Effects of vinblastine and colchicine on neural regulation of the fast and slow skeletal muscles of the rat

Albuquerque, Edson X.; Warnick, Jordan E.; Tasse, J.R.; Sansone, Frances M.

doi:10.1016/0014-4886(72)90103-3

Cited by 236 publications

(55 citation statements)

References 39 publications

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“…However, one cannot assume that cholinergic transmission plays an equivalent role D. B. DRACHMAN AND D. M. JOHNSTON in neurotrophic regulation of all properties of muscle. Indeed, there is now evidence that more than one factor is involved in the regulation of certain other properties of muscle, including ACh receptor distribution (Albuquerque, Warnick, Tasse & Sansone, 1972;Hofmann & Thesleff, 1972) and the localization of acetylcholinesterase (Drachman, 1972). Therefore each such property must be considered as a separate system, and the neurotrophic factors which influence it must be assessed quantitatively.…”

Section: Discussionmentioning

confidence: 99%

Neurotrophic regulation of dynamic properties of skeletal muscle: effects of botulinum toxin and denervation.

Drachman¹,

Johnston²

1975

The Journal of Physiology

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SUMMARY1. In order to determine the role of acetylcholine (ACh) transmission in neurotrophic regulation of dynamic properties of muscle, the effects of botulinum toxin treatment were compared with those of denervation. The extensor digitorum longus (EDL) and soleus muscles of rats were either denervated or injected with botulinum toxin. At times up to 25 days the isometric properties of these muscles were determined.2. Both botulinum treatment and denervation produced progressive slowing of the time to peak of the twitch (TPT) and half-relaxation time of the twitch (ART), which was more pronounced in the EDL than in the soleus.3. Both treatments produced slowing of the relaxation curve following tetanic contraction, more marked in the EDL than in the soleus muscle. This indicates a slowing of relaxation, and suggests a prolongation of the active state of the muscle.4. The maximum rate of rise of the tetanus did not change significantly in the EDL and soleus muscles after botulinum treatment or denervation. This suggests that there is no major change in the speed of contraction under conditions of botulinum treatment or denervation.5. The changes produced by botulinum treatment and denervation were virtually identical in all parameters tested. This is interpreted meaning that cholinergic transmission (including muscle usage), or some other factor closely related to cholinergic transmission, accounts for the motor nerve's trophic influence in maintaining these dynamic properties of skeletal muscles.

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Section: Discussionmentioning

confidence: 99%

Neurotrophic regulation of dynamic properties of skeletal muscle: effects of botulinum toxin and denervation.

Drachman¹,

Johnston²

1975

The Journal of Physiology

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“…fall in resting membrane potential, reduction in maximum rate of rise of the action potential) were more severe in the animals receiving high doses of (-)-emetine for 21-30 days than in those receiving lower doses for much longer periods. However, the precise significance of these changes is not clear since they occur in so many pathological conditions, involving directly or indirectly either peripheral nerve, skeletal muscle or both (see for example Harris, 1971;Albuquerque, Warnick, Tasse & Sansone, 1972;Harris & Ward, 1974) that they must be considered non-specific. The large increase in threshold for action potential generation seen in the muscles of the more severely affected animals may be of some significance.…”

Section: Discussionmentioning

confidence: 99%

Emetine Myopathy in the Rat

Bradley¹,

Fewings²,

Harris³

et al. 1976

British J Pharmacology

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(–)‐Emetine (0.25‐2.0 mg/kg i.p.) was administered to rats for up to 220 days. At doses of 1.0 mg/kg or less, the animals continued to gain weight but more slowly than the untreated control animals. The physiological changes in the muscles from these animals were minimal; there was a small reduction in both the resting membrane potential and in the maximum rate of rise of the action potential. There was no atrophy or loss of muscle fibres although in the occasional muscle, hyaline fibres, necrotic fibres and split fibres were observed. There was a focal loss of myofibrillar adenosine triphosphatase (ATPase) and nicotinamide adenine dinucleotide tetrazolium reductase (NADH‐TR) in Type II and Type III fibres, but no such loss in Type I fibres. The animals receiving 2.0 mg/kg of (–)‐emetine gained weight slowly for up to 20 days but then rapidly lost weight and by 30 days they were weak and emaciated. The muscles from these animals were severely atrophied and the total muscle wet weight was reduced by almost 20%. The strength of the muscles from these animals was measured in vitro using direct stimulation. They were weaker than normal both in absolute terms and when expressed in terms of tension developed/unit wet weight. There was no evidence of either functional or structural denervation but surgically denervated muscles from animals in this group were indistinguishable from denervated muscles from normal rats. Severe structural damage was obvious in the fibres of both extensor digitorum longus and soleus. Necrotic, hyaline and splitting fibres were common and the focal loss of myofibrillar ATPase and NADH‐TR activity was extensive and occurred in Type I fibres as well as in Type II and Type III fibres. It is concluded that the muscular weakness induced by (–)‐emetine is due to a direct effect on the muscle fibres and that this occurs at a subcellular level. There is no evidence that functional or structural denervation plays any role in the aetiology of emetine myopathy in the rat.

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“…"Products of nerve degeneration" also explain the local supersensitivity observed by Miledi around denervated endplates in multiply innervated frog muscle fibers. "Block of axonal transport" relates to the ACh supersensitivity and other denervation-like changes observed after the application of drugs such as colchicine to the sciatic nerve, effects that were attributed to blockage of axonal transport of trophic factors (94,95). However, as Cangiano and I showed independently (96,97), colchicine acts systemically, affecting innervated muscles in different parts of the body equally, regardless of the injection site.…”

Section: Trophic Factors Versus Products Of Nerve Degenerationmentioning

confidence: 99%

Scientific Discoveries: What Is Required for Lasting Impact

Lømo

2016

Annu. Rev. Physiol.

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I have been involved in two scientific discoveries of some impact. One is the discovery of long-term potentiation (LTP), the phenomenon that brief, high-frequency impulse activity at synapses in the brain can lead to longlasting increases in their efficiency of transmission. This finding demonstrated that synapses are plastic, a property thought to be necessary for learning and memory. The other discovery is that nerve-evoked muscle impulse activity, rather than putative trophic factors, controls the properties of muscle fibers. Here I describe how these two discoveries were made, the unexpected difficulties of reproducing the first discovery, and the controversies that followed the second discovery. I discuss why the first discovery took many years to become generally recognized, whereas the second caused an immediate sensation and entered textbooks and major reviews but is now largely forgotten. In the long run, discovering a new phenomenon has greater impact than falsifying a popular hypothesis.

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Effects of vinblastine and colchicine on neural regulation of the fast and slow skeletal muscles of the rat

Cited by 236 publications

References 39 publications

Neurotrophic regulation of dynamic properties of skeletal muscle: effects of botulinum toxin and denervation.

Neurotrophic regulation of dynamic properties of skeletal muscle: effects of botulinum toxin and denervation.

Emetine Myopathy in the Rat

Scientific Discoveries: What Is Required for Lasting Impact

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