Botulinum a Toxin Effects on Rat Jaw Muscle Spindles

Filippi, Guido Maria; Errico, Pierangelo; Santarelli, Rosamaria; Bagolini, B; Manni, E

doi:10.3109/00016489309135834

Cited by 323 publications

(196 citation statements)

References 13 publications

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“…Although unproven, BTX-A-induced alterations in proprioception could occur through an inhibition of acetylcholine release by the gamma-motoneurons of skeletal muscle. This could lead to a subsequent change in muscle spindle activity [ 12,231. Decreased sensitivity of muscle spindles would compromise a muscle's ability to detect and relay joint position and movement information to the central nervous system, reducing proprioceptive acuity and potentially muscle stiffness.…”

Section: Discussionmentioning

confidence: 99%

Proposed model of botulinum toxin-induced muscle weakness in the rabbit

et al. 2005

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Osteoarthritic patients show only a weak association between radiographic signs of joint disease and joint pain and disability. Conversely, muscle weakness is one of the earliest and most common symptoms of patients with osteoarthritis (OA). However, while many experimental models of osteoarthritis include a component of muscular weakness, no model has isolated this factor satisfactorily. Therefore, the purpose of this study was to develop and validate an experimental animal model of muscle weakness for future use in the study of OA. Botulinum Type-A toxin (BTX-A) was uni-laterally injected into the quadriceps musculature of New Zealand white rabbits (3.5 unitdkg). Isometric knee extensor torque at a range of knee angles and stimulation frequencies, and quadriceps muscle mass, were quantified for control animals, and at one-and six-months post-repeated injections, in both, the experimental and the contralateral hindlimb. Ground reaction forces were measured in all animals while hopping across two force platforms. Isometric knee extension torque and quadriceps muscle mass was systematically decreased in the experimental hindlimb. Vertical ground reaction forces in the push off phase of hopping were also decreased in the experimental compared to control hindlimbs. We conclude that BTX-A injection into the rabbit musculature creates functional and absolute muscle weakness in a reproducible manner. Therefore, this model may be used to systematically study the possible effects of muscle weakness on joint degeneration, either as an isolated intervention, or in combination with other interventions (anterior cruciate ligament transection, meniscectomy) known to create knee joint degeneration.

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Section: Discussionmentioning

confidence: 99%

Proposed model of botulinum toxin-induced muscle weakness in the rabbit

et al. 2005

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“…[47][48][49] During the initial weeks after injection, muscles treated with BTX-A show some variability in the size of muscle fibers, and demonstrate intra-cellular changes consistent with denervation (i.e. central mitochondria dispersed toward the periphery).…”

Section: Action On Striated Versus Smooth Musclementioning

confidence: 99%

Drug Insight: biological effects of botulinum toxin A in the lower urinary tract

et al. 2008

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SUMMARYBotulinum toxins can effectively and selectively disrupt and modulate neurotransmission in striated muscle. Recently, urologists have become interested in the use of these toxins in patients with detrusor overactivity and other urological disorders. In both striated and smooth muscle, botulinum toxin A (BTX-A) is internalized by presynaptic neurons after binding to an extracellular receptor (ganglioside and presumably synaptic vesicle protein 2C). In the neuronal cytosol, BTX-A disrupts fusion of the acetylcholine-containing vesicle with the neuronal wall by cleaving the SNAP-25 protein in the synaptic fusion complex. The net effect is selective paralysis of the low-grade contractions of the unstable detrusor, while still allowing high-grade contraction that initiates micturition. Additionally, BTX-A seems to have effects on afferent nerve activity by modulating the release of ATP in the urothelium, blocking the release of substance P, calcitonin gene-related peptide and glutamate from afferent nerves, and reducing levels of nerve growth factor. These effects on sensory feedback loops might not only help to explain the mechanism of BTX-A in relieving symptoms of overactive bladder, but also suggest a potential role for BTX-A in the relief of hyperalgesia associated with lower urinary tract disorders.

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“…In addition to this, recent research has also suggested that Bt is active at the level multiple levels, namely sensory nerve terminals, and muscle spindles, which leads to a reduction in sensory input and fewer muscle contractions (Matak 2014;Filippi 1993;Rosales 1996;). …”

Section: How the Intervention Might Workmentioning

confidence: 99%