A dependence of neurohumoral release upon the presence of calcium ion in the bathing medium has been demonstrated in superior cervical ganglia (Harvey and MacIntosh, '40; Hutter and Kostial, '54 and '55), in the adrenal medulla (Douglas and Rubin, '61), and at the neuromuscular junction (see Hubbard, '61). These observations, together with the demonstration of calcium entry during electrical stimulation and/or K depolarization in skeletal muscle (Bianchi and Shanes, '59), cardiac muscle (Winegrad and Shanes, '62), and in peripheral nerve (Hodgkin and Keynes, '57), have led to speculation relating calcium entry to neurohumoral release (Hodgkin and Keynes, '57; Shanes, ' 5 8 ) . These speculations have been supported and furthered by Douglas and Poisner ('62) by demonstration of calcium entry in the secreting adrenal medulla.
The effects of magnesium ion on transmission have long been recognized (see Engbaek, '52) and more recently have been related specifically to interference with neurohumor release (e.g., Hubbard, '61). However, no information concerning the effect of magnesium upon calcium entry in any structure is as yet available. This will be described for rabbit cervical vagus nerve.
The present experiments were done to study the possibility of a correlation between potassium-induced calcium entry and acetylcholine output in isolated rabbit superior cervical ganglia. Enhancement of calcium entry on exposure of the ganglion to raised potassium concentrations is found to be about equal to the acetylcholine released. Moreover, increase of the extracellular magnesium concentration reduces potassium-enhanced calcium entry in vagus nerve.
METHODS