Differential expression of two adhesion molecules of the immunoglobulin superfamily, F3 and polysialylated NCAM, in hypothalamic magnocellular neurones capable of plasticity.

The adult hypothalamo-neurohypophysial system undergoes activity-dependent, reversible morphological changes which result in reduced astrocytic coverage of its neurones and an increase in their synaptic contacts. Our recent observations show that neurones and glia of the hypothalamo-neurohypophysial system continue to express 'embryonic' molecular features which may underlie their capacity to undergo such plasticity. These include expression of cell surface molecules like the glycosyl phosphatidyl inositol (GPI)-linked glycoprotein F3, which intervenes in axonal outgrowth, and the polysialylated isoform of the neural cell adhesion molecule (PSA-NCAM), which reduces cell adhesion and promotes dynamic cell interactions. F3 is colocalised with vasopressin and oxytocin hormones in neurosecretory granules and follows an activity-dependent, regulated pathway for surface expression on neurohypophysial axons. In contrast, PSA-NCAM appears to follow a constitutive pathway, independent of the activity of the hypothalamo-neurohypophysial system, for expression on axonal and glial surfaces, in the hypothalamic magnocellular nuclei and in the neurohypophysis. The role of F3 remains to be determined but in view of its presumptive functions during development, we propose that it promotes remodelling of neurosecretory terminals. On the other hand, we provide direct evidence that surface expression of PSA on NCAM is essential to morphological plasticity since its specific enzymatic degradation in vivo inhibited the neuronal-glial and synaptic changes normally induced by stimulation of secretion from the hypothalamo-neurohypophysial system.