HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS		QUICK SEARCH:   [advanced] Author: Keyword(s): Year:  Vol:  Page:

This Article Full Text (PDF) Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via Google Scholar Google Scholar Articles by Kosterlitz, H. W. Articles by Wallis, D. I. Search for Related Content PubMed PubMed Citation Articles by Kosterlitz, H. W. Articles by Wallis, D. I.

1. Evoked ganglionic action potentials and drug-induced changes in resting potential were recorded by the sucrose-gap method. The height of the action potential was 10-20 mV.

2. Since the amplitude of the P wave is inversely proportional to the external potassium concentration between 0·5 and 12 mM, the P wave is probably caused by a phase of increased permeability to K⁺.

3. In the absence of an anticholinesterase, the depolarizing actions of choline and acetylcholine on the ganglion are almost equal, whereas acetylcholine is 2-3 times more potent than choline on the fibres of the internal carotid nerve. In the presence of eserine, acetylcholine induces a depolarization of the ganglion of up to 14 mV, while increase in [K⁺]_o causes a depolarization of up to 55 mV.

4. Although the post-ganglionic fibres in the distal pole of the ganglion are depolarized by drugs, for example, acetylcholine, they contribute little to drug-induced potential changes and probably little to evoked action potentials.

5. The hyperpolarization which occurs after exposure of the ganglion to acetylcholine is not due to a phase of increased permeability to K⁺.