Light-microscopic immunocytochemical localization of tyrosine hydroxylase in prenatal rat brain. II. Late ontogeny
Article first published online: 9 OCT 2004
Copyright © 1981 Alan R. Liss, Inc.
Journal of Comparative Neurology
Volume 199, Issue 2, pages 255–276, 20 June 1981
How to Cite
Specht, L. A., Pickel, V. M., Joh, T. H. and Reis, D. J. (1981), Light-microscopic immunocytochemical localization of tyrosine hydroxylase in prenatal rat brain. II. Late ontogeny. J. Comp. Neurol., 199: 255–276. doi: 10.1002/cne.901990208
- Issue published online: 9 OCT 2004
- Article first published online: 9 OCT 2004
The immunocytochemical localization of tyrosine hydroxylase is examined at embryonic (E) days 18 and 21 in rat brain in order to determine changes in the distribution and cytology of neurons showing immunoreactivity for the enzyme during late prenatal developmnt. As compared with earlier stages of development, the distribution and morphology of the tyrosine hydroxylasecontaining neurons at E18 and E21 more closely resemble catecholaminergic neurons in the adult brain. The changes occuring from the early to the late prenatal stages of development appear to be the result of an increase in number of cells and continued aggregation and migration of the labeled neurons.
The major differences in the distribution of labeled perikarya between E18 and E21 are in the olfactory bulb and cerebral cortex. In the olfactory bulb, tyrosine hydroxylase-containing neurons are not detected until E21. In contrast in the cerebral cortex, a few neurons are transiently labeled for the enzyme at E18, but are not detected at E21 and have not been reported in the adult brain.
The most striking change in the tyrosine-hydroxylase labeled structures in the late prenatal period is the increase in detectable immunoreactivity in bundles of axons and in terminal aborizations. The orderly appearance of tyrosine hydroxylase-labeled axons in the neostriatum and cortex are discussed in relation to the formation of these two contrasting regions innervated by catecholaminergic neurons.