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. 1977 Oct;271(3):847–862. doi: 10.1113/jphysiol.1977.sp012028

A long-lasting potentiation of transmitter release related to an increase in transmitter stores in a sympathetic ganglion

R I Birks
PMCID: PMC1353635  PMID: 926023

Abstract

1. High frequency preganglionic nerve stimulation increases the acetylcholine (ACh) stores of the cat superior cervical ganglion. The increase reaches a maximum 20 min following 60 min conditioning stimulation at 20/s. The effect of this conditioning on ACh release in ganglia perfused with plasma and test stimulated at 4 or 5/s has been studied, and the relationship of ACh stores to ACh release in conditioned ganglia determined.

2. The rate of ACh release in response to test stimulation at 5/s for 15 min, starting 20 min following conditioning, was 174% of the rate found in unconditioned ganglia. The ACh stores of the conditioned ganglia at the end of the test were calculated to be 173% of the control ganglion stores.

3. When test stimulation at 4/s was started 5 min following conditioning, the rate of ACh release showed a variable pattern of increase and decrease over a 75 min period. The mean peak rate of release was about 150% of the control rate, and the duration of potentiation was about 75 min.

4. When conditioned, unperfused ganglia were tested by stimulation at 4/s the ACh stores were found to increase and decrease in parallel with the increase and decrease in ACh release rates found in the perfusion experiments.

5. It was found also that the magnitude of the increase in ACh stores and ACh release was related to the amount of ACh in the ganglionic stores at the onset of conditioning, being greater for the ganglia with the smaller initial stores.

6. It is concluded that the potentiation of ACh release in ganglia conditioned in this way is directly related to the accompanying increase in ACh stores.

7. The possible significance of alterations of ACh stores and ACh release as a mechanism of modulatory control of ganglionic transmission is discussed.

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Selected References

These references are in PubMed. This may not be the complete list of references from this article.

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