Expression of tyrosine hydroxylase and vasopressin in magnocellular neurons of salt-loaded aged rats
Laboratoire de Neurobiologie des Signaux Intercellulaires, Université Pierre et Marie Curie, CNRS UMR 7101, 75252 Paris, France.Microscopy Research and Technique (Impact Factor: 1.15). 01/2002; 56(2):81-91. DOI: 10.1002/jemt.10018
Tyrosine hydroxylase (TH) is expressed in catecholaminergic neurons. However, under certain conditions it is also ectopically expressed in magnocellular neurons of the hypothalamus. To test the hypothesis that this expression of TH is related to the cellular activation of these neurons and/or to the vasopressin (VP) expression, we studied the expression of both TH and VP in control and salt-loaded aged rats. Our results demonstrate that aged rats show a marked TH expression in VP cells which is further increased by osmotic stimulation in the absence of increase in VP synthesis in the supraoptic nucleus. The presence of TH-immunopositive dendritic swellings in the ventral part of this nucleus reveals the high state of plasticity of these neurons. Furthermore, the lack of several actors of catecholamine biosynthesis in these neurons suggests a different role for TH. This study further demonstrates an ectopic expression of TH in hypothalamic neurons of aged rats and a TH expression linked to the activation of VP neurons but unrelated to VP synthesis.
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ABSTRACT: During the last stages of neuronal maturation, tyrosine hydroxylase is transiently expressed in the absence of the other catecholamine-synthesizing enzymes. We show here that it is expressed in rat spiral ganglion neurons between postnatal days 8 and 20, with a peak of expression at postnatal day 12. These tyrosine hydroxylase-immunoreactive neurons did not display aromatic amino acid decarboxylase- or dopamine-beta-hydroxylase-immunoreactivities, ruling out the possibilities of dopamine or noradrenaline synthesis. They also did not display peripherin- or intense neurofilament 200-kDa-immunoreactivities, two indicators of type II primary auditory neurons. Tyrosine hydroxylase-immunoreactive dendrites were seen in synaptic contact with the inner hair cells and expressed the GluR2 subunit of alpha-amino-3-hydroxy-5-methyl-4-isoxazole propionic acid receptors, further confirming the type I nature of the neurons transiently expressing the enzyme. The end of the tyrosine hydroxylase expression was not due to cell death because the immunoreactive neurons did not show TUNEL-labelled nuclei. Finally, all the type I neurons expressed the tyrosine hydroxylase mRNA at postnatal day 12, suggesting that the expression of the enzyme is a maturational step common to all these neurons and that the expression of the protein is not synchronized. Because the period of transient expression of tyrosine hydroxylase in type I neurons parallels the periods of maturation of evoked exocytosis in inner hair cells and of appearance and maturation of the cochlear potentials, we propose that the expression of the enzyme indicates the onset of hearing in individual type I primary auditory neurons. This enzyme expression could rely on a Ca2+ activation of its encoding gene subsequent to a sudden and massive Ca2+ entry through voltage-activated Ca2+ channels.
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ABSTRACT: Hypoosmolality produces a dramatic inhibition of vasopressin (VP) and oxytocin gene expression in the supraoptic nucleus (SON). This study examines the effect of sustained hypoosmolality on global gene expression in the oxytocin and VP magnocellular neurons of the hypothalamo-neurohypophysial system, to identify genes associated with the magnocellular neuron's adaptation to this physiological condition. Using laser microdissection of the SON, T7-based linear amplification of its RNA, and a 35,319-element cDNA microarray, we compare gene expression profiles between SONs in normoosmolar (control), 1-desamino-[8-D-arginine]-VP-treated normoosmolar, and hypoosmolar rats. We found 4959 genes with statistically significant differences in expression between normosmolar control and the hypoosmolar SONs, with 1564 of these differing in expression by more than 2-fold. These genes serve a wide variety of functions, and most were up-regulated in gene expression in hypoosmolar compared with control SONs. Of these, 90 were preferentially expressed in the SON, and 44 coded for transcription-related factors, of which 15 genes were down-regulated and 29 genes were up-regulated in the hypoosmolar rat SONs. None of these transcription-related factor genes significantly changed in expression after sustained 1-desamino-[8-D-arginine]-VP-treatment alone, indicating that these changes were associated with the hypoosmolar state and not due solely to a decreased activity in the SON. Quantitative in situ hybridization histochemistry was selectively used to confirm and extend these microarray observations. These results indicate that the hypoosmolar state is accompanied by a global, but selective, increase in expression of a wide variety of regulatory genes in the SON.
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ABSTRACT: Besides the monoaminergic neurons possessing the whole set of the enzymes of monoamine synthesis from the precursor amino acid and the monoamine membrane transporter, the neurons partly expressing monoaminergic phenotype, one of the enzymes of monoamine synthesis and/or monoamine membrane transporter, have been discovered. The monoenzymatic neurons are widely distributed through the brain being even more numerous than monoaminergic neurons suggesting their important functional role. Most numerous monoenzymatic neurons express individual enzymes of dopamine (DA), tyrosine hydroxylase (TH) or aromatic L-amino acid decarboxylase (AADC). TH is enzymatically active in most monoenzymatic neurons converting L-tyrosine to L-DOPA. AADC is enzymatically active in all studied monoenzymatic neurons converting extracellular L-dihydroxyphenylalanine (L-DOPA) or 5-hydroxytryptophan captured from the extracellular space, to DA or serotonin, respectively. Monoenzymatic neurons expressing complementary enzymes of the DA synthetic pathway synthesize this neurotransmitter in cooperation. The cooperative synthesis of monoamines by non-monoaminergic neurons is believed to be a compensatory reaction under the functional insufficiency of monoaminergic neurons. In addition to monoenzymatic neurons, less numerous non-monoaminergic neurons expressing the serotonin membrane transporter but lacking all the enzymes or only rate-limiting enzymes of monoamine synthesis have been discovered. Although the functional significance of these neurons remains uncertain, they most probably represent a temporal store of serotonin captured within the brain either from the intercellular space or the cerebrospinal fluid. Thus, a substantial number of the brain neurons express partly the monoaminergic phenotype, probably, serving to compensate the functional deficiency of monoaminergic neurons.
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