Action of glucosamine on acetylcholine-sensitive channels

Marchais, Dominique; Marty, Alain

doi:10.1007/bf01869350

Cited by 11 publications

(3 citation statements)

References 22 publications

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“…There seems no necessity to invoke such a complicated scheme to explain the present results. 414 CHANNEL BLOCKADE BY CHLORISONDAMINE Nature of the stable-blocked state Several studies have examined the effects of various permeant ions on channel lifetime and proposed the view that occupation of the lumen of ionic channels by an ion effectively hinders the normal closure of the channel (Marchais & Marty, 1980;Ascher, Marty & Neild, 1978b;Gage & Van Helden, 1979; reviewed by Steinbach, 1980). Similar observations have been made for the potassium channel of the squid axon and of frog muscle (Swenson & Armstrong, 1981;Stanfield, Ashcroft & Plant, 1981).…”

Section: Factors Influencing Recovery From the Blocked Conditionmentioning

confidence: 99%

Blockade of cholinergic channels by chlorisondamine on a crustacean muscle.

Lingle¹

1983

The Journal of Physiology

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SUMMARY1. Details of the blocking action of chlorisondamine, a ganglionic nicotinic blocker, on the excitatory cholinergic currents ofthe spiny lobster gastric mill 1 (g.m. 1) muscle are described.2. The steady-state block of cholinergic ionophoretic currents produced by chlorisondamine is strongly voltage-dependent.3. During a hyperpolarizing voltage step, a sequence of ionophoretic agonist pulses in the presence of chlorisondamine shows a large interpulse interaction manifested as a gradual diminution in response amplitude. The extent of diminution is dependent on the number of the pulse in a series and not on the duration of the interval between pulses. The slowly developing blockade is entirely dependent on agonist application.4. If agonist application is suspended for various time intervals following the development of a given blocked level in chlorisondamine, no recovery from the block is observed whether the rest interval is at the step potential or at more depolarized potentials.5. Recovery from a given blocked level can be observed if, during a depolarizing voltage step (to -60 mV) away from the potential at which the block was established (-140 mV), agonist is applied before return to the initial potential (-140 mV).6. Chlorisondamine produces a dose-dependent reduction in excitatory junctional current (e.j.c.) decay rate that is linear with chlorisondamine concentration and markedly dependent on voltage ( -35 mV/e-fold change). 7. Reduction in the amplitude of e.j.c.s occurred at concentrations of chlorisondamine that produced no detectable effect on e.j.c. decay.8. Alterations in e.j.c. amplitude showed time-and use-dependent aspects similar to those observed for ionophoretic currents.9. These results are discussed primarily in terms of a sequential model in which, following the binding of chlorisondamine to the opened ion channel, the channel can undergo a transition to a stable-blocked state that requires reactivation by agonist to become unblocked. This stable-blocked state is considered a closed-blocked channel.

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Section: Factors Influencing Recovery From the Blocked Conditionmentioning

confidence: 99%

Blockade of cholinergic channels by chlorisondamine on a crustacean muscle.

Lingle¹

1983

The Journal of Physiology

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“…In addition, it has been reported that DGL reduces the elementary current amplitude and increases the mean channel open time [31]. Because DGL has a weak binding site in the channel itself, the channel cannot be closed [31].…”

Section: Discussionmentioning

confidence: 99%

“…Because DGL has a weak binding site in the channel itself, the channel cannot be closed [31]. Voltage-gated sodium channels, which are necessary for electrogenesis and nerve impulse conduction, can be dynamically regulated after nerve injury or peripheral inflammation and can play important roles in modulating neural excitability [32, 33].…”

Section: Discussionmentioning

confidence: 99%

Suppressive Effects of D-Glucosamine on the 5-HT Sensitive Nociceptive Units in the Rat Tooth Pulpal Nerve

Kaida

Yamashita

Toda

et al. 2014

BioMed Research International

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It is well known that D-glucosamine hydrochloride (DGL) has a variety of biological activities and is regarded as a nutritional supplement effective in improving various disorders, including osteoarthritis and atherosclerosis. Although it has been reported that DGL has a significant pain relief effect in treating osteoarthritis, little is known about the characteristics of the effects of this compound on dental pain. The present study was undertaken to evaluate the applicability of DGL as a medicament to control pulpalgia. Using an in vitro rat mandible-inferior alveolar nerve preparation (jaw-nerve preparation), we evaluated the effects of DGL on 5-hydroxytryptamine (5-HT) sensitive nociceptive responses in the tooth pulpal nerve. 5-HT-induced nociceptive responses were fairly suppressed by direct application of DGL, suggesting that DGL have a pain relief effect on patients with dental pain.

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The Contribution of D-Glucosamine to Cell Membrane Stability: Mechanisms and Applications in Regenerative Medicine

Hayashi

2019

Sustainable Agriculture Reviews 35

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Action of glucosamine on acetylcholine-sensitive channels

Cited by 11 publications

References 22 publications

Blockade of cholinergic channels by chlorisondamine on a crustacean muscle.

Blockade of cholinergic channels by chlorisondamine on a crustacean muscle.

Suppressive Effects of D-Glucosamine on the 5-HT Sensitive Nociceptive Units in the Rat Tooth Pulpal Nerve

The Contribution of D-Glucosamine to Cell Membrane Stability: Mechanisms and Applications in Regenerative Medicine

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