Steady-state Levels Of Norepinephrine Research Articles

Fluid flow and metasomatism in the genesis of the amphibolites-facies, pelite-hosted Kanmantoo copper deposit, South Australia

Daily treatment of neonatal rats with 1-triiodothyronine for 30 days increased locomotor activity as well as the synthesis and presumably, release of brain norepinephrine, dopamine and 5-hydroxytryptamine. Whereas administration of lithium carbonate (60 mg/kg) to normal rats for 10 days, beginning from the 20th day of age, produced no significant effect, this antimanic drug significantly decreased the observed increase in spontaneous locomotor activity in l-triiodothyronine-treated rats. Lithium treatment in normal rats increased the activity of striatal tyrosine hydroxylase, but produced no significant effect on the endogenous levels of norepinephrine and dopamine in several discrete brain regions examined. Lithium, enhanced deamination of catecholamines as evidenced by increased level of 3,4-dihydroxyphenylacetic acid and monoamine oxidase activity in normal rats. The activity of catechol o-methyltransferase was decreased to 82 and 59% in midbrain and crebral cortex of normal rats, respectively. Furthermore, chronic treatment with lithium increased endogenous levels of tryptophan, tryptophan hydroxylase, 5-hydroxytryptamine and its metabolite, 5-hydroxyindoleacetic acid, in normal animals. In contrast to the effects seen in normal rats, admininstration of lithium in l-triiodothyronine-treated animals significantly decreased tyrosine hydroxylase as well as dopamine and its metabolite, 3,4-dihydroxyphenylacetic acid, suggesting that this antimanic drug reduced the synthesis and turnover of dopamine. However, the steady-state levels of norepinephrine were raised in hypothalamus, pons-medulla, midbrain and striatum of lithium-treated hyperthyroid rats. As seen in normal animals, lithium in l-triidothyronine-treated rats increased trytophan, tryptophan hydroxylase and 5-hydroxytryptamine levels, but decreased the concentration of 5-hydroxyindoleacetic acid. The results show that the suppressed behavioral activity seen in lithium-treated hyperthyroid rats may be associated with decreased synthesis of norepinephrine and dopamine in the brain. Finally, the effects exerted by lithium on the brain catecholamine metabolizing system of young hyperthyroid rats were not similar to those seen in normal rats of the corresponding age group.

Alterations in catecholamine levels and turnover in discrete brain areas after food deprivation

The present study determined the levels and turnover of norepinephrine (NE), epinephrine (EPI) and dopamine (DA) in discrete brain areas of rats after 48 hr food deprivation. The steady-state levels of NE, EPI and DA in saline-treated food-deprived rats, relative to satiated rats, remained basically unchanged. However, 48 hr deprivation caused a site-selective potentiation specifically in the hypothalamic paraventricular nucleus, in the depletion of NE after α-methyl-p-tyrosine injection (IP, 200 mg/kg), indicating an increase in NE turnover. While changes in EPI turnover could not be demostrated, an apparent increase in DA turnover was detected in the perifornical lateral hypothalamus and anterior hypothalamic nucleus after deprivation, while decreased DA turnover was seen in the hypothalamic dorsomedial nucleus and caudate nucleus. These results may reflect specific functions of hypothalamic catecholamines in control of food intake.

Differential effects of chronic morphine and naloxone on opiate receptors, monoamines, and morphine-induced behaviors in preweanling rats

Rats were administered either chronic morphine, naloxone or saline from 1 to 21 days of age. At 22 days of age, animals were sacrificed and various CNS areas were assayed for specific binding of [ 3H]naloxone and steady-state levels of norepinephrine, dopamine and serotonin, as well as turnover of norepinephrine and dopamine. In addition, some animals at 22 days of age were assessed for morphine-induced changes in activity, hot-plate paw-lick latency, and rectal body temperature. Chronic naloxone treatment produced an increase in the number of ligand binding sites in hypothalamus, striatum and cortex, but did not alter monoamine systems or the efficacy of morphine. In contrast, chronic morphine treatment produced tolerance to the hypoactive and antinociceptive effects of morphine, but did not alter ligand binding or monoamine systems. These results demonstrate that developing opiate receptor systems in brain are more responsive to chronic receptor blockade than to chronic receptor activation and that an alteration in the development of opiate receptor systems does not necessarily produce a concomitant alteration in either monoamine systems or the behavioral efficacy of morphine.

EFFECTS OF ETHANOL ON CATECHOLAMINE LEVELS AND RELATED ENZYME ACTIVITIES IN DIFFERENT BRAIN REGIONS OF RATS

AbstractThe effects of ethanol on the contents of norepinephrine (NE) and dopamine (DA) and the activities of related enzymes in the various regions of rat brains with different doses and mode of administration of ethanol were investigated. In acute ethanol intoxication, steady-state levels of NE were not altered. Continuous ethanol intoxication, however, significantly reduced NE contents and tended to decrease the activity of dopamine-β-hydroxylase in the hippocampus. The decrease in NE contents became more significant during ethanol withdrawal, especially in the medulla oblongata and the striatum. DA contents were increased in the brain-stem region in all ethanol-treated rats. The increase in DA contents correlated with the increase in tyrosine hydroxylase activity. The present data suggest that the dopaminergic system may contribute to the development of physical dependence on ethanol.

Effects of ethanol on catecholamine levels and related enzyme activities in different brain regions of rats.

The effects of ethanol on the contents of norepinephrine (NE) and dopamine (DA) and the activities of related enzymes in the various regions of rat brains with different doses and mode of administration of ethanol were investigated. In acute ethanol intoxication, steady-state levels of NE were not altered. Continuous ethanol intoxication, however, significantly reduced NE contents and tended to decrease the activity of dopamine-beta-hydroxylase in the hippocampus. The decrease in NE contents became more significant during ethanol withdrawal, especially in the medulla oblongata and the striatum. DA contents were increased in the brain-stem region in all ethanol-treated rats. The increase in DA contents correlated with the increase in tyrosine hydroxylase activity. The present data suggest that the dopaminergic system may contribute to the development of physical dependence on ethanol.

Thyrotropin releasing hormone: neurochemical evidence for the potentiation of imipramine effects on the metabolism and uptake of brain catecholamines.

The effects of chronic exposure to imipramine and thyrotropin-releasing hormone, alone and in combination, have been investigated on tyrosine hydroxylase activity as well as on the levels of norepinephrine, dopamine, and their respective metabolites in certain areas of rat brain. Repeated injections of thyrotropinreleasing hormone (20 mg/kg/24h, in two equally divided doses) for 10 days increased catecholamine synthesis and release, as shown by the increased activity of tyrosine hydroxylase and the enhanced levels of metabolites, homovanillic acid, and 4-hydroxy-3-methoxyphenylglycol. Chronic thyrotropin-releasing hormone treatment altered neither the steady state levels of norepinephrine in several brain areas, nor the uptake of 3H-norepinephrine in a crude synaptosomal (P2 pellet) fraction. By contrast, daily administration of imipramine (10 mg/kg) for 10 days significantly decreased the uptake of 3H-norepinephrine in P2 pellets by 27%. Whereas the levels of brain norepinephrine and dopamine were decreased, the concentrations of homovanillic acid and 4-hydroxy-3-methoxyphenylglycol were elevated after imipramine treatment. Furthermore, chronic imipramine treatment decreased the activity of striatal tyrosine hydroxylase, probably by receptor-mediated negative feedback mechanism. When thyrotropin-releasing hormone was injected concurrently with imipramine (10 mg/kg), this tripeptide significantly potentiated the effects of imipramine on the levels of homovanillic acid and 4-hydroxy-3-methoxyphenylglycol. These findings demonstrate that whereas thyrotropin-releasing hormone elicits its rapid mood-elevating effect probably by increasing the turnover of catecholamines, imipramine acts by blocking their neuronl re-uptake. In addition, our data provide a possible neurochemical basis for the reported potentiation of tricyclic antidepressant action by thyrotropin-releasing hormone in depressed patients.

Changes in pituitary oxytocin and vasopressin during the estrous cycle and after ovarian hormones: evidence for mediation by norepinephrine.

Pituitary levels of oxytocin and vasopressin were maximal on the morning of proestrus, declined during estrus, and were lowest on metestrus in cycling female rats. Norepinephrine levels in the paraventricular nucleus were decreased on proestrus and estrus when compared with metestrus-diestrus. Norepinephrine did not vary in the supraoptic nucleus. Administration of estradiol benzoate to ovariectomized rats elevated oxytocin in the pituitary 54 hr later. This elevation was not affected by a subsequent injection of estrogen or progesterone. Estrogen priming did not affect vasopressin levels in the pituitary, but a second injection of estrogen or of progesterone 48 hr later increased vasopressin in the pituitary when measured 6 hr after the second injection. Vasopressin was decreased 30 hr after a second injection of estrogen. The ovarian hormone treatments that elevated pituitary vasopressin decreased steady state levels of norepinephrine in the paraventricular nucleus and reduced the depletion of norepinephrine after administration of the catecholamine synthesis inhibitor α-methyltyrosine, suggesting a decrease in turnover. Ovarian hormones did not affect norepinephrine in the supraoptic nucleus. The present results suggest a role for posterior pituitary hormones in reproductive processes and a role for noradrenergic mechanisms in the paraventricular nucleus in mediating the effects of ovarian steroids on pituitary vasopressin.

Effects of estrogen and progesterone on plasma gonadotropins and on catecholamine levels and turnover in discrete brain regions of ovariectomized rats

Estradiol benzoate (EB) was administered, either alone or followed 48 h later by progesterone to ovariectomized rats. Plasma gonadotropins (FSH and LH) and steady state levels of norepinephrine (NE) and dopamine (DA) in 17 individual brain nuclei were assayed. In addition, catecholamines were measured after administration of the synthesis inhibitor α-methyltyrosine (α-MT) in order to assess hormonal influences on turnover. Treatment with EB, which lowered plasma FSH and LH, reduced the depletion of NE produced by α-MT in the lateral septum, interstitial nucleus of the stria terminalis, and central gray catecholamine area, and reduced the depletion of DA in the nucleus of the tractus diagonalis. EB enhanced NE depletion in the periventricular and anterior hypothalamic nuclei, and raised steady state levels of NE in the medial amygdaloid nucleus. These effects were reversed by subsequent treatment with progesterone, which stimulated FSH and LH release. EB plus progesterone enhanced the α-MT-induced depletion of NE over that observed with EB alone in the arcuate nucleus, and similarly enhanced DA depletion in the interstitial nucleus of the stria terminalis. EB plus progesterone prevented the depletion of NE by α-MT in the paraventricular and ventromedial nuclei, and also lowered resting NE levels in the paraventricular nucleus. The results suggest that catecholamine neurons in several discrete brain regions participate in the stimulatory and inhibitory feedback effects of ovarian hormones on gonadotropin secretion, and perhaps also on the hormonal induction of sexual receptivity.

Effects of lithium chloride on norepinephrine and dopamine metabolism in the rat brain

Lithium chloride (LiCl) was injected acutely (2.4 mEq/kg and 1.2mEq/kg X 2 for 3 hr, i.p.) or subacutely (2.5 mEq/kg X 2/day for 4.5 days, i.p.) in rats, and behavioral effects, steady state levels of norepinephrine (NE), dopamine (DA) and serotonin (5HT) and the metabolism of intraventricularly administered 14C-NE and 14C-DA in the brain were investigated. Acute and subacute administratin of LiCl suppressed the spontaneous motor activity, but had no effect on the levels of NE, DA and 5HT in the brain. Acute administration of LiCl did not influence the total radioactivity and the levels of NE and its metabolites in NE metabolism, while subacute administration of LiCl increased the deaminated metabolites. In DA metabolism, the deaminated metabolites were decreased by acute administration of LiCl and the O-methylated deaminated metabolites were increased by subacute administration. From these results, it is suggested that LiCl stimulates the monoamine oxidase pathway in NE and DA metabolism and the behavioral sedative effects of LiCl are attributed to the reduced functional activity of brain NE and DA neurons.

Alterations in turnover and endogenous levels of norepinephrine in cerebral cortex following electrical stimulation and acute axotomy of cerebral noradrenergic pathways

The turnover and endogenous levels of norepinephrine (NE) in the cerebral cortex (including the hippocampus) were measured after acute axotomy and electrical stimulation of the ascending NE pathways originating from the locus coeruleus. Acute unilateral axotomy of the dorsal NE pathway induces a small increase of NE in the cerebral cortex (ipsilateral vs. contralateral) and a decreased metabolism of NE (as estimated after synthesis inhibition by α-methyl-p-tyrosine). Electrical stimulation (20 Hz) of the locus coeruleus leads to a rapid decrease of NE levels to about 60% of the controls and new steady state levels of NE were reached in 7.5 min. After terminating the stimulation, the levels of NE in the cerebral cortex returned to normal within about 30 min. Electrical stimulation (20 Hz) of the locus coeruleus, after inhibition of NE synthesis, results in a biphasic decline of NE. The first phase is ended in about 2 min (30% decrease) after stimulation, the second phase persists for at least 30 min. The rate of decline of levels of NE in the cerebral cortex in the first phase is about 10 times higher than the rate of decline of the second phase. These results indicate that the level of NE in the cerebral cortex is in part dependent on the nerve impulse flow through the adrenergic fibres and are in favor of the concept of a multiple storage form for NE in the central nerve terminals.