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1.
Neurol India ; 70(2): 543-547, 2022.
Article in English | MEDLINE | ID: mdl-35532617

ABSTRACT

Background and Introduction: Botulinum neurotoxin (BoNT) is a potent biological toxin extracted from Clostridium Botulinum bacteria. BoNT injection is mainly used for medical purposes; it is frequently used for cosmetic purposes as well. The hypothesis that frequent application of this treatment modality may also affect the central nervous system constitutes the subject of our study. Objective: We aimed to demonstrate the possible central effects of BoNT in hemifacial spasm patients. Methods and Materials: Diffusion tensor imaging was used for this study. Patients were divided into two groups, and the measured values for each determined bilateral neuroanatomic region were compared within the relevant group. Results: Fractional anisotropy (FA) and apparent diffusion coefficient (ADC) values were found to be closer to the pathological values in the right motor cortex and in the left internal capsule areas of the patients who were injected with BoNT into the left side, in the left motor cortex area of the patients who were injected with BoNT into the right side. No significant changes were detected in other regions. Conclusion: Botulinum neurotoxin administration in patients with hemifacial spasms may cause some changes in the central nervous system as well as peripheral effects. In the case of similar studies supporting pathological changes, BoNT treatment modalities or appropriate indications may be reviewed, and regulation on excessive cosmetic use may be in question.


Subject(s)
Botulinum Toxins, Type A , Hemifacial Spasm , Neuromuscular Agents , Anisotropy , Botulinum Toxins, Type A/therapeutic use , Diffusion Tensor Imaging , Hemifacial Spasm/diagnostic imaging , Hemifacial Spasm/drug therapy , Humans , Neuromuscular Agents/therapeutic use
2.
Toxicon ; 147: 58-67, 2018 Jun 01.
Article in English | MEDLINE | ID: mdl-29031941

ABSTRACT

Tetanus (TeNT) and botulinum (BoNT) neurotoxins, the causative agents of tetanus and botulism, respectively, are the most potent toxic molecules known to mankind. This extreme potency is attributed to: i) their specificity for essential components of the neurotransmitter release machinery present at vertebrate synapses, and ii) their high-affinity targeting to motor neurons by binding to polysialogangliosides and protein receptors. Comprising the clostridial neurotoxin family, TeNT and BoNTs engage distinct surface receptors and intracellular sorting pathways in neurons. BoNTs bind to the intraluminal domain of specific synaptic vesicle proteins that are exposed to the extracellular milieu upon exocytosis, and are taken up by synaptic vesicle recycling. A sizeable proportion of BoNT molecules remain at the neuromuscular junction, where their protease moiety is released into the cytoplasm, blocking synaptic transmission and causing flaccid paralysis. In contrast, TeNT undergoes binding to specific components of the basal membrane at the neuromuscular junction, is endocytosed into motor neurons and sorted to axonal signalling endosomes. Following this, TeNT is transported to the soma of motor neurons located in the spinal cord or brainstem, and then transcytosed to inhibitory interneurons, where it blocks synaptic transmission. TeNT-induced impairment of inhibitory input leads to hyperactivity of motor neurons, causing spastic paralysis, which is the hallmark of tetanus. This review examines the molecular mechanisms leading to the entry, sorting and intracellular trafficking of TeNT and BoNTs.


Subject(s)
Botulinum Toxins/metabolism , Botulinum Toxins/toxicity , Protein Transport/physiology , Tetanus Toxin/metabolism , Tetanus Toxin/toxicity , Animals , Humans
3.
Article in Chinese | WPRIM (Western Pacific) | ID: wpr-537414

ABSTRACT

Objective To study the retrograde axonal transport of Schwann cell derived neurotrophic factor(SDNF)by motor neurons Methods SDNF was labeled with Chloramine T, 125 I SDNF and 100 fold excess of unlabelled SDNF was injected into the right hindlegs of neonatal rats separately The spinal cords was removed for counting in a  counter Results The radioactive level of experimental side was more than contralateral side The transport was blocked by 100 fold excess of unlabelled SDNF Conclusion SDNF was transported retrogradely by spinal motor neurons

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