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Query: UMLS:C0009443 (cold)
 92,137 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A single exposure to a severe stressor (either cold swim or inescapable shock) impairs subsequent performance in a shuttle avoidance-escape task (1), a deficit attributed to reduction in brain noradrenergic activity produced by these stressors. In the present paper, two experiments are described which examine how repeated exposure to such stressors affects (a) shuttle avoidance-escape performance (Experiment 1), and (b) aspects of brain norepinephrine metabolism (Experiment 2). Experiment 1 showed that, whereas subjects receiving the single exposure to cold swim or shock showed a large avoidance-escape deficit, subjects that received repeated exposure to these stressors for 14 days performed similarly to the control group that received no stressor. Experiment 2 showed that, whereas subjects that received one session of the inescapable shock stressor showed a lower level of norepinephrine in hypothalamus and cortex than did subjects that received no shock, subjects that received repeated exposure to inescapable shock or cold swim showed neurochemical "habituation." Subjects that received repeated shock showed elevated tyrosine hydroxylase activity and no depletion of norepinephrine level, and both repeated shock and cold swim caused a decrease in uptake of 3H-norepinephrine by slices of cortex in vitro. Thus, it is concluded that the behavioral and neurochemical changes that were observed after the stressful conditions studied are consistent with the hypothesis that changes in avoidance-escape responding following exposure to these stressful events are due to changes in brain noradrenergic activity.
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PMID:Effects of chronic exposure to stressors on avoidance-escape behavior and on brain norepinephrine. 0 Jul 11

When rats were exposed to immobilized cold stress, adrenaline content in the adrenal gland as well as noradrenaline content in the brain stem were reduced drastically, while noradrenaline content in the atria was not altered by the application of stress. Oral administrations of taurine (4-7 g/kg/day, for 3 days) prevented the stress-induced decline of adrenaline in the adrenal gland and this preventive effect could not be duplicated by the administration of L-isoleucine or DL-methionine. In hypophysectomized rats, the stress also induced a significant fall in adrenaline content of the adrenal gland, however taurine administration did not show significant preventive effects on the decline in adrenal catecholamines. The immobilized cold stress induced a significant increase in blood sugar and this increase was antagonized by pretreatment with taurine. Taurine had no significant effects on the stress-induced increase in the activity of adrenal tyrosine hydroxylase and the turnover rate of adrenaline in the adrenal gland measured by the rate of decline of this amine following alpha-methyl-tyrosine administration. The administration of taurine, in both in vivo and in vitro, inhibited the release of adrenaline from adrenal medullary granules, but that of dopamine-beta-hydroxylase was not significantly affected. The stress-induced elevation of the blood level of corticosterone was not affected by taurine administration. These findings indicate that taurine antagonizes the stress-induced elevation of blood sugar by reducing adrenaline output from the adrenal gland. The regulatory mechanism most likly involves the inhibition of adrenaline release from adrenal medullary granules, possibly by stabilizing the membrane of the granules.
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PMID:Effect of taurine on alteration in adrenal functions induced by stress. 0 14

Norepinephrine turnover rates and tyrosine hydroxylase activities were determined in the interscapular brown fat pad of the rat during cold acclimation, hyperthyroxinism, and after thyroidectomy. Rats were cold acclimated by placement in a cold room, one rat to a cage, for a period of 6 wk. Hyperthyroxinism was induced by daily subcutaneous injections of L-thyroxine (1 mg/kg) for 6 days. Norepinephrine turnover rate and enzyme activity were determined at the end of each experimental period and at 8 wk after thyroidectomy. The rate of norepinephrine turnover increased during cold acclimation and hyperthyroxinism and decreased after thyroidectomy. Cold acclimation resulted in a significant increase in tyrosine hydroxylase activity, whereas no significant effect on enzyme activity was observed in hyperthyroxinism or after thyroidectomy. None of the conditions produced a change compared to controls in the apparent Km of tyrosine hydroxylase for L-tyrosine. Cold acclimation resulted in a significant decrease in the apparent Km of tyrosine hydroxylase for pterin cofactor, whereas thyroxine treatment and thyroidectomy had no effect.
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PMID:Thyroid cold acclimation influences on norepinephrine metabolism in brown fat. 1 13

Since thyroid hormones influence urinary excretion of catecholamines after exposure to cold, the effects of hyper- and hypo-thyroidism on adrenal tyrosine hydroxylase (TH) (EC 1.14.16.2), phenylethanolamine-N-methyl transferase (PNMT) (EC 2.1.1.28), and serum dopamine-beta-hydroxylase (DbetaH) (EC 1.14.17.1) of rats of 23 and 4 degrees C were studied. TH changes resembled the urinary excretion pattern at 4 degrees C in being higher after 8 days than after 1 day of exposure, and in declining as acclimation occurred. At 23 degrees C, TH activity of hypothyroid rats was significantly higher than in euthyroid or hyperthyroid animals, and after 1 day at 4 degrees C the value increased even more. While in the hypothyroid animals at 4 degrees C the concentration of adrenal catecholamines was less, the epinephrine to norepinephrine ratio was higher than at 23 degrees C. Very high TH activity with a decline in catecholamine concentration suggests that the capacity of TH had been exceeded. PNMT activity was significantly elevated in this group. TH activity was not decreased in the hyperthyroid group at 23 degrees C, and was increased after 8 days at 4 degrees C, suggesting that circulating thyroid hormones have no direct inhibitory effect on TH. Serum DbetaH was elevated after exposure to 4 degrees C, regardless of thyroid hormonal status. The activation of adrenal TH in hypothyroid rats at 23 degrees C and of TH, PNMT, and serum DbetaH at 4 degrees C is probably the result of increased activity of the sympathetic nervous system.
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PMID:Influence of cold exposure and thyroid hormones on regulation of adrenal catecholamines. 2 Feb 13

Tyrosine hydroxylase (TH) and phenylethanolamine-N-methyltransferase (PNMT) activities were assayed in adrenal glands of the following groups of the Alaskan red-backed vole (Clethrionomys rutilus dawsoni): 1) laboratory reared at 20 degrees C and 2) exposed to 5 degrees C for 1, 3, 7, and 28 days; 3) wild, summer acclimatized; 4) wild, fall acclimatized; and 5) wild, winter acclimatized. TH activity in laboratory-acclimated voles exposed to 5 degrees C was increased by 2 times after 3 days and remained elevated after 28 days. PNMT activity in these same voles was increased after 7 days and also remained elevated after 28 days of cold exposure. In wild-acclimatized voles TH activity and PNMT activity in summer were equivalent to levels in 28-day cold-acclimated laboratory voles. In fall, TH activity was increased to 2.5 times the summer value. It decreased by midwinter, but remained elevated above the summer level. In contrast, PNMT activity appeared unchanged from summer through fall and winter. Pregnant summer voles had markedly increased TH activity. Adrenal norepinephrine and epinephrine did not change significantly with cold acclimation or seasonal acclimatization. Thus, acclimatization of wild voles to fall and winter conditions involved aquisition of a greater capacity to synthesize adrenal catecholamines than that produced by exposing laboratory-reared voles to an extended period of cold.
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PMID:Catecholamine-synthesizing enzymes in adrenals of seasonally acclimatized voles. 2 32

Treatments that increase the release of acetylcholine from the splanchnic nerve have previously been shown to induce the enzyme tyrosine hydroxylase in adrenal chromaffin cells. Such treatments include the systemic administration of the drugs phenoxybenzamine and 6-hydroxydopamine, insulin-induced hypoglycemia, and prolonged exposure to cold. We have reported that the administration of choline also induces the adrenal enzyme and have suggested that the mechanism of this induction involves an increase in the amount of acetylcholine released each time the splanchnic nerve fires. In the present studies, rats received both choline and one of the above treatments. Choline caused an augmentation of the adrenomedullary response to each of the treatments, but it had no apparent effect on a presynaptic enzyme, choline acetyltransferase. These observations strongly support the view that choline availability determines both the amount of acetylcholine present in nerve terminals and the amount liberated when cholinergic neurons fire.
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PMID:Enhancement by choline of the induction of adrenal tyrosine hydroxylase by phenoxybenzamine, 6-hydroxydopamine, insulin or exposure to cold. 2 31

The cellular localization of the enzymes tyrosine hydroxylase (TH), aromatic amino-acid decarboxylase (or dopa decarboxylase, DDC), dopamine beta-hydroxylase (DBH) and phenylethanolamine N-methyltransferase (PNMT) in the adrenal medulla of adult rats and rat fetuses (14th, 17th, 18th, 19th and 21st day) was examined. In the prenatal stages the medullary blastema and an adjacent part of the primitive sympathetic trunk were also investigated. Tissues were fixed in ice-cold 4% paraformaldehyde in 0.1 M phosphate buffer (pH 7.2). Cryostat sections (10 micron in thickness) were stained by the indirect immunofluorescence technique. Rabbit antibodies to TH (isolated from human pheochromocytoma), DDC, DBH and PNMT (the latter three isolated from bovine adrenal medulla) were used. Sections incubated with serum of non-immunized rabbits were used as controls. In the adult adrenal medulla, two cell types can be distinguished. One cell type contains only TH, DDC and DBH. The other cell type contains PNMT in addition. It is concluded that these cells correspond to the noradrenaline-(NA-) and adrenaline- (A-)storing cells respectively. In all prenatal stages TH, DDC and DBH are found in the primitive sympathetic trunk, in the medullary blastema, and in the medullary cells which have migrated into the cortical "anlage". PNMT is observed for the first time on the 18th day. Moreover, PNMT could only be demonstrated inside the adrenal gland. From these observations it is concluded that the capacity to synthesize NA is developed even before the "medullary" cells have reached the cortical "anlage". On the contrary, the capacity to synthesize A seems to be acquired only after this contact is established. The hypothesis is put forward that this phenomenon might indicate the induction of PNMT by glucocorticoids secreted by the fetal cortex.
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PMID:Appearance of tyrosine hydroxylase, aromatic amino-acid decarboxylase, dopamine beta-hydroxylase and phenylethanolamine N-methyltransferase during the ontogenesis of the adrenal medulla: an immunohistochemical study in the rat. 4 Jul

1. We utilized the induction of tyrosine hydroxylase, a catecholamine-synthesizing enzyme, in sympathetic ganglia and adrenal medullae to explore the central and peripheral mechanisms through which choline, various environmental stresses, and drugs that alter blood pressure or central neurotransmission affect various portions of the sympathetic nervous system. Animals received each treatment chronically, and enzyme activity was measured in the superior cervical, stellate, and coeliac ganglia and in the adrenal medullae.2. Choline administration increased tyrosine hydroxylase activity in all four tissues, probably by increasing the release of acetylcholine from preganglionic sympathetic neurones that synapse on catecholamine-producing ganglion and chromaffin cells; carbachol and nicotine had similar effects.3. Insulin enhanced tyrosine hydroxylase activity primarily in the coeliac ganglion and the adrenal medullae, but not in the superior cervical ganglia.4. Reserpine and phenoxybenzamine increased the activity of the enzyme in all four tissues.5. Prolonged exposure to a cold environment increased enzyme activity in all four tissues, but especially in the stellate and coeliac ganglia; forced swimming affected tyrosine hydroxylase only in these two ganglia.6. Several drugs known to modify central neurotransmission were found to increase tyrosine hydroxylase activity in some portions of the sympathetic nervous system but not in others. 5,7-Dihydroxytryptamine, which destroys terminals of serotoninergic neurones, enhanced enzyme activity in all four tissues, but primarily in the coeliac ganglion and adrenal medullae. ET-495 (a dopaminergic agonist), D-amphetamine, and morphine induced tyrosine hydroxylase activity in the adrenal medullae and the coeliac ganglion, but not in the superior cervical ganglia. Oxotremorine, a centrally acting muscarinic agonist, increased tyrosine hydroxylase activity only in the adrenal medullae; its effect was not blocked by methylatropine, a peripheral muscarinic blocker.7. These data indicate that specific neurones in the central nervous system, which utilize specific neurotransmitters and which are differentially affected by drugs and environmental inputs, selectively influence the outflows through the various zones of the sympathetic nervous system.
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PMID:Selective response of rat peripheral sympathetic nervous system to various stimuli. 4 Oct 93

Immunofluorescence specific for tyrosine hydroxylase (TH) or dopamine-beta-hydroxylase (DBH) was accentuated in both proximal and distal segments of the sciatic nerve after ligation. Estimations of the enzyme activities confirmed the above results. Mean axoplasmic flow rates of TH and DBH in bullfrog sciatic nerve were found to be 8 and 123 mm/day, respectively. They were decreased by colchicine or by cold temperatures (4 degrees C).
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PMID:Immunofluorescent and biochemical studies on tyrosine hydroxylase and dopamine-beta-hydroxylase of the bullfrog sciatic nerves. 8 31

Turnovers of dopamine (DA), norepinephrine (NE), epinephrine (E), and 5-hydroxytryptamine (5-HT) were determined in the brains of male turkeys during acute, chronic, and posttemperature stress. Changes induced in the depletion of endogenous monoamine levels 6 h after tyrosine hydroxylase or tryptophan hydroxylase inhibitions were regarded as changes in turnovers. High or low ambient temperature had no effect on brain DA turnover, whether the temperature stress was acute (6 h) or chronic (5 wk). Brain NE turnover increased upon acute exposure to either a cold (5 degrees C) or warm (32 degrees C) environment. Chronic exposure (5 wk) to such temperatures reduced significantly (P less than 0.001) the elevated NE turnover. The central E and 5-HT turnovers of birds kept at 32 degrees C for 6 h decreased and increased, respectively, whereas determination of E and 5-HT of birds kept at 5 degrees C showed an opposite pattern. Five weeks of continuous exposure to high and low environmental temperatures did not alter the changes in E and 5-HT turnovers from those observed during acute stress. Exposure of heat- or cold-reared turkeys to 24 degrees C reversed the changes in E and 5-HT turnovers. Thus the results indicated an increase in NE turnover only during acute exposure to thermal stress. However, the changes in E and 5-HT turnovers persisted during chronic exposure.
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PMID:Brain indole and catecholamines of turkeys during exposure to temperature stress. 13 76


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