The relationship between calcium uptake and hormone release in the isolated neurohypophysis. A reassessment

The release of peptide hormones and uptake of radiolabelled calcium were measured in isolated rat neurohypophyses incubated in vitro. Neuropeptide release was provoked either by depolarising the tissue with raised extracellular potassium, or by application of biphasic electrical stimulus pulses. Potassium stimulation increased uptake of radiolabelled calcium, but electrical stimulation caused no measurable change, suggesting that non-neuronal elements unresponsive to electrical stimulation were responsible for the uptake. This possibility is supported by the results of 2 further series of experiments, in which the neurohypophyses were manipulated in vivo before incubation in vitro. First, the experimental animals were given a 2% solution of sodium chloride in place of drinking water for 3 days, to deplete the neuropeptide content of the incubated tissue. After such treatment, potassium-stimulated neuropeptide release was greatly reduced, but calcium uptake was increased relative to that of normal tissue. Secondly, the pituitary stalk was lesioned electrolytically 14 days before the incubation, thus completely eliminating the neural elements of the neurohypophysis. Potassium stimulation then released no neuropeptide, but calcium uptake increased as in normal tissue. It thus appears that calcium uptake does not always closely parallel neuropeptide release, in contrast with previous results, and that depolarisation of the non-neuronal elements is responsible for the measurable uptake of calcium. The results do not contradict existing concepts of the central role of calcium influx in stimulus-secretion coupling in neurohypophyseal terminals, but serve to emphasise the need for care in the interpretation of calcium uptake data in tissues which are not homogeneous. The neurohypophyseal glial cells (pituicytes) are a likely site for the calcium uptake caused by potassium depolarisation.