The effect of choline mustard on the rat superior cervical ganglia.

The effect of choline mustard aziridinium ion (ChM) on the isolated superior cervical ganglion of the rat was investigated. In the presence of ChM (22.5 microM), stimulation at 1 Hz resulted in a slowly developing blockade of transmission, which did not occur at a stimulus frequency of 0.1 Hz. Choline (0.1 mM) slowed the onset of the blockade produced by stimulation at 1 Hz in the presence of ChM. The presence of excess thiosulphate ions prevented the action of ChM on the transmission in the superior cervical ganglion. Treatment of the ganglion with ChM (22.5 microM) only slightly inhibited the depolarization produced by carbachol (dose ratio 1.3), suggesting the drug produced a small degree of receptor blockade. [3H]-choline accumulation in the rat superior cervical ganglia displays several components: (a) sodium-dependent high affinity uptake (SDHAU) that can be activated further by preincubation in a high concentration of K+ ions; (b) sodium-dependent low affinity uptake (SILAU); (c) linear diffusional accumulation which does not saturate. Hemicholinium-3 selectively inhibits the activated sodium-dependent high affinity uptake, but is a weak inhibitor of resting sodium-dependent high affinity uptake and sodium-independent low affinity uptake. ChM inhibits both activated and resting sodium-dependent high affinity uptake, but is a very weak inhibitor of sodium-independent low affinity uptake. Homocholine shows similar selectivity. ChM inhibition of activated sodium-dependent high affinity uptake is very much more persistent than that of hemicholinium-3. Hemicholinium-3 and ChM both inhibit [3H]-acetylcholine synthesis.