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Anesth Analg. 1985 Apr;64(4):395-9.

Choline uptake, acetylcholine synthesis and release, and halothane effects in synaptosomes.

Erratum in

  • Anesth Analg 1986 Feb;65(2):210.


Synaptosomes isolated from rat cerebra were used as a model to study the effects of halothane on choline uptake and acetylcholine synthesis and release processes. Synaptosomes are membrane-bound particles that are formed by gentle disruption of brain tissue. These particles include the presynapse, cleft, portions of postsynaptic membrane, and all other components contained in brain nerve terminals necessary for neurotransmitter synthesis, storage, and release. Halothane (3% in air, vol/vol) caused a "competitive-like" inhibition of choline uptake in synaptosomes but had no effect on the enzymatic activity of choline acetyl-transferase (ChAT). Three percent halothane depressed synaptosomal acetylcholine (ACh) synthesis by 86% while ACh release from synaptosomes was inhibited 50%. It is suggested that halothane inhibits ACh synthesis by directly interfering with the carrier-mediated transport system of choline. Since halothane also inhibits ACh release, as well as choline uptake, it is probable that the anesthetic is acting upon more than one site in these cholinergic nerve terminals. These data require an interpretive evaluation that cannot fit the "unitary" hypothesis as the mechanism of action of general anesthetics.

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