Effect of oestradiol-17ß on the metabolism of noradrenaline in brain slices of ovariectomized rats

1981 ◽  
Vol 98 (1) ◽  
pp. 1-7 ◽  
Author(s):  
G. Köster ◽  
H. Breuer
Keyword(s):  
Chromatographic Separation ◽  
Mandelic Acid ◽  
Competitive Inhibition ◽  
Single Injection ◽  
Brain Slices ◽  
Ovariectomized Rats ◽  
Brain Areas ◽  
Methyl Transferase ◽  
Hypothalamic Tissue ◽  
Metabolism Of Noradrenaline

Abstract. Ovariectomized rats received a single injection of 10 μg oestradiol-17β 3-benzoate; 90 min or 19 h after injection, slices of various brain areas were prepared and incubated with tritiated noradrenaline for 30 min. Methylated and non-methylated metabolites of tritiated noradrenaline were determined after chromatographic separation. Nineteen h after administration of oestradiol-17β 3-benzoate, the formation of normetanephrine, 3-methoxy 4-hydroxy phenylglycol and 3-methoxy 4-hydroxy mandelic acid was decreased (P < 0.05) in hypothalamic tissue, whereas that of 3,4-dihydroxy mandelic acid was increased (P < 0.001). In thalamus tissue a decrease of normetanephrine (P < 0.05) and an increase of 3,4-dihydroxy mandelic acid (P < 0.01) were also observed. No conclusive results were obtained with hypophyseal tissue. The present findings suggest that oestrogens reduce the methylation of noradrenaline, probably through a competitive inhibition of the catechol-O-methyl-transferase by 2-hydroxylated oestrogens.

scholarly journals ICI 182,780 Penetrates Brain and Hypothalamic Tissue and Has Functional Effects in the Brain after Systemic Dosing

Endocrinology ◽  
2008 ◽  
Vol 149 (10) ◽  
pp. 5219-5226 ◽  
Author(s):  
Peter D. Alfinito ◽  
Xiaohong Chen ◽  
James Atherton ◽  
Scott Cosmi ◽  
Darlene C. Deecher
Keyword(s):  
Body Weight ◽  
Skin Temperature ◽  
Ethinyl Estradiol ◽  
Ovariectomized Rats ◽  
Ici 182,780 ◽  
Hot Flush ◽  
Hypothalamic Tissue ◽  
Dependent Model ◽  
The Brain ◽  
Neuroendocrine Functions

Previous reports suggest the antiestrogen ICI 182,780 (ICI) does not cross the blood-brain barrier (BBB). However, this hypothesis has never been directly tested. In the present study, we tested whether ICI crosses the BBB, penetrates into brain and hypothalamic tissues, and affects known neuroendocrine functions in ovariectomized rats. Using HPLC with mass spectrometry, ICI (1.0 mg/kg·d, 3 d) was detected in plasma and brain and hypothalamic tissues for up to 24 h with maximum concentrations of 43.1 ng/ml, and 31.6 and 38.8 ng/g, respectively. To evaluate antiestrogenic effects of ICI in the brain after systemic dosing, we tested its ability to block the effect of 17 α-ethinyl estradiol (EE) (0.3 mg/kg, 8 d) on tail-skin temperature abatement in the morphine-dependent model of hot flush and on body weight change. In the morphine-dependent model, EE abated 64% of the naloxone-induced tail-skin temperature increase. ICI pretreatment (1.0, 3.0 mg/kg·d) dose dependently inhibited this effect. ICI (3.0 mg/kg·d) alone showed estrogenic-like actions, abating 30% the naloxone-induced flush. In body weight studies, EE-treated rats weighed 58.5 g less than vehicle-treated rats after 8 d dosing. This effect was partially blocked by ICI (3.0 mg/kg·d) pretreatment. Similar to EE treatment, rats receiving 1.0 or 3.0 mg/kg·d ICI alone showed little weight gain compared with vehicle-treated controls. Thus, ICI crosses the BBB, penetrates into brain and hypothalamic tissues, and has both antiestrogenic and estrogenic-like actions on neuroendocrine-related functions.

RESTORATION BY OESTRADIOL BENZOATE OF A NEURAL AND HORMONAL RHYTHM IN THE OVARIECTOMIZED RAT

1975 ◽  
Vol 64 (1) ◽  
pp. 27-35 ◽  
Author(s):  
F. R. BURNET ◽  
P. C. B. MACKINNON
Keyword(s):  
Single Injection ◽  
Time Of Day ◽  
Ovariectomized Rats ◽  
Female Rat ◽  
Functional Link ◽  
Initial Injection ◽  
Oestradiol Benzoate ◽  
Before And After ◽  
Lh Release ◽  
The Brain

SUMMARY The rate of [35S]methionine incorporation into protein in discrete cerebral areas was measured before and after the administration of oestradiol benzoate (OB) to chronically ovariectomized rats. The circadian rhythm of incorporation which is normally seen in the intact cyclic female rat was deleted by ovariectomy. A daily rhythm of incorporation reappeared, however, in all the brain areas studied 30 h after a single injection of OB (20 μg), and was still present 12 days later. The release of luteinizing hormone (LH) after administration of 20 μg OB was measured in chronically ovariectomized animals and was found to be biphasic. High levels of LH after ovariectomy were initially reduced by negative feedback, but this phase was followed 52 h later by a facilitation of LH release between 15.00 and 18.00 h. The facilitation of LH release at this time of day was still detectable 12 days after the initial injection. The evidence for a functional link between the rhythm of neural activity which is reflected by [35S]methionine incorporation, and the ability to 'time' the facilitation of LH release is discussed.

Alterations in brain dopamine and serotonin metabolism during the development of tolerance to human β-endorphin in rats

1978 ◽  
Vol 56 (6) ◽  
pp. 1067-1071 ◽  
Author(s):  
Glen R. Van Loon ◽  
Errol B. De Souza ◽  
Chul Kim
Keyword(s):  
Homovanillic Acid ◽  
Single Injection ◽  
Serotonin Release ◽  
Serotonin Metabolism ◽  
Brain Dopamine ◽  
Brain Areas ◽  
Dopamine Metabolites ◽  
Initial Injection ◽  
Hydroxyindoleacetic Acid ◽  
Development Of Tolerance

Repeated intracisternal injections of human β-endorphin lead to development of tolerance with respect to the catalepsy, analgesia, and hypothermia which are seen following a single injection. The initial injection of β-endorphin results in increases in the dopamine metabolites, 3,4-dihydroxyphenylacetic acid (DOPAC) and homovanillic acid (HVA), in neostriatum, as well as increases in the serotonin metabolite, 5-hydroxyindoleacetic acid (5-HIAA), in hypothalamus and brainstem and a decrease in 5-HIAA in hippocampus. In the present study, we report changes in metabolism of dopamine and serotonin in specific brain areas during the development of tolerance to β-endorphin. Thus, the development of tolerance to β-endorphin with respect to catalepsy, analgesia, and hypothermia may be mediated by development of tolerance to the effects of β-endorphin on brain dopamine and serotonin release.

ALTERATIONS INDUCED BY CLOMIPHENE IN THE CONCENTRATIONS OF OESTROGEN RECEPTORS IN THE UTERUS, PITUITARY GLAND AND HYPOTHALAMUS OF FEMALE RATS

1980 ◽  
Vol 87 (3) ◽  
pp. 383-392 ◽  
Author(s):  
E. Y. ADASHI ◽  
A. J. W. HSUEH ◽  
S. S. C. YEN
Keyword(s):  
Pituitary Gland ◽  
Nuclear Receptors ◽  
Single Injection ◽  
Clomiphene Citrate ◽  
Female Rats ◽  
Ovariectomized Rats ◽  
Oestrogen Receptors ◽  
Prolonged Retention

Alterations in the concentrations of oestrogen receptors in the uterus, pituitary gland and hypothalamus during the 2 weeks following a single administration of clomiphene citrate (Clomid) to immature, bilaterally ovariectomized rats were investigated. Examination of the uterine wet weight at 1, 7 and 14 days following a single injection of Clomid (100 μg, 250 μg or 10 mg) indicated significant time- and dose-related increments from a control value of 45 ± 2 (s.e.m.) mg to a maximum of 123 ± 3 mg (250 μg dose at 14 days). In contrast, a single injection of oestradiol led to a transient increase in the uterine weight on day 1 to 94 ± 6 mg, but was without effect by days 7 and 14. Analysis of the uterine DNA content 7 and 14 days after treatment with Clomid revealed significant increments from control values of 390 ± 10 μg to a high level of 558 ± 8 μg (10 mg dose at 7 days). There was a transient retention of nuclear oestrogen receptors and rapid replenishment of cytoplasmic oestrogen receptors in less than 24 h in the uteri of animals treated with oestradiol (25 μg), but determinations of receptor content in Clomid-treated animals revealed prolonged retention of nuclear receptors and delayed replenishment of cytoplasmic receptors. The duration and extent of retention of nuclear receptors and depletion of cytoplasmic receptors after treatment with Clomid were found to be dose-dependent. Fourteen days after Clomid treatment, levels of oestrogen receptors in nuclei from the uterus were still raised in all treatment groups, whereas replenishment of cytoplasmic receptors was complete in animals treated with the lower doses (100 and 250 μg) of Clomid. A single injection of Clomid (250 μg) induced similar prolonged retention of nuclear receptors and delayed depletion of cytoplasmic receptors in pituitary tissue. In contrast, changes in the content of oestrogen receptors in the hypothalamus following Clomid treatment were minimal. The limited effect of Clomid on hypothalamic tissue may mean that the pituitary gland is a more important target for this compound than is the hypothalamus. The findings have confirmed earlier reports on the long-term uterotrophic effect of Clomid and have suggested that under these long-term, in-vivo conditions, Clomid acts in the uterus and pituitary gland as a long-acting oestrogen characterized by prolonged retention of oestrogen receptors in the nucleus and delayed, but otherwise effective, replenishment of the oestrogen receptors in the cytoplasm.

Astrocytic iNOS-Dependent Enhancement of Synaptic Release in Mouse Neocortex

2010 ◽  
Vol 103 (3) ◽  
pp. 1322-1328 ◽  
Author(s):  
Yossi Buskila ◽  
Yael Amitai
Keyword(s):  
Pyramidal Neurons ◽  
Brain Slices ◽  
Selective Inhibition ◽  
Inhibitory Neurons ◽  
Small Subset ◽  
Excitatory Synapses ◽  
Brain Areas ◽  
Synaptic Release ◽  
Cellular Source ◽  
Inos Inhibition

Nitric oxide (NO) has been recognized as an atypical neuronal messenger affecting synaptic transmission, but its cellular source has remained unresolved as the neuronal NO synthase isoform (nNOS) in brain areas such as the neocortex is expressed only by a small subset of inhibitory neurons. The involvement of the glial NOS isoform (iNOS) in modulating neuronal activity has been largely ignored because it has been accepted that this enzyme is regulated by gene induction following detrimental stimuli. Using acute brain slices from mouse neocortex and electrophysiology, we found that selective inhibition of iNOS reduced both spontaneous and evoked synaptic release. Moreover, iNOS inhibition partially prevented and reversed the potentiation of excitatory synapses in layer 2/3 pyramidal neurons. NOS enzymatic assay confirmed a small but reliable Ca2+-independent activity fraction, consistent with the existence of functioning iNOS in the tissue. Together these data point to astrocytes as a source for the nitrosative regulation of synaptic release in the neocortex.

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