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.

scholarly journals Transmitter Regulation of Plateau Properties in Turtle Motoneurons

1998 ◽  
Vol 79 (1) ◽  
pp. 45-50 ◽  
Author(s):  
Gytis Svirskis ◽  
Jørn Hounsgaard
Keyword(s):  
Membrane Potential ◽  
Metabotropic Glutamate Receptors ◽  
Input Resistance ◽  
Pattern Generation ◽  
Synaptic Activity ◽  
Membrane Properties ◽  
Resting Membrane Potential ◽  
Type I ◽  
Plateau Potentials ◽  
Inward Current

Svirskis, Gytis and Jørn Hounsgaard. Transmitter regulation of plateau properties in turtle motoneurons. J. Neurophysiol. 79: 45–50, 1998. In motoneurons, generation of plateau potentials is promoted by modulators that block potassium channels. In voltage-clamp experiments with triangular voltage ramp commands, we show that cis-(±)-1-aminocyclopentane-1,3-dicarboxylic acid ( cis-ACPD) and muscarine promote the generation of plateau potentials by increasing the dihydropyridine sensitive inward current, by increasing the input resistance, and by depolarizing the resting membrane potential. Type I metabotropic glutamate receptors (mGluR I) mediate the effects of cis-ACPD. Baclofen suppresses generation of plateau potentials by decreasing the dihydropyridine sensitive inward current, by decreasing the input resistance, and by hyperpolarizing the resting membrane potential. These results suggest that membrane properties of motoneurons are continuously modulated by synaptic activity in ways that may have profound effects on synaptic integration and pattern generation.

scholarly journals GABA-like immunoreactivity in nonspiking interneurons of the locust metathoracic ganglion

2002 ◽  
Vol 205 (23) ◽  
pp. 3651-3659 ◽  
Author(s):  
M. Wildman ◽  
S. R. Ott ◽  
M. Burrows
Keyword(s):  
Membrane Potential ◽  
Motor Neurons ◽  
Lucifer Yellow ◽  
Current Injection ◽  
Aminobutyric Acid ◽  
Homogeneous Population ◽  
Metathoracic Ganglion ◽  
Nonspiking Interneurons ◽  
Intracellular Microelectrodes ◽  
Gaba Immunohistochemistry

SUMMARYNonspiking interneurons are important components of the premotor circuitry in the thoracic ganglia of insects. Their action on postsynaptic neurons appears to be predominantly inhibitory, but it is not known which transmitter(s) they use. Here, we demonstrate that many but not all nonspiking local interneurons in the locust metathoracic ganglion are immunopositive for GABA (γ-aminobutyric acid). Interneurons were impaled with intracellular microelectrodes and were shown physiologically to be nonspiking. They were further characterized by defining their effects on known leg motor neurons when their membrane potential was manipulated by current injection. Lucifer Yellow was then injected into these interneurons to reveal their cell bodies and the morphology of their branches. Some could be recognised as individuals by comparison with previous detailed descriptions. Ganglia were then processed for GABA immunohistochemistry. Fifteen of the 17 nonspiking interneurons studied were immunopositive for GABA, but two were not. The results suggest that the majority of these interneurons might exert their well-characterized effects on other neurons through the release of GABA but that some appear to use a transmitter other than GABA. These nonspiking interneurons are therefore not an homogeneous population with regard to their putative transmitter.

scholarly journals Methylene blue counteracts cyanide cardiotoxicity: cellular mechanisms

2018 ◽  
Vol 124 (5) ◽  
pp. 1164-1176 ◽  
Author(s):  
Joseph Y. Cheung ◽  
JuFang Wang ◽  
Xue-Qian Zhang ◽  
Jianliang Song ◽  
Dhanendra Tomar ◽  
...  
Keyword(s):  
Methylene Blue ◽  
Membrane Potential ◽  
Adenosine Triphosphate ◽  
Early Stage ◽  
Left Ventricular ◽  
Smoke Inhalation ◽  
Resting Membrane Potential ◽  
Cellular Mechanisms ◽  
Oxidation Reduction ◽  
Intracellular Ca

In adult left ventricular mouse myocytes, exposure to sodium cyanide (NaCN) in the presence of glucose dose-dependently reduced contraction amplitude, with ~80% of maximal inhibitory effect attained at 100 µM. NaCN (100 µM) exposure for 10 min significantly decreased contraction and intracellular Ca2+ concentration ([Ca2+]i) transient amplitudes, systolic but not diastolic [Ca2+]i, and maximal L-type Ca2+ current ( ICa) amplitude, indicating acute alteration of [Ca2+]i homeostasis largely accounted for the observed excitation-contraction abnormalities. In addition, NaCN depolarized resting membrane potential ( Em), reduced action potential (AP) amplitude, prolonged AP duration at 50% (APD50) and 90% repolarization (APD90), and suppressed depolarization-activated K+ currents but had no effect on Na+-Ca2+ exchange current ( INaCa). NaCN did not affect cellular adenosine triphosphate levels but depolarized mitochondrial membrane potential (ΔΨm) and increased superoxide (O2·−) levels. Methylene blue (MB; 20 µg/ml) added 3 min after NaCN restored contraction and [Ca2+]i transient amplitudes, systolic [Ca2+]i, Em, AP amplitude, APD50, APD90, ICa, depolarization-activated K+ currents, ΔΨm, and O2·− levels toward normal. We conclude that MB reversed NaCN-induced cardiotoxicity by preserving intracellular Ca2+ homeostasis and excitation-contraction coupling ( ICa), minimizing risks of arrhythmias ( Em, AP configuration, and depolarization-activated K+ currents), and reducing O2·− levels. NEW & NOTEWORTHY Cyanide poisoning due to industrial exposure, smoke inhalation, and bioterrorism manifests as cardiogenic shock and requires rapidly effective antidote. In the early stage of cyanide exposure, adenosine triphosphate levels are normal but myocyte contractility is reduced, largely due to alterations in Ca2+ homeostasis because of changes in oxidation-reduction environment of ion channels. Methylene blue, a drug approved by the U.S. Food and Drug Administration, ameliorates cyanide toxicity by normalizing oxidation-reduction state and Ca2+ channel function.

scholarly journals MOTOR NEURONES OF THE CRAYFISH WALKING SYSTEM POSSESS TEA+-REVEALED REGENERATIVE ELECTRICAL PROPERTIES

1994 ◽  
Vol 188 (1) ◽  
pp. 339-345
Author(s):  
D Cattaert ◽  
A Araque ◽  
W Buno ◽  
F Clarac
Keyword(s):  
Membrane Potential ◽  
Outward Current ◽  
Rhythmic Activity ◽  
Input Resistance ◽  
Stomatogastric Ganglion ◽  
Resting Membrane Potential ◽  
Delayed Rectifier ◽  
Muscarinic Agonist ◽  
M Current ◽  
Motor Neurones

In crustaceans, some motor neurones (MNs) have been shown to be part of the central pattern generator in the stomatogastric system (Harris-Warrick et al. 1992; Moulins, 1990), the swimmeret system (Heitler, 1978) or the walking system (Chrachri and Clarac, 1990). These MNs induce changes in the central rhythm when depolarized and are conditional oscillators in the stomatogastric ganglion. Moreover, in the walking system, rhythmic activity can be triggered by muscarinic cholinergic agonists (Chrachri and Clarac, 1987). We have recently analyzed the role of muscarinic receptors in crayfish walking leg MNs (D. Cattaert and A. Araque, in preparation) and demonstrated that oxotremorine, a muscarinic agonist, evoked long-lasting depolarizing responses associated with an increased input resistance. The outward current blocked by oxotremorine is likely to be carried by K+, as is the case for the M current (IM) in vertebrates (Brown and Adams, 1980). In most neurones, K+ conductances play a principal role in maintaining the membrane potential at rest: for example, IM is active at the resting membrane potential, thus contributing to its maintenance, and the 'delayed-rectifier' (IK) assists the fast repolarization after an action potential. Some K+ conductances are Ca2+-dependent (IK,Ca) and are activated by an increase in internal Ca2+ concentration. In such cases, Ca2+ currents may result in hyperpolarization of the neurone through activation of IK,Ca. In opposition to these K+ currents, the direct effect of Na+ and Ca2+ conductances is to depolarize the neurone. For example, the persistant Na+ current (INap) that is responsible for the slow subthreshold depolarization termed slow pre-potentials (Gestrelius et al. 1983; Leung and Yim, 1991) participates in the formation of pacemaker depolarization (Barrio et al. 1991) and generates plateau-type responses in control conditions (Barrio et al. 1991; Llinas and Sugimori, 1980). Similarly Ca2+ or non-specific (Na+/Ca2+) conductances generate such events in Aplysia californica burster neurones (Adams and Benson, 1985), crustacean cardiac ganglion (Tazaki and Cooke, 1990), insect neurones (Hancox and Pitman, 1991) and crustacean stomatogastric ganglion (Kiehn and Harris-Warrick, 1992). Since crustacean MNs can participate in rhythm production, such depolarizing conductances may exist in most of them and may contribute to the long-lasting MN depolarizations and spike bursts present during locomotion.

Effect of low chloride on relaxation in hamster diaphragm muscle

1986 ◽  
Vol 61 (1) ◽  
pp. 180-184 ◽  
Author(s):  
S. A. Esau ◽  
N. Sperelakis
Keyword(s):  
Membrane Potential ◽  
Muscle Fatigue ◽  
Time Constant ◽  
Diaphragm Muscle ◽  
Resting Membrane Potential ◽  
Krebs Solution ◽  
Sarcolemmal Membrane ◽  
Cl Conductance

With muscle fatigue the chloride (Cl-) conductance of the sarcolemmal membrane decreases. The role of lowered Cl- conductance in the prolongation of relaxation seen with fatigue was studied in isolated hamster diaphragm strips. The muscles were studied in either a Krebs solution or a low Cl- solution in which half of the NaCl was replaced by Na-gluconate. Short tetanic contractions were produced by a 160-ms train of 0.2-ms pulses at 60 Hz from which tension (T) and the time constant of relaxation were measured. Resting membrane potential (Em) was measured using KCl-filled microelectrodes with resistances of 15–20 M omega. Mild fatigue (20% fall in tension) was induced by 24–25 tetanic contractions at the rate of 2/s. There was no difference in Em or T in the two solutions, either initially or with fatigue. The time constant of relaxation was greater in low Cl- solution, both initially (22 +/- 3 vs. 18 +/- 5 ms, mean +/- SD, P less than 0.05) and with fatigue (51 +/- 18 vs. 26 +/- 7 ms, P less than 0.005). Lowering of sarcolemmal membrane Cl- conductance appears to play a role in the slowing of relaxation of hamster diaphragm muscle seen with fatigue.

Calcium channels and excitation–contraction coupling in cardiac cells. I. Two components of contraction in guinea-pig papillary muscle

1987 ◽  
Vol 65 (9) ◽  
pp. 1821-1831 ◽  
Author(s):  
E. Honoré ◽  
M. M. Adamantidis ◽  
B. A. Dupuis ◽  
C. E. Challice ◽  
P. Guilbault
Keyword(s):  
Membrane Potential ◽  
Guinea Pig ◽  
Papillary Muscle ◽  
Cardiac Cells ◽  
Resting Membrane Potential ◽  
Tonic Component ◽  
Contraction Coupling ◽  
Rich Solution ◽  
The Relationship ◽  
Guinea Pig Atria

Biphasic contractions have been obtained in guinea-pig papillary muscle by inducing partial depolarization in K+-rich solution (17 mM) containing 0.3 μM isoproterenol; whereas in guinea-pig atria, the same conditions led to monophasic contractions corresponding to the first component of contraction in papillary muscle. The relationships between the amplitude of the two components of the biphasic contraction and the resting membrane potential were sigmoidal curves. The first component of contraction was inactivated for membrane potentials less positive than those for the second component. In Na+-low solution (25 mM), biphasic contraction became monophasic subsequent to the loss of the second component, but tetraethylammonium unmasked the second component of contraction. The relationship between the amplitude of the first component of contraction and the logarithm of extracellular Ca2+ concentration was complex, whereas for the second component it was linear. When Ca2+ ions were replaced by Sr2+ ions, only the second component of contraction was observed. It is suggested that the first component of contraction may be triggered by a Ca2+ release from sarcoplasmic reticulum, induced by the fast inward Ca2+ current and (or) by the depolarization. The second component of contraction may be due to a direct activation of contractile proteins by Ca2+ entering the cell along with the slow inward Ca2+ current and diffusing through the sarcoplasm. These results do not exclude the existence of a third "tonic" component, which could possibly be mixed with the second component of contraction.

scholarly journals Activation of Ca(2+)-dependent K+ current by acetylcholine and histamine in a human gastric epithelial cell line.

1993 ◽  
Vol 102 (4) ◽  
pp. 667-692 ◽  
Author(s):  
E Hamada ◽  
T Nakajima ◽  
S Ota ◽  
A Terano ◽  
M Omata ◽  
...  
Keyword(s):  
Membrane Potential ◽  
Epithelial Cell ◽  
Cell Line ◽  
K Channel ◽  
Resting Membrane Potential ◽  
Induced Response ◽  
Epithelial Cell Line ◽  
Bathing Solution ◽  
Pipette Solution ◽  
K Current

The effects of acetylcholine (ACh) and histamine (His) on the membrane potential and current were examined in JR-1 cells, a mucin-producing epithelial cell line derived from human gastric signet ring cell carcinoma. The tight-seal, whole cell clamp technique was used. The resting membrane potential, the input resistance, and the capacitance of the cells were approximately -12 mV, 1.4 G ohms, and 50 pF, respectively. Under the voltage-clamp condition, no voltage-dependent currents were evoked. ACh or His added to the bathing solution hyperpolarized the membrane by activating a time- and voltage-independent K+ current. The ACh-induced hyperpolarization and K+ current persisted, while the His response desensitized quickly (< 1 min). These effects of ACh and His were mediated predominantly by m3-muscarinic and H1-His receptors, respectively. The K+ current induced by ACh and His was inhibited by charybdotoxin, suggesting that it is a Ca(2+)-activated K+ channel current (IK.Ca). The measurement of intracellular Ca2+ ([Ca2+]i) using Indo-1 revealed that both agents increased [Ca2+]i with similar time courses as they increased IK.Ca. When EGTA in the pipette solution was increased from 0.15 to 10 mM, the induction of IK.Ca by ACh and His was abolished. Thus, both ACh and His activate IK.Ca by increasing [Ca2+]i in JR-1 cells. In the Ca(2+)-free bathing solution (0.15 mM EGTA in the pipette), ACh evoked IK.Ca transiently. Addition of Ca2+ (1.8 mM) to the bath immediately restored the sustained IK.Ca. These results suggest that the ACh response is due to at least two different mechanisms; i.e., the Ca2+ release-related initial transient activation and the Ca2+ influx-related sustained activation of IK.Ca. Probably because of desensitization, the Ca2+ influx-related component of the His response could not be identified. Intracellularly applied inositol 1,4,5-trisphosphate (IP3), with and without inositol 1,3,4,5-tetrakisphosphate (IP4), mimicked the ACh response. IP4 alone did not affect the membrane current. Under the steady effect of IP3 or IP3 plus IP4, neither ACh nor His further evoked IK.Ca. Intracellular application of heparin or of the monoclonal antibody against the IP3 receptor, mAb18A10, inhibited the ACh and His responses in a concentration-dependent fashion. Neomycin, a phospholipase C (PLC) inhibitor, also inhibited the agonist-induced response in a concentration-dependent fashion. Although neither pertussis toxin (PTX) nor N-ethylmaleimide affected the ACh or His activation of IK,Ca, GDP beta S attenuated and GTP gamma S enhanced the agonist response.(ABSTRACT TRUNCATED AT 400 WORDS)

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