» Articles » PMID: 6140647

Spontaneous Release of Acetylcholine and Acetylhomocholine from Mouse Forebrain Minces: Cytoplasmic or Vesicular Origin

Overview
Journal Neurochem Res
Specialties Chemistry
Neurology
Date 1983 Oct 1
PMID 6140647
Citations 1
Authors
Affiliations
Soon will be listed here.
Abstract

The objective of this study was to determine the subcellular origin of cholinergic transmitter released spontaneously from mouse forebrain minces. To accomplish this objective, minces were pretreated in ionic media and then loaded with [14C]homocholine, an analog of choline, to form the false transmitter [14C]acetylhomocholine [( 14C]AHCh). The ratio of the false transmitter [14C]AHCh to the true transmitter ACh was then used as an index of cholinergic transmitter contents for both the cytoplasmic (S3) and vesicle-bound (P3) fractions. Three different pretreatment procedures were used to cause the following changes in S3 and P3 false to true transmitter ratios prior to spontaneous release: 1) a small increase in the S3 ratio of [14C]AHCh to acetylcholine (ACh) and a large increase in the P3 ratio of [14C] AHCh to ACh; 2) a decrease in the S3 ratio of [14C]AHCh to ACh and an increase in the P3 ratio of [14C]AHCh to ACh; 3) an increase in the P3 ratio of [14C]AHCh to ACh without affecting the S3 ratio of [14C]AHCh to ACh. The influence of each pretreatment on these subcellular ratios was then compared with its influence on the spontaneous release ratio of [14C]AHCh to ACh. In all 3 instances, the influence of pretreatment on the ratio of spontaneously released false and true cholinergic transmitters from minces coincided with the effect of pretreatment on the pre-release ratio of false to true transmitter in the S3 fraction. These results suggest that much of the cholinergic transmitter which is spontaneously released from mouse forebrain occurs from the cytroplasmic fraction.

Citing Articles

Evidence to suggest that the spontaneous release of acetylcholine from rat hippocampal tissue is carrier-mediated.

Ivy M, Carroll P Neurochem Res. 1988; 13(4):325-8.

PMID: 3393262 DOI: 10.1007/BF00972481.

References
1.
Carrol P, Nelson S . Cholinergic vesicles: ability to empty and refill independently of cytoplasmic acetylcholine. Science. 1978; 199(4324):85-6. DOI: 10.1126/science.199.4324.85. View

2.
SUSZKIW J, OLeary M . Differential labeling of depot and active acetylcholine pools in nondepolarized and potassium-depolarized rat brain synaptosomes. J Neurochem. 1982; 38(6):1668-75. DOI: 10.1111/j.1471-4159.1982.tb06648.x. View

3.
Drachman D, Stanley E, Pestronk A, Griffin J, Price D . Neurotrophic regulation of two properties of skeletal muscle by impulse-dependent and spontaneous acetylcholine transmission. J Neurosci. 1982; 2(2):232-43. PMC: 6564300. View

4.
Gundersen Jr C, Howard B . The effects of botulinum toxin on acetylcholine metabolism in mouse brain slices and synaptosomes. J Neurochem. 1978; 31(4):1005-13. DOI: 10.1111/j.1471-4159.1978.tb00140.x. View

5.
Katz B, Miledi R . Does the motor nerve impulse evoke 'non-quantal' transmitter release?. Proc R Soc Lond B Biol Sci. 1981; 212(1186):131-7. DOI: 10.1098/rspb.1981.0029. View