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Italian study shows surprising result: Botox has legs!

Science - Health



The botulinum toxin, from which Botox is made, is a highly poisonous substance.

It works by degrading a protein called SNAP-25 (synaptosome-associated protein of 25,000 daltons) that controls the release of neurotransmitters. When SNAP-25 is eliminated, sensory communications in those affected nerve cells is degraded, or even stopped.

Scientists have found, on the beneficial side, that they can control such maladies in patients as strabismus (eyes that involuntarily cross), migraine headaches, various muscle spasms, and diseases (such as cerebral palsy).

Small doses of the botulinum toxin are also used by plastic surgeons to paralyze facial muscles (aka, wrinkles) in order to make patients look younger.

The result of the Caleo study is found in the April 2, 2008 issue of the Journal of Neuroscience.

The study’s title is “Long-Distance Retrograde Effects of Botulinum Neurotoxin A.” Its authors are Flavia Antonucci, Chiara Rossi, Laura Gianfranceschi, Ornella Rossetto, and Matteo Caleo.

The abstract of the Caleo study states: “Botulinum neurotoxins (designated BoNT/A–BoNT/G) are bacterial enzymes that block neurotransmitter release by cleaving essential components of the vesicle fusion machinery.”

“BoNT/A, which cleaves SNAP-25 (synaptosomal-associated protein of 25 kDa), is extensively exploited in clinical medicine to treat neuromuscular pathologies, facial wrinkles, and various types of pain.”

“It is widely assumed that BoNT/A remains at the synaptic terminal and its effects are confined to the injection site.”

“Here we demonstrate that catalytically active BoNT/A is retrogradely transported by central neurons and motoneurons and is then transcytosed to afferent synapses, in which it cleaves SNAP-25. SNAP-25 cleavage by BoNT/A was observed in the contralateral hemisphere after unilateral BoNT/A delivery to the hippocampus. Appearance of cleaved SNAP-25 resulted in blockade of hippocampal activity in the untreated hemisphere.”

“Injections of BoNT/A into the optic tectum led to the appearance of BoNT/A-truncated SNAP-25 in synaptic terminals within the retina. Cleaved SNAP-25 also appeared in the facial nucleus after injection of the toxin into rat whisker muscles. Experiments excluded passive spread of the toxin and demonstrated axonal migration and neuronal transcytosis of BoNT/A.”

“These findings reveal a novel pathway of BoNT/A trafficking in neurons and have important implications for the clinical uses of this neurotoxin.”



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