Effects of acetaldehyde on the membrane potential and membrane resistance of the identified neurons in the abdominal ganglion of Aplysia kurodai.

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)

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

The Journal of General Physiology ◽

10.1085/jgp.45.6.1195 ◽

1962 ◽

Vol 45 (6) ◽

pp. 1195-1216 ◽

Cited By ~ 73

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.

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

AJP Gastrointestinal and Liver Physiology ◽

10.1152/ajpgi.1987.252.5.g654 ◽

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.

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

Journal of Neurophysiology ◽

10.1152/jn.1984.51.4.689 ◽

1984 ◽

Vol 51 (4) ◽

pp. 689-704 ◽

Cited By ~ 10

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

Journal of Neurophysiology ◽

10.1152/jn.00493.2005 ◽

2005 ◽

Vol 94 (4) ◽

pp. 2772-2784 ◽

Cited By ~ 18

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.

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Electrical Characteristics and Activation Potential of Bufo Eggs

The Journal of General Physiology ◽

10.1085/jgp.43.1.139 ◽

1959 ◽

Vol 43 (1) ◽

pp. 139-157 ◽

Cited By ~ 85

Author(s):

Takashi Maéno

Keyword(s):

Membrane Potential ◽

Action Potential ◽

Membrane Resistance ◽

Chloride Ions ◽

Potassium Ions ◽

Ionic Mechanism ◽

Electrical Characteristics ◽

Activation Potential ◽

Specific Permeability ◽

Toad Bufo

Electrical characteristics and their changes during activation were studied with the microelectrodes on the oocytes and eggs of the toad, Bufo vulgaris formosus Boulenger. In young oocytes, the membrane characteristics had some similarities to those of nerve and muscle, except for a relatively large resistance of 25 KΩcm.2 and an absence of the action potential in the former. After maturation, however, the membrane characteristics became entirely different from those of oocytes and other excitable tissues. In the mature eggs the membrane resistance was measured to be as high as 200 KΩcm.2, and no specific permeability of the membrane to potassium ions was observable. A slow monophasic change in the membrane potential was recorded in every activation produced by mechanical stimulation, and termed "activation potential." In fresh water, its amplitude was as large as 80 to 90 mv. with an overshoot of about 50 mv. The activation potential might be comparable to the action potential of nerve and muscle, but was fundamentally different in ionic mechanism from the latter, since the former was caused by a marked increase in permeability to chloride ions.

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The Effect of Aconitine on the Giant Axon of the Squid

The Journal of General Physiology ◽

10.1085/jgp.47.4.719 ◽

1964 ◽

Vol 47 (4) ◽

pp. 719-733 ◽

Cited By ~ 30

Author(s):

W. H. Herzog ◽

R. M. Feibel ◽

S. H. Bryant

Keyword(s):

Membrane Potential ◽

Action Potential ◽

Action Potentials ◽

Giant Axon ◽

Membrane Resistance ◽

Repetitive Stimulation ◽

Resting Membrane Potential ◽

Sustained Activity ◽

Frequency Of Stimulation ◽

Sodium And Potassium

In the giant axon of Loligo pealii, "aconitine potent" Merck added to the bath (10-7 to 1.25 x 10-6 gm/ml) (a) had no effect on resting membrane potential, membrane resistance and rectification, membrane response to subthreshold currents, critical depolarization, or action potential, but (b) on repetitive stimulation produced oscillations of membrane potential after the spike, depolarization, and decrease of membrane resistance. The effect sums with successive action potentials; it increases with concentration of aconitine, time of exposure, and frequency of stimulation. When the oscillations are large enough and the membrane potential is 51.6 ± SD 1.5 mv a burst of self-sustained activity begins; it usually lasts 20 to 70 sec. and at its end the membrane potential is 41.5 ± SD 1.9 mv. Repolarization occurs with a time constant of 2.5 to 11.1 min. Substitution of choline for external sodium after a burst hyperpolarizes the membrane to -70 mv, and return to normal external sodium depolarizes again beyond the resting membrane potential. The effect of aconitine on the membrane is attributed to an increase of sodium and potassium or chloride conductances following the action potential.

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