Activation of feline acetylcholine synthesis in the absence of release: dependence on sodium, calcium and the sodium pump.
Following a 15 min inhibition of the Na pump in the cat superior cervical ganglion by perfusion with K-free Locke solution, a 10 min recovery period in normal Locke produced a 51% increase in acetylcholine stores. The increase in acetylcholine stores occurred without increase in acetylcholine release. Thus this procedure of pump inhibition followed by recovery selectively activates acetylcholine synthesis. The increase in acetylcholine stores occurred entirely during the 10 min recovery period in which the Na pump was re-activated. This increase represents a rate of synthesis of acetylcholine of 5.1% of stores per minute, which equals the maximum rate that can be achieved during high-frequency preganglionic nerve stimulation. The increase in stores was not affected by substituting isethionate for all but 8 mM-Cl in the perfusion fluids. The increase in stores was prevented by reducing the Na concentration of the K-free Locke to 25 mM. The increase in stores was only 17% when Ca was omitted from the K-free Locke. Omission of Ca from the perfusion fluid in the recovery period as well as in the period of pump inhibition prevented any increase in stores. It is concluded that the selective activation of acetylcholine synthesis following the pause in Na pumping was a direct result of an increase in Na pump rate and an increase in internal Ca in the nerve terminals. It is proposed that similar changes in Na pump rate and internal Ca produced by repetitive nerve impulse activity likewise activate acetylcholine synthesis independently of release of transmitter or depletion of stores.[1]References
- Activation of feline acetylcholine synthesis in the absence of release: dependence on sodium, calcium and the sodium pump. Birks, R.I. J. Physiol. (Lond.) (1983) [Pubmed]
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