Serotonin and 5-hydroxyindoleacetic acid concentrations in individual hypothalamic nuclei and other brain areas of rat

1984 ◽  
Vol 40 (11) ◽  
pp. 1288-1290 ◽  
Author(s):  
K. Oomagari ◽  
H. Uchimura ◽  
T. Matsumoto ◽  
H. Yokoo ◽  
M. Hirano ◽  
...  
Keyword(s):  
Brain Areas ◽  
Hypothalamic Nuclei ◽  
Hydroxyindoleacetic Acid

scholarly journals Changes of serotonin and 5-hydroxyindoleacetic acid content in the discrete brain areas in rats by immobilization

1978 ◽  
Vol 28 ◽  
pp. 54
Author(s):  
Masatoshi Tanaka ◽  
Yasuko Kohno ◽  
Ryoichi Nakagawa ◽  
Tadashi Nishikawa ◽  
Kumiko Matsuo ◽  
...  
Keyword(s):  
Acid Content ◽  
Brain Areas ◽  
Hydroxyindoleacetic Acid

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.

Monoamine Mechanisms in Chronic Schizophrenia: Post-Mortem Neurochemical Findings

1979 ◽  
Vol 134 (3) ◽  
pp. 249-256 ◽  
Author(s):  
T. J. Crow ◽  
H. F. Baker ◽  
A. J. Cross ◽  
M. H. Joseph ◽  
R. Lofthouse ◽  
...  
Keyword(s):  
Monoamine Oxidase ◽  
Corpus Striatum ◽  
Chronic Schizophrenia ◽  
Monoamine Oxidase Activity ◽  
Brain Areas ◽  
Direct Support ◽  
Metabolite Concentrations ◽  
Hydroxyindoleacetic Acid ◽  
Monoamine Metabolite ◽  
The Brain

SummaryDopamine and its metabolites homovanillic acid and dihydroxyphenylacetic acid, noradrenaline, serotonin and its metabolite 5-hydroxyindoleacetic acid, and tryptophan and its metabolite kynurenine have been assayed in 9 schizophrenic and 10 control brains, together with the monoamine-related enzymes tyrosine hydroxylase monoamine oxidase, dopamine-β-hydroxylase, and catechol-o-methyltransferase. In schizophrenic brains dopamine, noradrenaline and serotonin were significantly increased in some areas of corpus striatum, but there were no significant changes in enzyme activity or monoamine metabolite concentrations in any of the brain areas examined. The findings are not consistent with theories that serotonin or noradrenaline stores are grossly depleted or noradrenaline neurones have degenerated, or that monoamine oxidase activity is abnormal, in schizophrenia, and provide no direct support for the hypothesis that dopamine neurones are overactive.

Changes in Brain Monoaminergic Neurotransmitter Concentrations in Rat after Intracerebroventricular Injection of Streptozotocin

1992 ◽  
Vol 12 (1) ◽  
pp. 103-109 ◽  
Author(s):  
Andreas Ding ◽  
Roger Nitsch ◽  
Siegfried Hoyer
Keyword(s):  
Frontal Cortex ◽  
Electrochemical Detection ◽  
Entorhinal Cortex ◽  
Turnover Rate ◽  
Brain Metabolism ◽  
Intracerebroventricular Injection ◽  
Brain Areas ◽  
Tissue Concentrations ◽  
Hydroxyindoleacetic Acid ◽  
Monoaminergic Neurotransmitter

The tissue concentrations of the monoaminergic neurotransmitters noradrenaline (NA), dopamine, and serotonin (5-HT) and of their major metabolites were measured by HPLC and electrochemical detection in several rat brain areas after intracerebroventricular injection of streptozotocin (STZ). NA levels were found to be decreased in the frontal cortex by 14%, in the entorhinal cortex by 18%, and in the striatum by 38%. In the entorhinal cortex, 5-HT levels were decreased by 19% and the 5-HT turnover rate, measured as the 5-hydroxyindoleacetic acid/5-HT ratio, was found to be increased by 48%. These results may be indicative of a distinct susceptibility of some neurotransmitters in certain brain areas after a more general impairment of brain metabolism by means of intracerebroventricular application of the diabetogenic compound STZ.

Synaptosomal uptake of norepinephrine and 5-hydroxytryptamine and synthesis of catecholamines during benzodiazepine treatment

1978 ◽  
Vol 56 (5) ◽  
pp. 777-784 ◽  
Author(s):  
R. B. Rastogi ◽  
Y. D. Lapierre ◽  
R. L. Singhal
Keyword(s):  
Locomotor Activity ◽  
Homovanillic Acid ◽  
Single Injection ◽  
Brain Areas ◽  
Catecholamine Synthesis ◽  
Endogenous Level ◽  
Hydroxyindoleacetic Acid ◽  
Previously Treated ◽  
Low Levels ◽  
Chronic Diazepam

Administration of diazepam (10 mg/kg, sc) acutely or for 22 consecutive days decreased spontaneous locomotor activity and presumably the release of norepinephrine and dopamine as evidenced by increased levels of these amines in crude synaptosomes and low levels of their metabolites, 4-hydroxy-3-methoxyphenylglycol in brain and homovanillic acid in striatum of rats. Acute or chronic diazepam elevated the levels of synaptosomal 5-hydroxytryptamine by 21 and 50%, respectively, suggesting that the release of this indoleamine was also diminished. Whereas a single injection of diazepam failed to alter the synaptosomal uptake of 5-[3H]hydroxytryptamine or rate of synthesis of this indoleamine, repeated exposure for 22 days enhanced it by 31 and 28%, respectively. Acute diazepam treatment also enhanced 5-hydroxyindoleacetic acid levels in hypothalamus, pons–medulla, and midbrain of rats. The endogenous level of tryptophan in P2 pellet also was increased (by 117%) in chronic diazepam-treated rats. Diazepam given acutely or chronically failed to change the rate of catecholamine synthesis. However, discontinuation of diazepam for 48 h in rats previously treated for 20 days significantly increased locomotor activity and synaptosomal catecholamine synthesis above the values of 'treated' as well as normal control animals. Despite their increased synthesis, the synaptosomal levels of norepinephrine and dopamine in 'withdrawn' groups were decreased to 46 and 62%, respectively. This could presumably be due to a compensatory release of these monoamines and partly to altered uptake of norepinephrine which was diminished by 24%. Additionally, the levels of homovanillic acid in striatum and 4-hydroxy-3-methoxyphenylglycol in brain were enhanced to 196 and 193%, respectively, taking the values of chronically exposed rats as 100%. Withdrawal of rats from diazepam decreased the rate of synthesis of 5-hydroxytryptamine and the level of 5-hydroxytryptamine within the crude synaptosomes; the latter could be attributed to enhanced release and impeded uptake of this indoleamine. The view gains support from enhanced levels of the metabolite 5-hydroxyindoleacetic acid seen in several brain areas of withdrawn rats.Our data suggest that diazepam exerts its central effects on mood and behaviour by impairing the release of catecholamines and 5-hydroxytryptamine. It is also suggested that enhanced release and decreased uptake of these monoamines may, in part, be responsible for the hyperexcitability seen during the 'rebound' phase in anxious patients withdrawn from benzodiazepine therapy.

scholarly journals Lactation decreases angiotensinogen mRNA expression in the midcaudal arcuate nucleus of the rat brain

2001 ◽  
Vol 280 (4) ◽  
pp. R1169-R1176 ◽  
Author(s):  
Robert C. Speth ◽  
M. Susan Smith ◽  
Kevin L. Grove
Keyword(s):  
Receptor Binding ◽  
Dopaminergic Neurons ◽  
Arcuate Nucleus ◽  
Prolactin Secretion ◽  
Male Rat ◽  
Mrna Levels ◽  
Ang Ii ◽  
Brain Areas ◽  
Hypothalamic Nuclei

In lactating rats, ANG II receptor binding in the arcuate nucleus (ARH) and median eminence is decreased. To further evaluate brain angiotensinergic activity during lactation, we assessed angiotensinogen (AON) mRNA by in situ hybridization in forebrains of day 10or 11 postpartum lactating and diestrous rats. AON mRNA was abundantly expressed in the ARH, preoptic, suprachiasmatic, supraoptic, paraventricular, and dorsomedial hypothalamic nuclei, and other regions, similar to that reported in male rat brains. AON mRNA levels were decreased 27% in the midcaudal ARH of lactating rats but did not differ between lactating or diestrous rats in any of the other brain areas examined. Immunofluorescence for AON and glial fibrillary acidic protein or tyrosine hydroxylase confirmed that the AON immunoreactivity in the ARH was limited to astrocytes. Confocal microscopy revealed close appositions of AON-positive astrocytes to dopaminergic neurons in the ARH. The decrease in AON mRNA in the midcaudal ARH during lactation coupled with decreased ARH ANG II receptor binding suggests that lactating rats are less subject to ANG II-mediated inhibition of prolactin secretion.

Effects of acute and chronic administrations of phencyclidine on the levels of serotonin and 5-hydroxyindoleacetic acid in discrete brain areas of mouse

Life Sciences ◽  
1985 ◽  
Vol 36 (10) ◽  
pp. 939-946 ◽  
Author(s):  
Toshitaka Nabeshima ◽  
Masayuki Hiramatsu ◽  
Hiroshi Furukawa ◽  
Tsutomu Kameyama
Keyword(s):  
Brain Areas ◽  
Hydroxyindoleacetic Acid
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