.5 +/- 0.4 s, P less than 0.01). At higher concentrations of CCK-OP (greater than 10(-10) M), the slow-wave pattern became disorganized. Addition of increasing concentrations of [K+]o or bethanechol, but not CCK-OP, stimulated a concentration-dependent increase in the maximum rate of rise (dV/dtmax) of an evoked spike potential. These studies suggest 1) bethanechol decreased the membrane potential without altering the slow-wave activity, whereas CCK-OP has a minimal effect on the membrane potential but distorted the slow-wave shape; 2) an increased amplitude of the spike and dV/dtmax of the spike were associated with an increase in phasic contractions after bethanechol or increased [K+]o; 3) the lack of an increase in the spike amplitude and the dV/dtmax to CCK-OP was associated with no increase in phasic contraction.

Cooperative Mechanisms Between Leg Joints of Carausius morosusI. Nonspiking Interneurons That Contribute to Interjoint Coordination

1998 ◽  
Vol 79 (6) ◽  
pp. 2964-2976 ◽  
Author(s):  
Dennis E. Brunn
Keyword(s):  
Membrane Potential ◽  
Motor Neuron ◽  
Motor Neurons ◽  
Stick Insect ◽  
Interjoint Coordination ◽  
Antagonistic Muscle ◽  
Nonspiking Interneurons ◽  
Active Motor ◽  
Thoracic Part ◽  
Depressor Muscle

Brunn, Dennis E. Cooperative mechanisms between leg joints of Carausius morosus. I. Nonspiking interneurons that contribute to interjoint coordination. J. Neurophysiol. 79: 2964–2976, 1998. Three nonspiking interneurons are described in this paper that influence the activity of the motor neurons of three muscles of the proximal leg joints of the stick insect. Interneurons were recorded and stained intracellularly by glass microelectrodes; motor neurons were recorded extracellularly with oil-hook electrodes. The motor neurons innervate the two subcoxal muscles, the protractor and retractor coxae, and the thoracic part of the depressor trochanteris muscle. The latter spans the subcoxal joint before inserting the trochanter, thus coupling the two proximal joints mechanically. The three interneurons are briefly described here. First, interneuron NS 1 was known to become more excited during the swing phase of the rear and the stance phase of the middle leg. When depolarized it excited several motor neurons of the retractor coxae. This investigation revealed that it inhibits the activity of protractor and thoracic depressor motor neurons when depolarized as well. In a pilocarpine-activated animal, the membrane potential showed oscillations in phase with the activity of protractor motor neurons, suggesting that NS 1 might contribute to the transition from swing to stance movement. Second, interneuron NS 2 inhibits motor neurons of protractor and thoracic depressor when depolarized. In both a quiescent and a pilocarpine-activated animal, hyperpolarizing stimuli excite motor neurons of both muscles via disinhibition. In one active animal the disinhibiting stimuli were sufficient to generate swing-like movements of the leg. In pilocarpine-activated preparations the membrane potential oscillated in correlation with the motor neuronal activity of the protractor coxae and thoracic depressor muscle. Hyperpolarizing stimuli induced or reinforced the protractor and thoracic depressor bursts and inhibited the activity of the motor neurons of the retractor coxae muscle, the antagonistic muscle of the protractor. Therefore interneuron NS 2 can be regarded as an important premotor interneuron for the switching from stance to swing and from swing to stance. Finally, interneuron NS 3 inhibits the spontaneously active motor neurons of both motor neuron pools in the quiescent animal. During pilocarpine-induced protractor bursts, depolarizing stimuli applied to the interneuron excited several protractor motor neurons with large action potentials and one motor neuron of the thoracic depressor. No oscillations of the membrane potentials were observed. Therefore this interneuron might contribute to the generation of rapid leg movements. The results demonstrated that the two proximal joints are coupled not only mechanically but also neurally and that the thoracic part of the depressor appears to function as a part of the swing-generating system.

Insulin release, cGMP, cAMP, and membrane potential in acetylcholine-stimulated islets.

1978 ◽  
Vol 235 (5) ◽  
pp. E493 ◽  
Author(s):  
E Gagerman ◽  
L A Idahl ◽  
H P Meissner ◽  
I B T�ljedal
Keyword(s):  
Membrane Potential ◽  
Cyclic Amp ◽  
Insulin Release ◽  
Cyclic Gmp ◽  
Spike Activity ◽  
Obvious Effect ◽  
Ionic Fluxes ◽  
Mouse Islets ◽  
Silent State ◽  
Esterase Inhibitor

Acetylcholine potentiated the glucose-induced insulin release from microdissected mouse islets of Langerhans but had no effect on basal insulin release. Significant potentiation was obtained with 0.1 micron acetylcholine in the presence of 10 micron eserine and with 1 micron or more acetylcholine in the absence of a choline esterase inhibitor. Carbamylcholine, too, potentiated insulin release. Potentiation was blocked by methylatropine, whereas methylatropine alone had no effect on insulin release. Acetylcholine or carbamylcholine (5-500 micron) had no obvious effect on cyclic GMP or cyclic AMP in the islets. In the presence of 11.1 mM D-glucose, the membrane potential of beta-cells oscillated slowly between a polarized silent state of -50 to -55 mV and a depolarized active state of -33 to -39 mV, at which a fast spike activity occurred. Acetylcholine made the potential stay at the plateau and induced a continuous spike activity pattern. Atropine inhibited the electrical effects of acetylcholine but not those of glucose alone. It is suggested that cholinergic potentiation of insulin release is mediated by changes of transmembrane ionic fluxes, probably without the intervention of cyclic GMP or cyclic AMP.

Connectivity of slowly adapting pulmonary stretch receptors with dorsal medullary respiratory neurons

1987 ◽  
Vol 58 (6) ◽  
pp. 1259-1274 ◽  
Author(s):  
A. J. Berger ◽  
T. E. Dick
Keyword(s):  
Electrical Stimulation ◽  
Membrane Potential ◽  
Beta Cells ◽  
Spike Activity ◽  
Alpha Cells ◽  
Drg Neurons ◽  
Lung Inflation ◽  
Stretch Receptors ◽  
Pulmonary Stretch Receptors ◽  
P Cells

1. Intracellular recordings were made from 50 dorsal respiratory group (DRG) neurons in the region of the ventrolateral nucleus of the solitary tract in anesthetized, paralyzed cats ventilated with a cycle-triggered pump whose inflation stroke was triggered by the onset of phrenic nerve inspiratory (I) discharge. Activity was recorded simultaneously in the ipsilateral nodose ganglion from sensory cell bodies of slowly adapting pulmonary stretch receptors (PSRs). 2. Respiratory cycle-related membrane potential changes of DRG neurons were recorded. Twenty-six neurons that did not exhibit spikes were classified as I alpha, I beta or pump (P)-cells by comparing their membrane potential trajectories during I in the presence of lung inflation with that observed during I, but with lung inflation withheld. The remaining 24 neurons were classified similarly, but the classification was based upon a comparison of their I-phase spike activity responses with and without lung inflation. I phase-related histograms of either membrane potential or spike activity were constructed to facilitate DRG neuronal classification. Additionally, steady lung inflation of varying magnitudes was applied during the expiratory phase. This prolonged expiration and produced different responses in the neurons. Generally, I beta and P-cells were depolarized, whereas I alpha cells were hyperpolarized. 3. Low-intensity electrical stimulation of the ipsilateral vagus nerve evoked excitatory postsynaptic potentials (EPSPs) in all three DRG neuronal types. P-cells and I beta cells exhibited EPSPs in response to the lowest intensity; generally this intensity was below threshold for the simultaneously recorded PSR. Overall, EPSPs in I alpha cells had the highest thresholds, but some EPSPs could be evoked at thresholds similar to those of the I beta cells. The distributions of the average onset latency of the evoked EPSP overlapped considerably. Thus vagal electrical stimulation cannot be used for unequivocal classification of DRG neurons into I alpha, I beta, and P-cell subpopulations. 4. Using intracellular spike-triggered averaging, single PSRs were shown to generate monosynaptic EPSPs in I beta neurons and P-cells but not I alpha cells. Divergence of single PSR afferents also was observed. Relationships between EPSP shape factors, amplitudes, and PSR afferent conduction velocity are similar to those previously observed for monosynaptic EPSPs in hindlimb motoneurons generated by spinal afferents.

scholarly journals Membrane Potentials of the Lobster Giant Axon Obtained by Use of the Sucrose-Gap Technique

1962 ◽  
Vol 45 (6) ◽  
pp. 1195-1216 ◽  
Author(s):  
Fred J. Julian ◽  
John W. Moore ◽  
David E. Goldman
Keyword(s):  
Membrane Potential ◽  
Action Potential ◽  
Sea Water ◽  
Sucrose Solution ◽  
Chloride Concentration ◽  
Giant Axon ◽  
Membrane Resistance ◽  
Resting Potential ◽  
Gap Technique ◽  
Sucrose Gap

A method similar to the sucrose-gap technique introduced be Stäpfli is described for measuring membrane potential and current in singly lobster giant axons (diameter about 100 micra). The isotonic sucrose solution used to perfuse the gaps raises the external leakage resistance so that the recorded potential is only about 5 per cent less than the actual membrane potential. However, the resting potential of an axon in the sucrose-gap arrangement is increased 20 to 60 mv over that recorded by a conventional micropipette electrode when the entire axon is bathed in sea water. A complete explanation for this effect has not been discovered. The relation between resting potential and external potassium and sodium ion concentrations shows that potassium carries most of the current in a depolarized axon in the sucrose-gap arrangement, but that near the resting potential other ions make significant contributions. Lowering the external chloride concentration decreases the resting potential. Varying the concentration of the sucrose solution has little effect. A study of the impedance changes associated with the action potential shows that the membrane resistance decreases to a minimum at the peak of the spike and returns to near its initial value before repolarization is complete (a normal lobster giant axon action potential does not have an undershoot). Action potentials recorded simultaneously by the sucrose-gap technique and by micropipette electrodes are practically superposable.

Nonspiking interneurons in walking system of the cockroach

1975 ◽  
Vol 38 (1) ◽  
pp. 33-52 ◽  
Author(s):  
K. G. Pearson ◽  
C. R. Fourtner
Keyword(s):  
Membrane Potential ◽  
Periplaneta Americana ◽  
Rhythmic Activity ◽  
Synaptic Activity ◽  
Cobalt Sulfide ◽  
Resting Membrane Potential ◽  
Cellular Mechanisms ◽  
Metathoracic Ganglion ◽  
Nonspiking Interneurons ◽  
Leg Movements

Intracellular recordings were made from the neurites of interneurons and motoneurons in the metathoracic ganglion of the cockroach, Periplaneta americana. Many neurons were penetrated which failed to produce action potentials on the application of large depolarizing currents. Nevertheless, some of them strongly excited and/or inhibited slow motoneurons innervating leg musculature, even with weak depolariziing musculature, even with weak depolarizing currents. Cobalt-sulfide-straining of these nonspiking neurons showed them to be interneurons with their neurites contained entirely within the metathoracic ganglion. Two further characteristics of these interneurons were rapid spontaneous fluctuations in membrane potential and a low resting membrane potential. One nonspiking neuron, interneuron I, when depolarized caused a strong excitation of the set of slow levator motoneurons which discharge in bursts during stepping movements of the metathoracic leg. During rhythmic leg movements the membrane potential of interneuron I oscillated with the depolarizing phases occurring at the same time as bursts of activity in the levator motorneurons. No spiking or any other nonspiking neuron was penetrated which could excite these levator motoneurons. From all these observations we conclude that oscillations in the membrane potential of interneuron I are entirely responsible for producing the levator bursts, and thus for producing stepping movements in a walking animal. During rhythmic leg movements, bursts of activity in levator and depressor motoneurons are initiated by slow graded depolarizations. The similarity of the synaptic activity in these two types of motoneurons suggests that burst activity in the depressor motoneurons is also produced by rhythmic activity in nonspiking interneurons. The fact that no spiking neuron was found to excite the depressor motoneurons supports this conclusion. Interneuron I is also an element of the rhythm-generating system, since short depolarizing pulses applied to it during rhythmic activity could reset the thythm. Long-duration current pulses applied to interneuron I in a quiescent animal did not produce rhythmic activity. This observation, together with the finding that during rhythmic activity the slow depolarizations in interneuron I are usually terminated by IPSPs, suggests that interneuron I alone does not generate the rhythm. No spiking interneurons have yet been enccountered which influence the activity in levator motoneurons. Thus, we conclude that the rhythm is generated in a network of nonspiking interneurons. The cellular mechanisms for generating the oscillations in this network are unknown. Continued.

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

1984 ◽  
Vol 51 (4) ◽  
pp. 689-704 ◽  
Author(s):  
W. R. Schlue ◽  
J. W. Deitmer
Keyword(s):  
Nervous System ◽  
Membrane Potential ◽  
Sensory Neurons ◽  
Membrane Resistance ◽  
Equilibrium Potential ◽  
Bathing Medium ◽  
Membrane Hyperpolarization ◽  
K Concentration ◽  
Intracellular K Activity ◽  
K Activity

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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