The effect of lithium on acetylcholine release and synthesis

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When sodium concentration in Krebs solution was replaced by different concentrations of lithium to maintain isosmolarity, the acetylcholine release during resting conditions in rat cortex slices was increased depending on the lithium concentration. The maximal augmentation in ACh resting release was reached at a lithium concentration of 117.9 mM. This acetylcholine release proved to be tetrodotoxin (2.5 × 10-7 g ml) and noradrenaline (10-6 g ml) resistant. However, when sodium was partly replaced by lithium (117.9 mM LiCl and 25 mM NaCl) the synthesis was blocked completely. This inhibition can be attributed to the lithium ions present in the nerve terminals, since the acetylcholine release was unaffected at low sodium concentration (25 mM) when isosmolarity was maintained by glucose. Furthermore lithium (117.9 mM) reduced the acetylcholine output due to stimulation from the nerve terminals of guinea-pig ileum longitudinal muscle strip. It is suggested that lithium accumulating inside the nerve terminals inhibited the rate of synthesis of acetylcholine. The reduction of freshly synthetized acetylcholine led to a reduction of acetylcholine output due to stimulation.

Original languageEnglish
Pages (from-to)521-530
Number of pages10
Issue number4
Publication statusPublished - Jul 1972

ASJC Scopus subject areas

  • Pharmacology
  • Cellular and Molecular Neuroscience

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