Acetylcholine receptors and sodium channels in denervated and botulinum‐toxin‐treated adult rat muscle.

Bambrick, Linda L.; Gordon, Tessa

doi:10.1113/jphysiol.1987.sp016356

Cited by 30 publications

(15 citation statements)

References 52 publications

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“…BoNT exposure of limb skeletal muscle causes a trend toward larger motor endplates, but the overall size was not significantly different from that of controls (Bambrick and Gordon, 1987;Alderson et al, 1991;Witzemann et al, 1991;Ma et al, 2004). Similarly, our results of developing EOM indicate that BoNT induced a tendency, although not significant, for increased surface area of the motor endplates.…”

Section: Endplate Morphology and Terminal Sprouting Was Moderately Afsupporting

confidence: 64%

Acute and long-term effects of botulinum neurotoxin on the function and structure of developing extraocular muscles

Croes¹,

Baryshnikova²,

Kaluskar³

et al. 2007

Neurobiology of Disease

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Strabismus is a misalignment of the visual axes, due to an imbalance in extraocular muscle (EOM) function. Botulinum neurotoxin (BoNT) treatment can correct the misalignment with permanent therapeutic effects in infants, possibly because the toxin causes structural alterations in developing EOM. To determine whether BoNT indeed permanently weakens developing EOMs, we examined the chicken oculomotor system. Following injections of BoNT in hatchling chicks, we quantified physiological parameters (contractile force measurements) and morphological parameters (myofiber morphometry, innervation, quantitative transmission electron microscopy of mitochondria/fiber types). Treatment of developing EOM with BoNT caused acute reductions of muscle strength and mitochondrial densities, but minimal changes in muscle fiber diameter and neuromuscular junction structures. Contrary to expectations, contractile force was fully recovered by 3-4 months after treatment. Thus, permanent therapeutic effects of BoNT most likely do not cause permanent changes at the level of the peripheral effector organ, but rather involve central (CNS) adaptive responses.

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Section: Endplate Morphology and Terminal Sprouting Was Moderately Afsupporting

confidence: 64%

Acute and long-term effects of botulinum neurotoxin on the function and structure of developing extraocular muscles

Croes¹,

Baryshnikova²,

Kaluskar³

et al. 2007

Neurobiology of Disease

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“…A reduction in acetylcholine esterase levels leads to increased receptor sensitivity (24). There is upregulation of extrajunctional acetylcholine receptors along with increased lysosomal and endocytic activity, which may contribute to recovery (1,23). In animal studies sprouting of new terminal axons from affected motor nerves has also been seen.…”

Section: Recovery From the Effects Of Toxinmentioning

confidence: 90%

Poison as cure: a clinical review of botulinum toxin as an invaluable drug

Bali¹,

Thakur²

2005

J. Venom. Anim. Toxins incl. Trop. Dis

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Botulinum toxin is the most potent toxin known. It is readily absorbed from mucosal surfaces. If dispersed as an aerosol or mixed in the food or water it can lead to a large outbreak of botulism. The disease presents as a symmetric descending paralysis in an afebrile patient. Cranial nerve involvement with diplopia, dysarthria, dysphonia, dysphagia and respiratory paralysis is seen after a variable incubation period. The treatment is mainly supportive. The source of the toxin is Clostridium botulinum, an anaerobic gram-positive spore-forming organism. Some other species of Clostridium like C. butyricum and C. baratii also produce the toxin.The toxin is heat labile and can be inactivated by heating at 100°C for 10 minutes.The toxin acts at the peripheral cholinergic nerve terminals at the neuromuscular junctions, postganglionic parasympathetic ganglia, etc, and affects neurotransmitter release by inhibiting exocytosis. Clinical uses in various medical fields were found for it.

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“…It has been reported that the number and distribution area of acetylcholine receptors were increased in rat diaphragm [21] and hindlimb [22] after treatment with high-dose BoNT. In the present case of low-dose intoxication, however, we consider that increases in the number and distribution area of effective acetylcholine receptors do not contribute significantly, at least not at the parent motor nerve terminals.…”

Section: Postsynaptic Remodelingmentioning

confidence: 99%

Improved Calcium Utilization at Motor Nerve Terminals Exposed to Botulinum Neurotoxin in Mice

et al. 2008

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Abstract:We examined the fail-safe responses against lowdose botulinum intoxication (botulinum neurotoxin serotype A; 0.05 ng/35 g body weight) in electrically activated in vitro phrenic nerve-diaphragm preparations, since sustained ventilation is critical for the prognosis of clinical botulinum intoxication. At 0, 1, 2 and 4 wks after the peritoneal injection of the toxin, both contractility and neurotransmitter release were measured. There was an increase in directly induced twitch force without affecting directly induced tetanus throughout the observation period. Indirectly induced twitch force decreased by 60% at 1 wk, which gradually recovered only during the 4-wk observation period. Spontaneous neurotransmitter release, evaluated as the frequency of miniature end plate potentials, was largely abolished 1 wk after the injection and recovered only slightly during the 4-wk period. The effects on spontaneous release were independent of medium Ca 2+ concentration. Evoked release, evaluated as quantal content, was also mostly inhibited at 1 wk, but it recovered to approximately 50% of controls at 4 wks. The recovery of quantal content was more prominent at low medium Ca 2+ concentration. These results indicated two functional failsafe responses that compensate for the acute inhibitory effect of low dose of botulinum toxin on neuromuscular transmission; increased contractility of muscle, and improved efficiency of evoked quantum release. The increased contractility probably reflects remodeling of muscle fiber composition of the diaphragm. The improved efficiency of evoked quantum release probably involves remodeling of voltage-gated Ca 2+ channels, intracellular Ca 2+ store sites, or transmitter-releasing apparatuses.

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Acetylcholine receptors and sodium channels in denervated and botulinum‐toxin‐treated adult rat muscle.

Cited by 30 publications

References 52 publications

Acute and long-term effects of botulinum neurotoxin on the function and structure of developing extraocular muscles

Acute and long-term effects of botulinum neurotoxin on the function and structure of developing extraocular muscles

Poison as cure: a clinical review of botulinum toxin as an invaluable drug

Improved Calcium Utilization at Motor Nerve Terminals Exposed to Botulinum Neurotoxin in Mice

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