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dc.contributor.authorSumislawski, Joshua Joseph
dc.description.abstractBotulinum neurotoxin, the agent that causes the paralytic disease botulism, is the most poisonous substance known. The ability of botulinum neurotoxin serotype A (BoNT/A) to produce flaccid paralysis makes it both of public-health concern as a biological weapon and of medical interest as a versatile therapeutic agent (BOTOX). Less appreciated is the frequent observation that poisoned nerve endings respond by initiating and extending neurites. This phenomenon, termed sprouting, has now been proposed as an indication that the binding of BoNT/A to the neuronal membrane activates intracellular signals that are independent of its already well-characterized paralytic action. Supporting this novel idea, recent studies have demonstrated that the ability of the toxin to induce sprouting is concentration-dependent and counteracted by receptor antagonists. This study addressed the hypothesis that BoNT/A promotes neurite outgrowth through a signaling pathway that depends on the second messenger cyclic adenosine monophosphate (cAMP). To test this hypothesis, primary cultures of motor neurons from embryonic mice were exposed to BoNT/A with and without several inhibitors of cAMP-dependent pathways. In the presence of the inhibitors, the ability of the toxin to induce sprouting was eliminated. These results suggest that BoNT/A promotes neurite outgrowth of embryonic motor neurons via cAMP-dependent intracellular signaling. Additional studies are necessary to further our understanding of the neurotrophic action of this potent toxin.
dc.subjectBotulinum neurotoxin
dc.subjectNeurite outgrowth
dc.subjectEmbryonic motor neurons
dc.titleBotulinum neurotoxin serotype A promotes the neurite outgrowth of embryonic motor neurons via cAMP-dependent intracellular signaling
dc.description.departmentPhysiology and Pharmacology
dc.description.advisorJulie Coffield
dc.description.committeeJulie Coffield

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