Publications by authors named "M Pecot-Dechavassine"

The population of large dense-core vesicles (LDCVs) in motor nerve terminals of the frog cutaneous pectoris muscle was analysed after various experimental protocols leading to large acetylcholine release. Three types of LDCVs classified according to their size and the core density were detected. Vesicles, 100-150 nm in diameter, with a large and very dense core (type 1) or with an irregular and diffuse dense core (type 2) were present in similar proportions (45 and 50% respectively) in controls.

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Misdirection of sensory fibers into motor pathways is, in part, responsible for the poor results obtained after peripheral nerve repair. After avulsion of the C-5 root in rats, the authors connected a C-4 ventral rootlet to the musculocutaneous nerve by means of a sural nerve graft. In this way, they were able to increase the number of regenerating motor fibers and avoid growth of sensory fibers into the nerve grafts.

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In an attempt at repairing the injured spinal cord of adult mammals (rat, dog and marmoset) and its damaged muscular connections, we are currently using: 1) peripheral nerve autografts (PNG), containing Schwann cells, to trigger and direct axonal regrowth from host and/or transplanted motoneurons towards denervated muscular targets; 2) foetal spinal cord transplants to replace lost neurons. In adult rats and marmosets, a PNG bridge was used to joint the injured cervical spinal cord to a denervated skeletal muscle (longissimus atlantis [rat] or biceps brachii [rat and marmoset]). The spinal lesion was obtained by the implantation procedure of the PNG.

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Synaptic vesicle recycling after intense acetylcholine (ACh) release was studied at the frog neuromuscular junction (NMJ) using the synaptic vesicle transmembrane protein synaptophysin as immunocytochemical marker of the synaptic vesicle membrane during the process of exo-endocytosis. ACh release in cutaneous pectoris nerve-muscle preparations was stimulated by three different means: K+, Cd2+ in Ca(2+)-free medium, and electrical stimulation in the presence of 4-aminopyridine (4-AP). Cd2+ stimulation produced synaptic vesicle depletion and nerve terminal swelling.

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Synaptophysin and synaptobrevin, two integral proteins of synaptic vesicles, have been used as immunocytochemical markers of the synaptic vesicle membrane during Cd(2+)- or K(+)-induced ACH release at the frog neuromuscular junction. ACh release was stimulated in cutaneous pectoris nerve-muscle preparations by: (1) 1 mM Cd2+ in Ca(2+)-free medium for a period of 3 h, (2) 25 or 40 mM K+ in normal Ringer's solution. Synaptophysin and synaptobrevin were immunolabelled in single fibres teased from fixed muscles using rabbit antisera raised against synaptophysin and synaptobrevin revealed with fluorescein-conjugated IgG.

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