Accumulation, Acetylation, and Releasability of Diethylhomocholine from a Sympathetic Ganglion

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Abstract
Superior cervical ganglia of the cat perfused with [14C]diethylhomocholine ([14C]DEHCh) synthesized acetyldiethylhomocholine (ADEHCh), but rather little of this ester was released by subsequent preganglionic nerve stimulation. Stimulation evoked the release of an appreciable amount of unchanged DEHCh when ganglia had been exposed to the analogue in the absence of choline (Ch), but did not do so when exposed to both Ch and DEHCh. The release of DEHCh was Ca2+ dependent, and was not the result of the release and subsequent hydrolysis of ADEHCh. This is the first clear demonstration of the release of an unacetylated compound from mammalian tissue; therefore, the characteristics of the transmitter release mechanism are further defined. The effect of preganglionic nerve stimulation on the uptake and acetylation of DEHCh was also measured. Stimulated ganglia accumulated ∼4 times more labeled analogue and synthesized 7.5 times more ADEHCh than did rested ganglia. Stimulated ganglia perfused with 2‐(4‐phenylpi‐peridino)cyclohexanol, a compound considered to inhibit acetylcholine (ACh) release by inhibiting its transport into synaptic vesicles, accumulated 3.4 times as much and acetylated 6 times as much DEHCh as did rested ganglia. When the concentration of Mg2+ in the perfusion medium was increased to block ACh release, accumulation of the labelled analogue was enhanced by stimulation, but its acetylation was increased much less than during perfusion with normal medium. It is concluded that the synthesis of ADEHCh is subject to the same regulation as is ACh synthesis and that the activation of ester synthesis during activity can be dissociated from ester release. The relationship between stimulation‐induced increases of DEHCh accumulation and ADEHCh synthesis suggests that some other factor associated with nerve terminal impulse invasion, such as increased Ca2+ influx, is necessary for the manifestation of increased synthesis of the acetyl compound.