NEUROPHYSINS IN CENTRAL DIABETES-INSIPIDUS

When they were discovered by Acher and co-workers, neurophysins were t hought to act as carriers for the active nonapeptides vasopressin (AVP ) and oxytocin (OT) and were then recognized as the inactive fragment of a precursor with a higher molecular weight (propressophysin). The r ole of neurophysins in the hypothalamo-neurohypophyseal system is now being reconsidered in the light of crystallographic and molecular biol ogy research and the recent definition of the different deletions or s ubstitutions that cause central diabetes insipidus in rats (Brattlebor o) or human beings. Apparently, any disruption of the strucuture and/o r conformation of neurophysins (by genic substitution or deletion) may cause a decline in the binding and the activity of the endopeptidase responsible for the cleavage of the AVP. The disruption may also produ ce a change in the polymerization of neurophysins and salt bridges rel ating this to the neuropeptides, with the result that there is an acce lerated aspecific enzymatic degradation of the hormone revealing clini cal symptomatology. So, rather than being a mere inactive part of the precursor, neurophysins are now equally regarded as a system for carry ing and protecting nonapeptides.