MODULATION OF NCAM POLYSIALYLATION IS ASSOCIATED WITH MORPHOFUNCTIONAL MODIFICATIONS IN THE HYPOTHALAMONEUROHYPOPHYSEAL SYSTEM DURING LACTATION

Post-transcriptional modification of the neural cell adhesion molecule (NCAM) by polysialic acid significantly decreases NCAM adhesiveness a nd more generally modifies cell-cell interactions, Polysialic acid-NCA M (PSA-NCAM) is mainly expressed in the developing nervous system. In the adult, its expression is restricted to regions that retain morphol ogical plasticity, such as the hypothalamo-neurohypophysial system dur ing lactation in rats. Since cell-cell interactions and synaptic conta cts in the hypothalamo-neurohypophysial system are greatly increased d uring lactation, we examined whether PSA-NCAM expression is modified d uring this period. Immunohistochemistry and immunoblotting showed that , compared with virgin rats, PSA-NCAM dramatically decreased during la ctation in both the supraoptic nuclei and the neurohypophysis, and ret urned to its initial level only after weaning. This decrease was progr essive and became significant only at the end of the first week of lac tation. By contrast, modifications in the level of NCAM protein or cha nges in the splicing pattern of NCAM mRNAs could not be detected. The decline in polysialic acid on the NCAM molecule could strengthen membr ane appositions, thereby stabilizing the newly established synapses an d neurohaemal contacts in the hypothalamo-neurohypophysial system that accompany; the increased neuronal activity that occurs during lactati on. We also studied the regulation of the phosphorylated microtubule-a ssociated protein-1B (MAP1B-P), whose distribution pattern largely ove rlaps with that of PSA-NCAM in the adult brain. Expression of MAP1B-P was greatly increased during lactation in the hypothalamic axons proje cting into the neurohypophysis. Thus, the expression patterns of both PSA-NCAM and MAP1B-P may reflect the permanent structural plasticity c haracterizing the hypothalamo-neurohypophysial system in the adult.