Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “INDOLEACETIC ACID”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 919 records · Page 51Linked to original sources
PubMed1985

Analysis of 3-indolylacetic acid and abscisic acid by high-performance liquid chromatography and gas-liquid chromatography.

A method of analysis of 3-indolylacetic acid (IAA) and abscisic acid (ABA), allowing the simultaneous extraction of both regulators from plant material, has been developed. The method involves extraction with methanol, isolation of the acid fraction, diazomethane methylation, separation of the hormones through reverse-phase preparative high-performance liquid chromatography, and quantification of both compounds by gas-liquid chromatography. The recovery percentage at each step was monitored with radioactive compounds added at the beginning of the process. The final recovery was 70% for IAA and 96% for ABA. The method was applied to the analysis of the IAA and ABA content of stems of hazel (Corylus avellana L.).

Abscisic Acid↗
PubMed1985

Cerebrospinal fluid and plasma monoamines and their metabolites in euthymic bipolar patients.

In a search for trait markers in manic-depressive illness, we studied cerebrospinal fluid (CSF) and plasma monoamines and their metabolites in 25 lithium-treated euthymic bipolar patients (12 of whom provided unmedicated samples) and 30 normal volunteers. No group differences were found. Lithium treatment showed a trend to increase CSF hydroxy-indoleacetic acid (HIAA) (p = 0.05). Dopaminergic and serotonergic metabolites were highly correlated in the CSF of all three groups. We found no evidence of a trait marker for manic-depressive illness among CSF monoamines and their metabolites.

3,4-Dihydroxyphenylacetic Acid↗
PubMed1986

Infusion of a monoamine oxidase inhibitor into the locus coeruleus can prevent stress-induced behavioral depression.

Behavioral depression produced by exposing animals to a stressor that they cannot control (uncontrollable shock) was reversed by infusion of the monoamine oxidase (MAO) inhibitor pargyline into the locus coeruleus (LC) region of the brain stem. Following exposure to uncontrollable shock, rats were infused through bilateral cannulas implanted in the LC region with either pargyline or vehicle. At 110 min after infusion, animals were tested for behavioral activity in a swim tank. Immediately following the behavioral test, animals were sacrificed for determination of the monoamines [norepinephrine (NE), dopamine (DA), serotonin (5-HT)], as well as 5-hydroxy-indoleacetic acid (5-HIAA) in various brain regions. The results showed that animals exposed to uncontrollable shock and then infused with vehicle exhibited significantly less activity in the swim test than animals not exposed to shock and similarly infused with vehicle; thus, the usual behavioral depression following exposure to uncontrollable shock was observed. On the other hand, shocked animals infused with pargyline did not show reduced activity in the swim test. Unshocked animals infused with pargyline showed no more activity than did shocked animals infused with pargyline or unshocked animals infused with vehicle, which demonstrated that the infusion of pargyline into shocked animals did not eliminate the shock-induced depression of activity simply by generally stimulating motor activity. Measurement of the concentration of NE, DA, 5-HT, and 5-HIAA present in seven brain regions at the conclusion of the swim test showed that pargyline infusion into the LC eliminated the large depletion of NE in the LC that is normally observed after exposure to uncontrollable shock while having no effect on NE levels in the other brain regions examined. The level of 5-HT in the LC was also raised by infusion of pargyline into the LC, but again, there was no effect of pargyline infusion on 5-HT levels in any of the other brain regions. In conclusion, infusion of pargyline into the LC region of the brain eliminated both the large depletion of NE in the LC region and the behavioral depression that otherwise results from exposure of animals to uncontrollable shock.

Animals↗
PubMed1987

Obsessive-compulsive disorder: psychobiological approaches to diagnosis, treatment, and pathophysiology.

The diagnosis, treatment, and pathophysiology of obsessive-compulsive disorder (OCD) were examined in a series of studies utilizing psychobiological approaches. Putative biological markers previously reported in depression were studied in this disorder and revealed that on some measures [Dexamethasone Suppression Test and rapid eye movement (REM) latency on sleep electroencephalogram (EEG)], OCD patients resemble those with major depressive disorder (MDD), whereas on others [REM density, platelet serotonin uptake, probably platelet 3H-imipramine binding, and 5-hydroxy-indoleacetic acid (5-HIAA) in cerebral spinal fluid (CSF)] they do not. The relationship between OCD and MDD was further explored in a double-blind, randomized crossover study designed to compare the antiobsessional effects of two tricyclic antidepressants, clomipramine (CMI) and desipramine (DMI), in a nondepressed cohort of OCD patients. CMI was found to have significant antiobsessional effects in this group, whereas in the same patients, DMI lacked therapeutic effects. These results suggest that not all antidepressants are antiobsessive and that some property of CMI, such as its potent serotonergic effects, may be of pathophysiological relevance for OCD. The role of serotonin in this disorder was then tested using the pharmacological challenge strategy. A novel serotonin postsynaptic receptor (5HT-1) agonist, m-chlorophenylpiperazine (m-CPP), was administered orally (0.5 mg/kg) under double-blind, placebo-controlled conditions to OCD patients and controls. In addition, a serotonergic receptor antagonist, metergoline (4 mg), was given to a subset of OCD patients. Relative to healthy volunteers, the OCD patients became significantly more anxious, depressed, and dysphoric after m-CPP administration. Moreover, in the OCD patients, obsessive-compulsive symptoms increased markedly after m-CPP and decreased significantly following metergoline administration. These results demonstrate that agents that bind to the 5HT-1 receptor can acutely affect the symptoms of OCD patients. The striking behavioral effects of these direct postsynaptic receptor ligands and the relative specificity of clomipramine as an antiobsessional agent suggest that serotonergic neurons may play a role in the pathophysiology, as well as mediating the pharmacological reduction, of obsessional symptoms.

Adult↗
PubMed1983

Daily rhythms of serotonin metabolism in the medial hypothalamus of the chicken: effects of pinealectomy and exogenous melatonin.

Indoleamine levels in punches of the medial hypothalamus containing the suprachiasmatic nuclei (SCN) of 4-week-old cockerels were determined by HPLC-EC. Melatonin levels in punches were determined by radioimmunoassay (RIA). Daily rhythms of serotonin (5-HT) and of its metabolite 5-hydroxy-3-indoleacetic acid (5-HIAA) were observed; levels were higher at midnight than at midday. A daily rhythm with the same phase in punch melatonin content was also observed. Pinealectomy at 1 week after hatching abolished the 5-HIAA and melatonin rhythm in 4-week-old birds but did not abolish the 5-HT rhythm. Injections of melatonin (0.5 mg/kg) increased 5-HT, 5-HIAA and melatonin levels in the hypothalamic punches. These results indicate that circulating melatonin of pineal origin may act to increase 5-HT turnover and/or release in the SCN. They suggest a link between the circadian secretion of pineal melatonin and the regulation of 5-HT projections to the hypothalamus from the raphe nuclei in the brainstem of the chicken. We have previously shown that the rhythmic secretion of melatonin by the pineal is influenced by oscillators in the brain via the superior cervical ganglia. The results reported here indicate that melatonin in turn may regulate brain oscillators, suggesting a neuroendocrine loop within the avian circadian system.

Animals↗
PubMed1991

Age effects on monoamine turnover of the rat substantia nigra.

Measurement of turnover of dopamine (DA), noradrenaline (NA) and serotonin (5-hydroxytryptamine (5-HT), and their metabolites has been performed in 6- and 24-month-old rats. Dopamine synthesis in 24-month-old rats did not show any change with respect to 6-month-old rats. However, our results seem to indicate decreased DA release in 24-month-old rats. This hypothesis could be supported by the changes found in the 3-methoxytyramine (3-MT) accumulation rate after monoamine oxidase inhibition with pargyline. The turnover of NA and its main metabolite, 3-methoxy-4-hydroxyphenylglycol (MHPG) decreased in 24-month-old rats compared with 6-month-old rats. Serotonin synthesis did not change in 24-month-old rats with respect to 6-month-old rats. However, the metabolism of 5-HT quantified as turnover of 5-hydroxy-3-indoleacetic acid (5-HIAA) increased in 24-month-old rats with respect to 6-month-old rats. The monoamine oxidase B:monoamine oxidase-A ratio increased in 24-month-old rats. The significance of these changes is discussed.

3,4-Dihydroxyphenylacetic Acid↗
PubMed1996

Polyamine amides are neuroprotective in cerebellar granule cell cultures challenged with excitatory amino acids.

Primary cultures of rat cerebellar granule cells have been used to assess the potential neuroprotective effects of philanthotoxins and argiotoxin-636 (ArgTX-636). These polyamine amides are potent antagonists of ionotropic L-glutamate (L-Glu) receptors. In granule cells loaded with fluo-3, ArgTX-636 and philanthotoxin-343 (PhTX-343) antagonised increases of intracellular free calcium concentration ([Ca2+]i) that were stimulated by N-methyl-D-aspartate (NMDA). The antagonism was use-dependent. Antagonism by PhTX-343 was fully reversible, but recovery following antagonism by ArgTX-636 was slow and only partial during the time-course of an experiment. Neither compound inhibited K(+)-induced increases in [Ca2+]i. In excitotoxicity studies with cerebellar granule cells, the release of lactate dehydrogenase (LDH) and morphological observations were used to assess cell death. A 20-30 min exposure to 500 microM NMDA, 100 microM L-Glu or 500 microM kainate was sufficient to kill > 90% of the cells after 18-20 h. When added 5 min prior to, and during agonist exposure, PhTX-343 and ArgTX-636 provided total neuroprotection. ArgTX-636 was about 20-30 fold more potent than PhTX-343 against NMDA, but was approximately equipotent with PhTX-343 against a kainate challenge. Neither of the toxins showed any inherent toxicity even at 400 microM and 100 microM respectively. Some analogues of PhTX-343 are more potent, both in terms of antagonism of NMDA-stimulated increases of [Ca2+]i and neuroprotection, than PhTX-343 and ArgTX-636.

Amides↗
PubMed1975

Amantadin e tremor, a 5-hydroxytryptamine-mediated response?

Amantadine-induced tremor has been investigated using mice. Experiments with, mebanazine, reserpine, diethyldithiocarbamate, and p-chlorophenylalanine suggest that the tremorgenic action of amantadine is influenced by a balance between three putative central nervous system (CNS) transmitters: noradrenaline, dopamine and 5-hydroxytryptamine (5-HT). Drugs which reduce the concentration of the catecholamines in brain increase amantadine induced tremor. p-Chlorophenylalanine, which specifically depletes brain 5-HT, antagonises amantadine-induced tremor. An ED50 (tremor) dose of amantadine decreases the concentration of 5-hydroxy-indoleacetic acid (5-HIAA) in rat brain, particularly when this elevated due to pretreatment with 5-hydroxytryptophan. Neither inhibition of monoamine oxidase nor reduction of 5-HT-reuptake appear to be responsible for this decrease. Experiments on rat fundus suggest that amantadine increased the sensitivity of receptors to 5-HT. A similar mechanism of action in the CNS could explain both the tremor and the decrease in brain 5-HIAA. The possible relevance of these findings is discussed with respect to the known anti-Parkinson action of amantadine.

Amantadine↗
PubMed1977

Effects of mazindol and d-fenfluramine of 5-hydroxytryptamine uptake, storage and metabolism in blood platelets.

Mazindol induced a dose-related inhibition of the uptake of labelled 5-hydroxytryptamine (5-HT) by guinea pig blood platelets. It was more potent than d-fenfluramine. Mazindol and d-fenfluramine decreased 5-hydroxy-indoleacetic acid formation in intact platelets but not in sonicated ones. The inhibitory effects of both drugs appeared to the competitive in nature and were markedly reduced in platelets suspended in plasma instead of in Tyrode solution. Mazindol neither decreased the stored endogenous 5-HT nor caused efflux of the labelled amine from preloaded platelets, whereas d-fenfluramine induced a significant release of the amine. It is concluded that mazindol, like d-fenfluramine, competes with 5-HT for the same transport mechanisms at the cytoplasmic membrane level but this effect is not accompanied, as is the case with d-fenfluramine, by a concomitant release of the amine.

Animals↗
PubMed1986

d- and l-isomers of fenfluramine differ markedly in their interaction with brain serotonin and catecholamines in the rat.

Various doses of fenfluramine isomers were compared for their ability to affect monoamine levels, metabolism and synthesis in the rat brain. d-Fenfluramine was more potent than l-fenfluramine in reducing serotonin (5-HT) and 5-hydroxy-indoleacetic acid (5-HIAA) at 4 h after their administration. After decarboxylase inhibition, a low dose of d-fenfluramine (2.5 mg/kg) reduced 5-HT synthesis, assessed as 5-hydroxytryptophan (5-HTP) accumulation, in the hypotalamus and lower brain-stem only, whereas a higher dose (5 mg/kg) reduced 5-HT synthesis in all brain regions examined except the striatum. A higher dose of l-fenfluramine (10 mg/kg) was required to reduce 5-HT synthesis. Metergoline, a 5-HT antagonist, did not modify the effects of fenfluramine isomers on 5-HT synthesis. One h after its administration l-fenfluramine 5-20 mg/kg significantly increased brain 3-methoxy-4-hydroxyphenylethylene glycol sulfate (MHPG-SO4), striatal homovanillic acid (HVA) and dihydroxyphenylacetic acid (DOPAC) levels, while after 4 h only the highest dose raised HVA levels. No change of striatal HVA and DOPAC levels was seen 1 or 4 h after any dose of d-fenfluramine while the highest dose raised brain MHPG-SO4 levels. Neither l- nor d-fenfluramine changed striatal 3-methoxytyramine (3-MT) levels. The noradrenaline (NA) and dopamine (DA) levels were decreased 4 h after 10 and 20 mg/kg l-fenfluramine or 20 mg/kg d-fenfluramine. The results show that the d- and l-isomers of fenfluramine at relatively low doses have a specific action on brain 5-HT and catecholamines, respectively.(ABSTRACT TRUNCATED AT 250 WORDS)

5-Hydroxytryptophan↗
PubMed1989

Agonist activity of a novel compound, 1-[3-(3,4-methylenedioxyphenoxy)propyl]-4-phenyl piperazine (BP-554), at central 5-HT1A receptors.

We used an in vitro radioligand receptor binding assay with rat cerebral cortex, hippocampus and striatum membrane preparations to show that 1-[3-(3,4-methylenedioxyphenoxy)propyl]-4-phenyl piperazine (BP-554) had much higher affinity for 5-HT1A recognition sites than for 5-HT1-non-A, 5-HT2, benzodiazepine, dopamine D-2 and alpha 2-adrenergic recognition sites. The compound inhibited the activity of forskolin-stimulated adenylate cyclase in rat hippocampal membranes. Intraperitoneal injection of BP-554 to mice decreased the concentration of only 5-hydroxy-indoleacetic acid of the amines and their metabolites in the brain and decreased the accumulation of 5-hydroxytryptophan in the brain after decarboxylase inhibition by 3-hydroxybenzylhydrazine. Furthermore, the administration of BP-554 caused hypothermia and increased serum corticosterone levels in mice. The observed effects of BP-554 were similar to those of 8-hydroxy-2-(di-n-propylamino)tetralin. These results suggest that BP-554 acts as a selective 5-HT1A receptor agonist in vivo.

8-Hydroxy-2-(di-n-propylamino)tetralin↗
PubMed1990

Effects of calcium antagonists on biogenic amines in discrete brain areas.

Discrete brain sections were obtained from rats given i.p. verapamil, nifedipine, diltiazem or flunarizine (0, 10, 20 or 40 mg/kg). The biogenic amines and metabolites in the hypothalamus, brainstem hippocampus, striatum, thalamus-midbrain and cortex were determined by high-performance liquid chromatography with electrochemical detection. The treatments induced several changes in the levels of neurotransmitters and metabolites, displaying regional specificity and differences according to the various compounds. It was speculated that some effects could have been due to indirect actions and/or to interactions of the compounds with receptors other than the voltage-sensitive calcium channels. However blockade of these channels could account for the following effects. (a) The nifedipine-induced increases in the 5-hydroxy-3-indoleacetic acid levels and, in general, the signs of activation of the serotonergic systems. (b) The fall in the 3,4-dihydroxyphenylacetic acid levels and, in general, the signs of attenuation of dopaminergic neurotransmission induced by nifedipine, verapamil and diltiazem. (c) The fall in the norepinephrine levels induced by all the compounds studied.

Animals↗
PubMed1991

Comparison of some arthropod toxins and toxin fragments as antagonists of excitatory amino acid-induced excitation of rat spinal neurones.

Wasp and spider venom toxins, which block glutamatergic transmission at invertebrate neuromuscular junctions, have recently been shown to block transmission at glutamate-operated synapses in mammalian central nervous system. Using the technique of iontophoresis on spinal neurones in anaesthetised rats, we have compared the action of five arthropod toxins and two toxin fragments, on responses to excitatory amino acids including alpha-amino-3-hydroxy-5-methyl-4-isoxazolepropionate, kainate and N-methyl-D-aspartate (NMDA). All toxins caused greater than 70% mean reduction of non-NMDA responses. Only argiotoxin636 significantly reduced responses to NMDA. This blockade, like that induced by philanthotoxin-433 and -343, was readily reversible whereas blockade induced by Joro Spider toxin or Nephila Spider toxin was less readily reversible. Neither 2,4-dihydroxyphenylacetate nor 2,4-dihydroxyphenylacetylasparagine blocked NMDA or non-NMDA responses. It appears, therefore that small structural differences in the polyamine part of these toxin molecules give rise to different activity profiles with respect to selectivity and reversibility.

Action Potentials↗