Improved Calcium Utilization at Motor Nerve Terminals Exposed to Botulinum Neurotoxin in Mice
| Autor: | Toshiaki Ishii, Masakazu Nishimura, Seiichi Komori, Ryu Fujikawa |
|---|---|
| Rok vydání: | 2008 |
| Předmět: |
Male
medicine.medical_specialty Time Factors End-plate potential Physiology Diaphragm Presynaptic Terminals Neuromuscular transmission Motor nerve chemistry.chemical_element Calcium Contractility Mice chemistry.chemical_compound Internal medicine medicine Animals Botulinum Toxins Type A Neurotransmitter Motor Neurons Miniature Postsynaptic Potentials Recovery of Function Botulinum toxin Electric Stimulation Phrenic Nerve Endocrinology chemistry Anesthesia Female Injections Intraperitoneal Intracellular Muscle Contraction medicine.drug |
| Zdroj: | The Journal of Physiological Sciences. 58:419-424 |
| ISSN: | 1880-6562 1880-6546 |
| Popis: | We examined the fail-safe responses against low-dose 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 Ca2+ 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 Ca2+ concentration. These results indicated two functional fail-safe 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 Ca2+ channels, intracellular Ca2+ store sites, or transmitter-releasing apparatuses. |
| Databáze: | OpenAIRE |
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