Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: EC:3.4.24.69 (botulinum neurotoxin)
 1,901 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Botulinum C2 toxin has vascular permeability as well as lethal activities. Both activities are elicited by cooperation of two dissimilar protein components, designated components I and II, which individually have very low activities. The vascular permeability activity of C2 toxin, demonstrated as blueing response after intravenous injection of Evans blue, was markedly enhanced by treatment with trypsin and was abolished by neutralization with either anti-component I or II serum. Inflammatory reactions, such as edema, congestion, and hemorrhage, were found at the site of intradermal injection of trypsinized C2 toxin. No vascular permeability activity was demonstrated by the intradermal injection of the toxin of Clostridium botulinum types A through F. These results indicate that C2 toxin has a novel biological activity, which is not possessed by the neurotoxin elaborated by C. botulinum types A through F. This suggests that C2 toxin causes lethality in a different way from that of botulinum neurotoxin, which is known to inhibit the presynaptic release of acetylcholine at the neuromuscular junction.
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PMID:Vascular permeability activity of botulinum C2 toxin elicited by cooperation of two dissimilar protein components. 701 65

The purpose of this study was to use botulinum neurotoxin type A (BoNT/A) selectively to evaluate the influence of localized masticatory atrophy and paresis on craniofacial growth and development. 60 growing rats, 4 weeks old, weighing approximately 120g, were randomly divided according as follows (Long-Evans, N=15 per group): I (Mb+Tns); II (Mns+Tb); III (Mb+Tb); IV (Mns+Tns), where Mb or Tb is the BoNT/A-injected masseter or temporalis muscles (1.0U/muscle, 2.5ml) and Mns or Tns is the saline-injected muscles (2.5ml). After 7 weeks, the mature rats were killed, the muscles dissected and mean muscle mass recorded. Anthropometric cranial, maxillary and mandibular measurements were taken from the dried skulls. Changes in animal weight during the growth period were not statistically significant. The mean masticatory muscle mass was smaller for the BoNT/A-injected muscles of Mb and Tb. Anthropometric measurements of bony structures inserted by masseter and temporalis muscles revealed a significant treatment effect. The measurements showed a facial morphology typical of a dolichofacial profile: short upper face accompanied by a long lower face with an extended mandibular length and ramus height and constricted bicoronoidal and bigonial widths. The results suggest that induction of localized masticatory muscle atrophy with BoNT/A alters craniofacial growth and development.
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PMID:The influence of masticatory hypofunction on developing rat craniofacial structure. 2021 21

In this study, botulinum neurotoxin type A (BoTx/A) was injected into the temporalis and masseter muscles of growing rats to induce masticatory hypoactivity. Sixty, 30-day-old, male Long-Evans rats were randomly divided into four groups. BoTx/A was bilaterally injected in the masseter muscles in group I, in the temporalis muscles in group II, and into both the masseter and the temporalis muscles in group III. Group IV served as the control in which saline was bilaterally injected into both muscles. Forty-five days after the injections, the rats were sacrificed. Observation of cortical bone thickness from bone biopsies of the right halves of the mandibles, evaluation of the volume of masseter and temporalis muscles with a plethysmometer, and scanning of bone mineral density (BMD) of the skull and mandibular bone structure with dual-energy X-ray absorptiometry were performed. One-way analysis of variance was employed to analyse measurements of muscle volume, BMD, and cortical bone thickness among the groups. The least square difference was then used to determine significance. Reduced cortical bone thickness and BMD of the skull and mandibular bone structure were observed. The volumes of the temporalis and masseter muscles injected with BoTx/A were smaller. Masticatory hypofunction affects bone structure during development.
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PMID:Bone changes in the mandible following botulinum neurotoxin injections. 2088 20

We addressed the hypothesis that intraplantar botulinum toxin B (rimabotulinumtoxin B: BoNT-B) has an early local effect upon peripheral afferent terminal releasing function and, over time, will be transported to the central terminals of the primary afferent. Once in the terminals it will cleave synaptic protein, block spinal afferent transmitter release, and thereby prevent spinal nociceptive excitation and behavior. In mice, C57Bl/6 males, intraplantar BoNT-B (1 U) given unilaterally into the hind paw had no effect upon survival or motor function, but ipsilaterally decreased: (1) intraplantar formalin-evoked flinching; (2) intraplantar capsaicin-evoked plasma extravasation in the hind paw measured by Evans blue in the paw; (3) intraplantar formalin-evoked dorsal horn substance P (SP) release (neurokinin 1 [NK1] receptor internalization); (4) intraplantar formalin-evoked dorsal horn neuronal activation (c-fos); (5) ipsilateral dorsal root ganglion (DRG) vesicle-associated membrane protein (VAMP); (6) ipsilateral SP release otherwise evoked bilaterally by intrathecal capsaicin; (7) ipsilateral activation of c-fos otherwise evoked bilaterally by intrathecal SP. These results indicate that BoNT-B, after unilateral intraplantar delivery, is taken up by the peripheral terminal, is locally active (blocking plasma extravasation), is transported to the ipsilateral DRG to cleave VAMP, and is acting presynaptically to block release from the spinal peptidergic terminal. The observations following intrathecal SP offer evidence for a possible transsynaptic effect of intraplantar BoNT. These results provide robust evidence that peripheral BoNT-B can alter peripheral and central terminal release from a nociceptor and attenuate downstream nociceptive processing via a presynaptic effect, with further evidence suggesting a possible postsynaptic effect.
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PMID:Botulinum toxin B in the sensory afferent: transmitter release, spinal activation, and pain behavior. 2444 Aug 13