Campus Access Only

All rights reserved. This publication is intended for use solely by faculty, students, and staff of University of the Pacific. No part of this publication may be reproduced, distributed, or transmitted in any form or by any means, now known or later developed, including but not limited to photocopying, recording, or other electronic or mechanical methods, without the prior written permission of the author or the publisher.

Date of Award


Document Type


Degree Name

Master of Science (M.S.)



First Advisor

Alden E. Noble

First Committee Member

Carl C. Riedesel

Second Committee Member

T. H. Bullock

Third Committee Member

S. Anderson


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.



Included in

Life Sciences Commons



Rights Statement

Rights Statement

No Known Copyright. URI:
The organization that has made the Item available reasonably believes that the Item is not restricted by copyright or related rights, but a conclusive determination could not be made. Please refer to the organization that has made the Item available for more information. You are free to use this Item in any way that is permitted by the copyright and related rights legislation that applies to your use.