Thesis (Ph. D.)--University of Missouri-Columbia, 2003. / Typescript. Vita. Includes bibliographical references (leaves 234-254). Also available on the Internet.

Title from PDF of title page (University of Missouri--Columbia, viewed on Feb 25, 2010). The entire thesis text is included in the research.pdf file; the official abstract appears in the short.pdf file; a non-technical public abstract appears in the public.pdf file. Dissertation advisor: Dr. Anand Chandrasekhar. Vita. Includes bibliographical references.

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Thesis (doctoral)--Lund University, 1992. / Added t.p. with thesis statement inserted.

Thesis (Ph. D.)--University of Wisconsin--Madison, 1968. / Typescript. Vita. eContent provider-neutral record in process. Description based on print version record. Includes bibliographical references.

Thesis (doctoral)--Lund University, 1992. / Added t.p. with thesis statement inserted.

Thesis (M.Phil.) - University of Queensland, 2006. / Includes bibliography.

Thesis (M.S.)--University of Wisconsin--La Crosse, 2002. / Includes bibliographical references.

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The first proof of the chemical mediation of nerve impulses by the peripheral release of specific chemicals was made by Loewi (1921). He demonstrated that during stimulation of the vagus nerve leading to an excised frog’s heart (Figure 1) a chemical mediator that he called Vagus-substance was released which slowed the action of the heart. This chemical mediator entered a perfusion fluid consisting of isotonic sodium chloride which was pumped out of the ventricle of the heart and diverted so as to drip onto a second frog's heart. The dripping perfusion medium slowed the pulsation of the second heart upon stimulation of the donor heart. When the stimulus was removed, the donor heart returned to normal pulsation and shortly after the recipient heart returned to normal. The Vagus-substance in the perfusion fluid was identified by Feldberg and Krayer (1933) as acetylcholine. Cholineacetylase forms acetylcholine from acetic acid and choline at the neuromuscular junction (Figure 2) in the presence of energy. The energy is obtained as a result of the action potential produced by the nerve impulse traveling along the nerve to the neuromuscular junction. The acetylcholine proceeds to cross the synapse at the neuromuscular junction and activates the muscle causing its contraction. The persistent presence of the acetylcholine at the junction would result in constant depolarization of the muscle resulting in fibrillation. The acetylcholine is destroyed by acetylcholinesterase causing repolarization so that the muscle is able to respond to further nerve impulses. Acetylcholine possesses two actions in vertebrates: muscarinic and nicotinic. The muscarinic action is exhibited at the neuromuscular functions of smooth muscle and sweat glands and the nicotine action is exhibited at the neuromuscular junction of striated muscle and at the synapse within ganglia.