Long-lasting effects of serotonin deficiency on differentiating peptidergic neurons in the rat suprachiasmatic nucleus.

Serotonin (5-HT, 5-hydroxytryptamine) is known to be an inductor of the brain development [Whitaker-Azmitia, P.M., Druse, M.

The effects of serotonin on the differentiation of neurons producing vasoactive intestinal polypeptide in the suprachiasmatic nucleus of the rat.

The morphogenetic influences of serotonin on the differentiation of neurons synthesizing vasoactive intestinal polypeptide (VIP) in the suprachiasmatic nucleus were studied in rats. This was addressed by comparative morphofunctional analysis of VIP neurons in adult rats whose brains developed prenatally in conditions of normal and deficient serotonin metabolism. Serotonin deficiency was created in fetuses by treatment of their mothers with p-chlorophenylalanine (PCPA).

[The source of transitory innervation of suprachiasmatic nucleus by tyrosine hydroxylase-immunoreactive fibers during the postnatal period in rats].

Suprachiasmatic nucleus in the rats during early postnatal development is transitorily innervated by tyrosine hydroxylase-immunoreactive fibers that are neither catecholamine- nor serotoninergic. The goal of this immunocytochemical investigation was to find out if tyrosine hydroxylase-immunoreactive neurons of anterior hypothalamus could be the source of this innervation. According to the obtained immunocytochemical data, multiple multipolar tyrosine hydroxylase-immunoreactive neurons are localized around the suprachiasmatic nucleus in the rats at days 2 and 10 of postnatal development.

[Effect of serotonin on differentiation of neurons producing vasoactive intestinal polypeptide in the rat suprachiasmatic nucleus].

This study was aimed to evaluate the morphogenetic influence of serotonin on the differentiating vasoactive intestinal polypeptide (VIP) neurons of the suprachiasmatic nucleus (SCN) in rats. The comparative morpho-functional analysis of VIP neurons was made in adult rats which developed under normal metabolism of serotonin or in its deficiency. The serotonin deficiency was induced in foetuses by injections of p-chlorophenilalanine to pregnant mothers.