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Journal of Neuroscience, Vol 8, 3658-3669, Copyright © 1988 by Society for Neuroscience
Postmitotic, postmigrational expression of tyrosine hydroxylase in olfactory bulb dopaminergic neurons
JH McLean and MT Shipley
Department of Anatomy and Cell Biology, University of Cincinnati College of Medicine, Ohio 45267-0521.
The developmental expression of tyrosine hydroxylase (TOH) was studied in a
large, specific population of dopaminergic (DA) neurons in the main
olfactory bulb (MOB) of the rat. These DA neurons comprise an anatomically
distinctive population that has been well characterized in the adult
hamster (Davis and Macrides, 1983) and rat (Halasz et al., 1981; Baker et
al., 1983, 1984). We addressed a basic question in developmental
neurobiology: What factors regulate the expression of neuronal transmitter
phenotype during development? Olfactory bulb DA neurons are born in the
ventricular and subependymal zones and migrate through all intervening
layers to the most superficial layer in the bulb (Altman, 1969; Bayer,
1983). The time of TOH expression in these neurons was determined using
immunohistochemistry and light microscopic image-analysis techniques. The
results indicate that TOH phenotype is not expressed when the cells are
born in the subependymal zone nor during their migration to the
periglomerular region but only after they reached their final destination,
the glomerular layer. This suggests that epigenetic factors associated with
the glomeruli initiate the expression of the key transmitter synthesizing
enzyme in these neurons. Primary olfactory neurons in the nasal epithelium
project exclusively to glomeruli of the MOB; removal of this input in adult
rats (Kawano and Margolis, 1982; Baker et al., 1983, 1984), mice (Nadi et
al., 1981; Baker et al., 1983), dogs (Nadi et al., 1981), and hamsters
(Kream et al., 1984) appears to down-regulate the expression of the TOH in
periglomerular cells. The present results suggested that the input from the
primary olfactory nerve is also necessary for the initial expression of the
TOH phenotype. In support of this notion, we found that lesions of the
olfactory nerve during the first postnatal week caused a significant
reduction in the number of TOH-positive juxtaglomerular neurons in the
following weeks. Thus, the olfactory nerve appears to be necessary for both
the initiation and maintenance of TOH expression in olfactory bulb neurons.
These findings suggest that specific cell-cell interactions play a key role
in CNS neuronal transmitter phenotype regulation.(ABSTRACT TRUNCATED AT 400
WORDS)
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