Acetylcholine (ACh) release from sliced cerebral cortex of rats was measured when the tissue was incubated in a high K+ (46 mm) medium containing eserine. In the absence of hemicholinium (HC‐3), ACh release was well maintained, but in the presence of HC‐3, ACh release declined within 15–20 min. Subcellular fractions representing nerve‐ending free (cytoplasmic) ACh and nerve‐ending bound ACh were prepared from slices that had been stimulated to release ACh in the presence of HC‐3. Both nerve‐ending stores of ACh were depleted when their content was compared to tissue that had not been stimulated and there was no demonstrable difference in the rate of depletion of either of the two fractions. Stimulating slices with K+ in the absence of HC‐3 also depleted cytoplasmic and vesicle‐bound ACh. It is concluded that, under these experimental conditions, both nerve ending stores of ACh are available for release and that, in the absence of HC‐3, ACh synthesis can maintain ACh release, but cannot maintain tissue ACh content.
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Salehmoghaddam et al. (1976) studied this question.
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