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Results for “TYROSINE DECARBOXYLASE”

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At least 1,261 records · Page 70Linked to original sources
PubMed1977

The effect of chronic ethanol treatment on behaviour and central monoamines in the rat.

Rats weaned at 16 days of age were treated with various ethanol concentrations (8--24% w/v) for 270 days. The effect of the chronic ethanol treatment on the growth rate, the diurnal pattern of drinking, the open field activity, and the conditioned avoidance acquisition and retention of the rats were studied. Termination of the chronic ethanol administration caused two types of withdrawal syndromes. The first, an acute withdrawal syndrome was observed within 12 h after the discontinuation of the ethanol treatment and was characterized by extreme hyperexcitability. The second, a delayed withdrawal syndrome was characterized by a more coordinated behavioural stimulation and developed first after about 3 days after the discontinuation of the ethanol treatment. Biochemically, the latter withdrawal syndrome was accompanied by an increased rate of tyrosine hydroxylation (measured as the accumulation of dopa after inhibition of aromatic amino acid decarboxylase) in the striatum and dopamine-rich limbic structures. No differences in the accumulation of 5-hydroxytryptophan were observed. Furthermore, there was an increased level of dopamine concomitant with a decreased level of noradrenaline in the limbic areas during ongoing ethanol treatment. On the 4th day after withdrawal of ethanol the endogenous levels of dopamine and noradrenaline were statistically significantly reduced in the limbic structures. The data of the present study indicate that chronic ethanol administration induces various kinds of behavioural changes and that these changes at least partially are mediated via central catecholamine mechanisms.

Animals↗
PubMed1985

Effect of apomorphine, alpha-methylparatyrosine, haloperidol and reserpine on DOPA production in clonal cell lines (PC-12 and N1E-115).

The effect of various drugs on DOPA production in the pheochromocytoma clone PC-12 and the neuroblastoma clone N1E-115 was studied. The N1E-115 cells contain only very low amounts of dopamine due to a lack of the aromatic L-amino acid decarboxylase, whereas the PC-12 cells are rich in dopamine. alpha-Methyl-p-tyrosine and apomorphine blocked DOPA production in both cell clones. Reserpine and haloperidol reduced the intracellular dopamine in the PC-12 cells and simultaneously induced a blockade of cellular DOPA production. The released dopamine was primarily recovered as 3,4-dihydroxyphenylacetic acid indicating a release of dopamine into the cytoplasm. This transient increase of cytoplasmic dopamine by reserpine or haloperidol brings about the inhibition of DOPA production in the PC-12 cells. Our results show that the PC-12 clone especially reacts to various drugs like other in vitro systems and may serve as an additional model for studying drug effects on catecholamine biosynthesis and metabolism.

Adrenal Gland Neoplasms↗
PubMed1993

GABAergic synaptic interactions in the substantia nigra.

The substantia nigra receives a strong GABAergic input from the ipsilateral striatum and globus pallidus. Nigral GABAergic synaptic interactions have been described in the pars compacta (SNC) and pars reticulata (SNR) but not in the pars lateralis (SNL). The SNR and particularly the SNL are the nodal points of the GABAergic nigrotectal pathway. The present study analyzes the synaptic connections of GABAergic and dopaminergic neurons in each of the divisions of the substantia nigra by employing a double-labeling immunocytochemical technique at the light and electron microscope levels. Glutamic acid decarboxylase (GAD)-containing terminals make symmetrical synaptic contacts with dopaminergic neurons in the SNC and SNR. Neurons that contain GAD also receive a GABAergic input in the SNR and SNL. The proportion of GAD-GAD contacts appears to be highest in the SNL where virtually all GAD-positive terminals are found to be in synaptic contact with or apposed to GAD positive profiles. This study demonstrates a strong GABAergic input onto nigral dopaminergic neurons and GABAergic neurons in the SNR and SNL. This GABAergic influence which is ostensibly striatal or pallidal in origin is particularly prominent in relation to the SNL-mediated nigro-collicular pathway.

Animals↗
PubMed1978

Effect of pentoxifylline and aminophylline on biogenic amine metabolism of the rat brain.

In the brain of rats injected with pentoxifylline [3,7-dimethyl-1(5-oxo-hexyl)-xanthine] or aminophylline the following was observed: (i) dose-dependent increases of tryptophan and 5-hydroxyindoleacetic acid levels and of 5-hydroxytryptophan and dihydroxyphenylalanine accumulation after treatment with the decarboxylase inhibitor benserazide HCl; (ii) acceleration of norepinephrine turnover following alpha-methyl-p-tyrosine; (iii) increase of 3-methoxytyramine accumulation following pargyline. On a molar basis pentoxifylline was more potent than aminophylline in affecting brain biogenic amine metabolism.

Aminophylline↗
PubMed1982

Prenatal and postnatal ontogenesis of neurotransmitter-synthetizing enzymes and [125I]tetanus toxin binding capacity in the mouse hypothalamus.

In order to estimate the early neuronal maturation in the hypothalamus, we followed the development of 3 neurotransmitter-synthetizing enzymes (TH, GAD, ChAT) and a neuronal cell surface marker (tetanus toxin) in the hypothalamus as compared to cerebral hemispheres. This showed that TH, ChAT and GAD activities were present in both structures on the fourteenth fetal day. Yet, before birth, whereas GAD and ChAT activities remained low and followed a similar development in the 2 structures, TH activity was important and higher in hypothalamus than in brain hemispheres. After birth the activities of the 3 enzymes increased rapidly between day 5 and day 20, but their evolution in the hypothalamus always preceded that in the cerebral hemispheres. Tetanus toxin binding capacity was present on the thirteenth fetal day in the 2 structures, but during fetal life in the hypothalamus, the level of toxin binding was always higher than in the cerebral hemispheres. After birth, the toxin binding increased between day 2 and day 10 and reached adult level at the same time in both structures, around day 15. We conclude that neuronal maturation proceeds earlier in the hypothalamus than in brain hemispheres, and that the differentiation of a neuronal surface marker appears concomitantly with that of specific intraneuronal enzymes.

Animals↗
PubMed1985

Dexamethasone restores hormonal inducibility of ornithine decarboxylase in primary cultures of rat hepatocytes.

Induction of ornithine decarboxylase by various hormones was studied in quiescent primary cultures of adult rat hepatocytes maintained in a chemically defined medium. The following results were obtained: Enzyme activity rose transiently during the first day of cultivation in hormone-untreated cells. During this phase, insulin increased ornithine decarboxylase activity. Inducibility by insulin was maintained for more than 40 h only after pretreatment with 0.1 microM dexamethasone. Enzyme activity could be induced by 1 nM insulin and peaked after 7 h. Inducibility by glucagon and growth hormone required pretreatment with the glucocorticoid hormone. Ornithine decarboxylase activity was maximal 5 h after glucagon addition. Concentrations down to 0.1 nM were effective. Pretreatment with dexamethasone was most effective, when the hormone was present during the first 20 h of cultivation. The effect of the glucocorticoid during the pretreatment phase was diminished by colchicine and to a lesser extent by cytochalasine B. We suggest that part of the permissive effect of dexamethasone could be mediated by changes in the cytoskeleton and the function of hormone receptors. The fact that induction of ornithine decarboxylase was exerted by several hormones despite the absence of cell proliferation and DNA synthesis may indicate that polyamine biosynthesis has an important role in the quiescent hepatocyte.

Animals↗
PubMed1979

Methylazoxymethanol treatment of fetal rats results in abnormally dense noradrenergic innervation of neocortex.

A single injection of methylazoxymethanol in pregnant rats at 15 days of gestation results in severe cortical atrophy in the offspring. In the adult offspring, the neurochemical markers for the cortical gamma-aminobutyric acid-containing neurons are severely reduced, whereas the noradrenergic markers are minimally altered. Immunohistofluorescence microscopy demonstrates a marked increase in the density of noradrenergic axons which have an abnormal pattern of distribution in the atrophic cortex. The results suggest that the central noradrenergic neurons determine the number of axons to be formed early in brain development, but local factors in the terminal field regulate the ultimate distribution of the noradrenergic axons.

Adrenergic Fibers↗