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At least 145 records · Page 8Linked to original sources
PubMed1979

[Modification of curarization after acute administration of 2 antiepileptic drugs].

In rats anaesthetised with sodium pentobarbital the previous administration of a single dose of an anti-epileptic agent (carbamazepine or sodium valproate) significantly increases the curarising action of two short-action curare-like agents--pancuronium bromide and fazadinium bromide. It seems that this potentialisation of curare action might be the result of either a pharmacokinetic interference (competion for plasma protisen receptor sites), or due to a summation of depressor actions at the neuromuscular level, especially through changes in the levels of GABA and/or cAMP.

Animals↗
PubMedDate not supplied

[Principles of the interaction of curare-like agents with skeletal muscle cholinoreceptors].

The principles of interaction of curare-like agents with acetylcholine receptors of skeletal muscles are discussed. The possible types of interatomic bonds of substances with receptors are exemplified by different chemical compounds which possess the neuromuscular blocking action. Prior attention is given to the role of hydrophobic interactions in the activity and mechanism of action of curare-like agents.

Binding Sites↗
PubMed1980

Sprouting and regression of the nerve at the frog neuromuscular junction in normal conditions and after prolonged paralysis with curare.

A light microscopical, histochemical and electron microscopical investigation of the frog neuromuscular junction has been performed on muscles from animals in different functional states of activity. The combined staining of axon terminals and cholinesterase (ChE) allows a precise description of the nerve terminal arborization and its synaptic contacts. Most terminal arborizations form long continuous contacts with the muscle cell. Distinquishable from these are nerve branches (usually of small diameter)d or distal endings of branches with one or several small and isolated contacts. It is assumed that these are sprouts with newly-formed synaptic sites. Other sprouts end without apparent synaptic contact. At the uttrastructural levet, nerve sprouts end without apparent synaptic contact. At the uttrastructural levet, nerve sprouts growing into empty, well-differentiated synaptic gutters or inducing the formation of new synaptic sites were observed. In other sites, ChE is apparently located at postsynaptic gutters with no nerve present. Similarly, in the electron microscope, well-differentiated synaptic gutters lacking any nerve or Schwann cell elements were observed. In addition, synaptic gutters only partially occupied by the nerve were frequently seen. These features have been interpreted as signs of regression of the nerve terminals. Nerve regression and sprouting were found in animals chronically paralysed with curare over several weeks as well as in untreated frogs (winter and summer frogs, laboratory frogs, fed and unfed). When quantitatively evaluating the occurence of presumed features of nerve sprouting and nerve regression, differences were found between different experimental groups. From this it is concluded that, in addition to developmental changes, the degree of nerve sprouting and regression is controlled by external factors such as muscle activity and seasonal variations. Signs of sprouting and nerve regression can be simultaneously present in a single synapse. It appears that the frog neuromuscular synapse is not a static structure, but is in a state of permenent remodelling.

Acetylcholinesterase↗
PubMed1987

Chronic application of curare does not increase the level of motoneuron survival-promoting activity in limb muscle extracts during the naturally occurring motoneuron cell death period.

Naturally occurring motoneuron cell death during development is a well-described phenomenon and the existence of a survival factor provided by target muscles has been postulated. Blockade of activity by chronic application of a neuromuscular junction blocker rescues almost all motoneurons from cell death. The present study was conducted in order to examine the possibility that the motoneuron survival-promoting activity in muscles increases following activity blockade. Cell culture was used to assess the degree of motoneuron survival-promoting activity present in muscle extracts. Embryonic chick motoneurons were labeled by injecting the water-insoluble fluorescent dye, DiI (Molecular Probes, Inc.) into the spinal nerves both before and during the cell death period. The labeled cells extending long neurites were counted after 2 days of culture as viable motoneurons in low-density heterogeneous cell cultures. The culture medium, Ham F12/DMEM (1:1 mixture) supplemented with 10% horse serum, 5% chick serum, and 5% fetal calf serum, was employed as a basic culture medium for assessing motoneuron survival factor, since it supported the survival of a significantly higher number of motoneurons derived from embryos before cell death than those during the cell death period, thus representing the motoneuron's requirement for survival factor in vivo. The number of surviving motoneurons clearly increased in proportion to the amount of muscle extract added to the culture medium. In comparison with control chick embryos, the dose-response relation between the number of surviving motoneurons and the amount of muscle extract added did not change when embryos were used after chronic application of curare. These results therefore indicate that survival factor derived from target muscle is crucial to the in vitro motoneurons during the cell death period, but do not support the idea that inactive muscle contains a higher amount of the survival factor.

Age Factors↗
PubMed1988

Anti-curare action of stannous ion in the frog neuromuscular junction.

For the purpose of elucidating the mechanism of action of stannous ion (Sn2+), we investigated effects of stannous chloride (SnCl2) on the twitch and on the electrical phenomena in the muscle fiber. Sciatic nerve-sartorius muscle preparations from the bullfrog were used as the material. Effect of SnCl2 was examined on the twitch partially inhibited by pretreatment with d-tubocurarine. SnCl2 (1-100 microM) antagonized d-tubocurarine and enhanced the twitch dose-dependently. Tartaric acid, which is the solvent used for SnCl2 solution, had no augmentative effect on the twitch, even at a concentration as high as 250 microM. SnCl2 (1-50 microM) increased the amplitude of the endplate potential; that is, it exerted an anti-curare action. The resting potential and the membrane resistance of the muscle fiber were not altered by 30 microM SnCl2. These findings lead to the conclusion that Sn2+ enhances the twitch by increasing the endplate potential of the muscle fibers.

Animals↗
PubMed1992

Onset of CGRP expression and its restriction to a subset of spinal motor neuron pools in the chick embryo is not affected by treatment with curare.

Calcitonin gene-related peptide (CGRP) is expressed in and defines a subset of motor neuron pools in the lumbar spinal cord of the chick embryo. The onset of CGRP expression in individual pools coincides with both the period of the initial innervation of the leg and the beginning of naturally occurring cell death in the lumbar motor column. Administration of neuromuscular blocking agents at this time results in a striking reduction of normal motor neuron loss. It has been reported that such treatment also results in the abolition of CGRP expression at later stages of development. In this study, we have examined the effect of curare treatment on CGRP expression in motor neurons earlier in their development. We find that, in contrast to the effects reported at later stages, inhibition of neuromuscular activity does not affect either the onset of CGRP expression or its restriction to a subset of motor neuron pools. This demonstrates that the control of the onset of CGRP expression is unlikely to be linked to processes which are regulated by neuromuscular transmission including naturally-occurring cell death.

Animals↗
PubMedDate not supplied

Effects of chloral hydrate, pentobarbital, ketamine, and curare on the auditory middle latency response.

Changes in threshold, latency, and amplitude of the auditory middle latency response (MLR) with anesthesia and neuromuscular paralysis were studied in guinea pigs. Although each component of the surface-recorded MLR was altered by barbiturate and nonbarbiturate agents, the early positive wave (wave A) was always present, and the later waves were generally identifiable at moderate levels of anesthesia. MLR threshold was not affected by anesthesia or curare. Pentobarbital, chloral hydrate, and ketamine each caused an increase in the latency of all MLR components, with increases progressively marked for later waves. Amplitude changes were more complex. Wave A increased in amplitude with anesthesia, while wave C decreased or disappeared temporarily. Wave B showed mixed amplitude changes. Changes in MLR associated with anesthesia were generally more pronounced at a stimulation rate of 10/sec as compared to 4/sec. No changes in waveform morphology or latency were seen with neuromuscular paralysis. The results provide evidence in support of separate neurogenic substrates for the different components of the guinea pig temporal lobe MLR. The presence of the MLR with moderate levels of anesthesia indicates that this animal is an appropriate model for studying the MLR in experiments requiring anesthesia and immobilization.

Animals↗
PubMedDate not supplied

[Myotonic seizures; the action of curare or related compounds on myotonia (author's transl)].

Myotonic seizures with apnea are alarming but temporary incidents occurring during curaization of a myotonic patient. Experience with regional curaization in myotonia shows that it is induced only by suxamethonium and it is only an exaggeration of the fasciculations produced by this compound. In contrast, however, competitive curare compounds have no effect on myotonia. The myotonic seizure, which is specific to myotonia, is radically different from the other respiratory accidents common to muscular dystrophies.

Adolescent↗
PubMed1993

Molecular dissection of subunit interfaces in the acetylcholine receptor: identification of residues that determine curare selectivity.

The acetylcholine receptor from vertebrate skeletal muscle is a transmembrane channel that binds nerve-released acetylcholine to elicit rapid transport of small cations. Composed of two alpha subunits and one beta, one gamma, and one delta subunit, the receptor is a cooperative protein containing two sites that bind agonists, curariform antagonists, and snake alpha-toxins. Until recently the two binding sites were thought to reside entirely within each of the two alpha subunits, but affinity labeling and expression studies have demonstrated contributions by the gamma and delta subunits. Affinity labeling and mutagenesis studies have identified residues of the alpha subunit that contribute to the binding site, but the corresponding gamma- and delta-subunit residues remain unknown. By making gamma-delta chimeras and following the nearly 100-fold difference in curare affinity for the two binding sites, the present work identified residues of the gamma and delta subunits likely to be near the binding site. Two sets of binding determinants were identified in homologous positions of the gamma and delta subunits. The determinants lie on either side of a disulfide loop found within the major extracellular domain of the subunits. This loop is common to all acetylcholine, gamma-aminobutyrate, and glycine receptor subunits.

Animals↗
PubMed1978

O2 uptake and developed tension during and after fatigue, curare block, and ischemia.

The purpose of this study was to investigate the effect of changes in developed tension on the ratio between O2 uptake and isometric developed tension in the in situ dog gastrocnemius-plantaris muscle group. O2 uptake and isometric developed tension of the muscle were measured during contractions at 1 twitch/s before and after fatigue with both single and twin impulses (6.5 V, 0.2-ms duration; the twins were separated by 10--20 ms). Twin impulses prior to fatigue raised developed tension to two times the tension developed with single impulses. Fatigue was obtained by stimulation at 10--20 impulses/s for 30--40 min. Twin impulses after fatigue returned developed tension to the level of single impulses before fatigue. O2 uptake and developed tension were also measured during the slower development of fatigue produced by continuous stimulation (3, 4, 5, and 6 impulses/s) as well as during "fatigue" induced by partial neuromuscular block with curare or ischemia. In all cases, there was no change in the O2 uptake per unit of tension developed, indicating a constant coupling between O2 uptake and developed tension.

Animals↗
PubMed2005

Curare: the South American arrow poison.

The history of curare is both curious and convoluted. A product of South American culture it emerged in the sixteenth century from the mists of antiquity at the same time as quinine, coca, and chocolate. Like quinine, at first came the extract but no plant, and later the plant but no chemical compound. It took more than 300 years and the efforts of many explorers and scientists to resolve the problem. These included Condamine, Humboldt, Brodie, Waterton, Bernard, Dale, Walker, and King. Finally, the pure compound d-tubocurarine was isolated from the liana Chondrodendron and synthesised. Its specific physiological action was blockade of the effect of acetylcholine at the neuro-muscular junction. Such a paralytic poison could be used to kill oneself or others. The bizarre plot to kill the Prime Minister, Lloyd George, during the First World War is described. Fortunately this nefarious plan was thwarted by the Secret Service!

Botany↗
PubMed1991

[Acetylcholine receptor antibody titer, sensitivity to curare electromyogram and disease severity in myasthenia gravis].

All of 39 rabbits immunized with acetylcholine receptors invariably formed anti-AChR Abs and some of them developed muscular weakness or flaccid paralysis. Pharmacological, physiological and ultrastructural studies indicated that the pathology of experimental autoimmune myasthenia gravis in rabbits resembled that of human myasthenia gravis. The titer of anti-AChR Abs correlated poorly with disease severity and did not simply predicted the muscular weakness. The results ruled out the possibility that antigenic modulation of AChR was sufficient to account for the induction of myasthenia gravis. There was a close relationship between the sensitivity to curare and disease severity, but only part of immunized animals appeared electromyogram change. This led us to conclude that serum anti-AChR concentration would not be the single pathological factor in myasthenia gravis and disease severity may correlate with amount of normal AChR.

Animals↗
PubMed1990

[Anesthesiologic aspects of narco-curare-electroshock treatment].

The physiology and side-effects of narco-curare-electric shock treatment are reviewed on the basis of the literature and, similarly, risk groups are delimited. Directives for preoperative assessment, the anaesthesiological procedure and per- and postoperative observation are given. It is concluded that the NCE procedure is associated with a low risk and slight mortality provided the above-mentioned conditions are observed. Patients with cardiovascular disease constitute the greatest risk group and should receive optimal medical treatment prior to NCE. In cases with raised intracranial pressure, NCE should only be employed with great reservation. ECG monitoring, treatment with atropine and preliminary treatment with oxygen are advised in general. Withdrawal of psychocopharmaca prior to NCE is rarely indicated.

Anesthesia, General↗
PubMed1990

[Clinical correlation of anti-receptor antibody titer, sensitivity to curare and electromyographic changes in experimental autoimmune myasthenia gravis].

Experimental autoimmune myasthenia gravis (EAMG) was studied in 39 rabbits which were repeatedly immunized with purified membrane-bound Torpedo (Nacine timilei) acetylcholine receptor (N-AchR). These rabbits invariably formed anti-AChR antibodies and some of them developed muscular weakness or flaccid paralysis. Pharmacological, physiological and ultrastructural studies showed that the pathological features of EAMG in rabbits closely resembled those of human myasthenia gravis. Antibody titer to AChR of the rabbit sera was determined with ELISA. In some of the rabbits, a rise in antibody Level occurred without appearance of weakness, while it is still likely that AChR antibody could be necessary for the induction of neuromuscular blockage. The sensitivity to curare was found to correlates closely with the severity of the disease. Typical electromyographic changes were found only in some of the EAMG rabbits with these studies. It was considered that anti-AChR concentration would not be the single pathological factor in EAMG.

Animals↗
PubMed1987

[Postsynaptic potentiation of miniature currents of muscle fiber endplates in the rat diaphragm. The effect of an acetylcholinesterase inhibitor, temperature and curare].

Miniature end-plate currents (MEPC) were recorded in voltage-clamped end-plates of the rat diaphragm. A positive correlation between the amplitude and half-decay time of individual MEPC was found in control, after acetylcholinesterase (AChE) inhibition the correlation increased: correlation coefficients--0.29 and 0.49, respectively (28 degrees C). Addition of curare after the AChE inhibition caused a decrease in the amplitude and duration of MEPC, but had no effect on the correlation between these parameters. Cooling down to 18 degrees C led to the essential reduction of this correlation in control as well as after the AChE inhibition. Effect of the prolongation of the half-decay time due to the AChE inhibition was more significant at 28 degrees C than at 18 degrees C. The Q10 value for duration of the rising MEPC phase (about 2) was less than that for the half-decay time (about 3). The role of factors determining the MEPC duration is discussed. The results are explained by the postsynaptic potentiation in terms of the cooperative action of agonists on cholinoreceptors and of peculiarities of the acetylcholine diffusion from the synaptic cleft.

Animals↗
PubMed1978

Hofmann elimination with diazomethane on curare bases and selected quaternary tetrahydroisoquinoline alkaloids.

Use of a large excess of alkali-free diazomethane resulted in a Hofmann elimination with selected curare bases and some other quaternary tetrahydroisoquinoline alkaloids. (+)-Tubocurarine chloride provided a monostilbene methine, O,O-dimethyltubocurinemethine, and a monostilbene--monostyrene compound, O,O-dimethyltubocurinedimethine. The major elimination products of (+)-isotubocurarine chloride and (+)-carnegine methiodide were monostyrene methines, O,O-dimethyltubocurineisomethine and carneginemethine, respectively. Treatment of (+)-laudanosine methiodide with potassium hydroxide, under the conditions of Hofmann degradation, or alkali-free diazomethane solution provided the same stilbene compound, laudanosinemethine. The structures of the elimination compounds were further confirmed by catalytic reduction and quaternization with methyl iodide.

Alkaloids↗
PubMed1976

Hypothalamic chemostimulation and autonomic changes in curarized rats.

Rats previously implanted with chronic double walled cannulae aimed at the lateral hypothalamic area (LHA) ate and drank reliably after minute injections of norepinephrine and carbachol respectively. Later on the rats were curarized and artificially respirated. After an habituation period during which rectal temperature, cardiac rate and peripheral vasomotor activity were continuously recorded, half of the subjects were injected with 1 mul of norepinephrine (40 x 10(-9) moles) and the other half with 1 mul of carbachol (2.4 x 10(-9)moles). Both drugs elicited hypothermia, bradycardia and vasodilatation. Bradycardia after carbachol was significantly greater than after norepinephrine and hypothermia and vasodilatation after norepinephrine were significantly greater than after carbachol. When the treatments were reversed essentially the same effects were observed.

Animals↗