1. 1. High potassium (50 mM)-evoked acetylcholine (ACh) release from rat basal forebrain slices under conditions without an exogenous choline supply was determined using a radioimmunoassay for ACh. 2. 2. A consistent amount of ACh release was observed at each repetitive stimulation and ACh content in brain slices was not altered by potassium stimulations. These results indicate the existence of a large intracellular releasable ACh store, which is independent of new synthesis from exogenous choline. 3. 3. Atropine, even at a concentration of 10-6 M, did not affect the potassium-evoked ACh release. Thus, modulation of ACh release by the muscarinic autoreceptor was not revealed under the conditions employed. 4. 4. Thyrotropin-releasing hormone (TRH, 10-4 M) caused a slight and statistically insignificant increase in potassium-evoked ACh release. DN-1417, a TRH analogue, at a concentration of 10-4 M significantly increased potassium-evoked ACh release. These findings indicate that DN-1417 is able to enhance ACh output independently of ACh synthesis from exogenous choline.
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