About: Catecholamine is a(n) research topic. Over the lifetime, 10753 publication(s) have been published within this topic receiving 379056 citation(s). The topic is also known as: catecholamines.
TL;DR: A single cell clonal line which responds reversibly to nerve growth factor (NGF) has been established from a transplantable rat adrenal pheochromocytoma and should be a useful model system for neurobiological and neurochemical studies.
Abstract: A single cell clonal line which responds reversibly to nerve growth factor (NGF) has been established from a transplantable rat adrenal pheochromocytoma. This line, designated PC12, has a homogeneous and near-diploid chromosome number of 40. By 1 week's exposure to NGF, PC12 cells cease to multiply and begin to extend branching varicose processes similar to those produced by sympathetic neurons in primary cell culture. By several weeks of exposure to NGF, the PC12 processes reach 500-1000 mum in length. Removal of NGF is followed by degeneration of processes within 24 hr and by resumption of cell multiplication within 72 hr. PC12 cells grown with or without NGF contain dense core chromaffin-like granules up to 350 nm in diameter. The NGF-treated cells also contain small vesicles which accumulate in process varicosities and endings. PC12 cells synthesize and store the catecholamine neurotransmitters dopamine and norepinephrine. The levels (per mg of protein) of catecholamines and of the their synthetic enzymes in PC12 cells are comparable to or higher than those found in rat adrenals. NGF-treatment of PC12 cells results in no change in the levels of catecholamines or of their synthetic enzymes when expressed on a per cell basis, but does result in a 4- to 6-fold decrease in levels when expressed on a per mg of protein basis. PC12 cells do not synthesize epinephrine and cannot be induced to do so by treatment with dexamethasone. The PC12 cell line should be a useful model system for neurobiological and neurochemical studies.
01 Nov 1965-American Journal of Psychiatry
Abstract: The "catecholamine hypothesis of affective disorders" proposes that some, if not all, depressions are associated with an absolute or relative decrease in catecholamines, particularly norepinephrine, available at central adrenergic receptor sites. Elation, conversely, may be associated with an excess of such amines. Evidence supporting this hypothesis was reviewed. Data from pharmacological studies, mainly in animals, suggest that the actions of both major classes of antidepressant drugs are mediated through the catecholamines. The monoamine oxidase inhibitors increase brain concentrations of norepinephrine while imipramine-like agents potentiate the physiological effects of norepinephrine. Reserpine, a drug which can cause clinical depression, depletes catecholamines, but other amines may also be involved in its mechanism of action. A rigorous extrapolation from pharmacological studies to pathophysiology clearly cannot be made. Clinical studies relevant to the catecholamime hypothesis are limited and the ...
TL;DR: The results suggest that p -chlorophenylalanine may effect 5HT depletion by inhibiting the biosynthesis of this monoamine, possibly by blocking tryptophan hydroxylation.
Abstract: p -Chlorophenylalanine has been found to be a potent and selective depletor of brain serotonin (5HT) in mice, rats and dogs. Brain 5-hydroxy-3-indolylacetic acid (5HIAA) content was also depleted by the drug, but catecholamine concentrations were only slightly decreased. Peripheral stores of 5HT were also lowered. In rats, p -chlorophenylalanine reduced the normal increase in brain 5-hydroxyl-3-indolyl compounds following L-tryptophan loading (without apparently affecting tryptophan uptake into brain), completely prevented the increase in brain 5HT accompanying inhibition of monoamine oxidase by pargyline and blocked the increase in brain 5HIAA usually observed after reserpine treatment. p -Chlorophenylalanine slightly diminished the usual increase in brain 5HT in rats following 5-hydroxytryptophan (5HTP) administration, but decreased the rate of disappearance of excess 5HT and antagonized the increase in brain 5HIAA. p -Chlorophenylalanine did not inhibit monoamine oxidase or 5HTP-decarboxylase in vitro and exerted no effect on monoamine oxidase or 5HTP decarboxylase activity of rat tissues in vivo. In contrast, p -chlorophenylalanine inhibited liver tryptophan hydroxylase in vitro and strongly suppressed the tryptophan- and phenylalanine-hydroxylating capabilities of livers of rats treated with it. These results suggest that p -chlorophenylalanine may effect 5HT depletion by inhibiting the biosynthesis of this monoamine, possibly by blocking tryptophan hydroxylation. A blockade of uptake of amino acid precursor might also contribute to the effect of decreasing 5HT biosynthesis. The slow depletion (2-3 days) of brain 5HT induced by p -chlorophenylalanine suggests that an active metabolite might be formed. p -Chlorophenylpyruvic acid exerted essentially the same pharmacologic effects as the amino acid, but it cannot be ascertained at present whether it is the active metabolite because of the interconversion of α-amino acids and α-keto acids in vivo. p -Chlorophenethylamine may be excluded as the metabolite responsible for the action of p -chlorophenylalanine because of the brief duration of the amine in brain and the short lasting, nonselective decrease of both 5HT and norepinephrine produced by the amine. A study of structural variation in the phenylalanine series indicated a specific requirement of a single chlorine substituent in the para position for potent in vivo activity. Rats treated with p -chlorophenylalanine displayed few apparent signs, and certainly not sedation. p -Chlorophenylalanine did not block characteristic signs elicited by reserpine or tetrabenazine in rats. Accordingly, the central actions of reserpine and reserpine-like drugs may possibly be dissociated from both 5HT concentrations and the formation of new 5HT in brain.
04 May 1984-Science
TL;DR: Together these agents appear to determine the complex physiologic responses to a variety of stressors.
Abstract: Stress stimulates several adaptive hormonal responses. Prominent among these responses are the secretion of catecholamines from the adrenal medulla, corticosteroids from the adrenal cortex, and adrenocorticotropin from the anterior pituitary. A number of complex interactions are involved in the regulation of these hormones. Glucocorticoids regulate catecholamine biosynthesis in the adrenal medulla and catecholamines stimulate adrenocorticotropin release from the anterior pituitary. In addition, other hormones, including corticotropin-releasing factor, vasoactive intestinal peptide, and arginine vasopressin stimulate while the corticosteroids and somatostatin inhibit adrenocorticotropin secretion. Together these agents appear to determine the complex physiologic responses to a variety of stressors.
01 Jun 1966-Pharmacological Reviews
TL;DR: A good case can be made for the concept that the physiological activity of the brain dopamine is quite different from that of brain norepinephrine, although there are as yet no experiments to positively show that dopamine is a true neuro-transmitter substance in the brain.
Abstract: The whole body of evidence discussed in this article shows that brain dopamine can be regarded as a strong candidate for a physiologically active substance, regulating the functioning of some extrapyramidal centers, especially substantia nigra, striatum and pallidum. The following findings provide strong support for this view: The dopamine is mainly confined to the extrapyramidal regions mentioned; in these regions, the amine is localized in specific neurons and nerve terminals; its rate of turnover is of a high order of magnitude; is there a correlation between itsconcentration in the brain and the functional state of the extrapyramidal centers following administration of certain drugs; there is a striking relationship between some extrapyramidal disorders (drug-induced and genuine parkinsonism) and the lack of the amine in the substantia nigra, the striatum and the pallidum; and, finally, that substantia nigra exerts a direct influence on the concentration of the amine in the striatum by virtue of the nigro-striatal dopamine-containing fibers. In the extrapyramidal centers, dopamine may have either inhibitory or excitatory activity. Neurophysiological evidence obtained in different species points to a predominantly inhibitory activity of dopamine on single neurons of the brain. Evidence showing that in the retina and in the median eminence (including the pituitary stalk) dopamine may be the predominant catecholamine argues in favor of a specific function of the amine in these brain structures, although there are at present no direct findings to prove this suggestion. From the evidence discussed in this article a good case can be made for the concept that the physiological activity of the brain dopamine is quite different from that of brain norepinephrine. There are as yet., however, no experiments to positively show that dopamine is a true neuro-transmitter substance in the brain. All central dopamine effects could equally well be explained by assuming that the amine is a modifier of synaptic transmission. Therefore, in order to establish dopamine unequivocally as a central neurotransmitter substance, there is still one crucial experiment to be done: to demonstrate that upon stimulation of the relevant parts of the brain, dopamine is in fact released at synapses to exert by itself an effect on the neurons standing in synaptic relationship with the stimulated dopamine-containing terminals. It is to be hoped that we shall not have to wait too long for this experiment to be performed.