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F Hery

Publications and source records attributed to F Hery.

At least 37 records · Page 2Linked to original sources
PubMed1984

In vitro 3H-serotonin (5-HT) synthesis and release in BALBc and C57BL mice. II. Cell body areas.

"In vitro" 3H-5-HT and 3H-5-HIAA, newly synthesized from 3H-TRP, are measured in the brainstem, the anterior raphe nuclei and the locus coeruleus of C57BL and BALBc mice. As found for the caudate nucleus and the hippocampus, higher synthesis and release are determined in C57BL than in BALBc, for the locus coeruleus and more globally, for the brainstem. But these differences disappear when the study is carried on the raphe dorsalis and the raphe centralis nuclei. Therefore the serotonergic activity could be independently regulated at the level of cell bodies and at those of terminals. However, the 5-HT metabolism of NRD of BALBc mice could be submitted to a specific autoinhibition which could explain a lower 5-HT synthesis and release at the corresponding terminal level, compared to C57BL.

Animals↗
PubMed1982

In vivo release of serotonin in two raphe nuclei (raphe dorsalis and magnus) of the cat.

The release of 3H-serotonin (3H-5-HT) endogenously synthesized from 3H-tryptophan was estimated in both dorsalis and magnus (MRN) raphe nuclei of anaesthetized "encéphale isolé" cats, by using push-pull cannulae. Resting steady state in the release of 3H-5-HT was observed 30 min after the beginning of superfusion with L-3H-tryptophan. The amounts of 3H-5-HT released in the DRN and the MRN are much greater than those measured simultaneously in the caudate nucleus. A marked increase either in the 5-HT release was seen in the presence of fluoxetine, a potent reuptake blocker of 5-HT, or during local depolarization with potassium chloride. The spontaneous release was diminished by removing Ca++ and by adding cobalt to the medium. Tetrodotoxin (TTX) decreased the 5-HT release in the DRN and, based on previously established, blocked the stimulating effect of batrachotoxin. According to the pharmacological characteristics of the monoamine dendritic release determined for dopamine in the substantia nigra [17], our results suggest that 5-HT release processes in the DRN correspond to a release from nerve endings, not from dendrites. The purpose of this study was to determine if the 5-HT released in the DRN is released from either axon terminals or dendrites. Morphological studies performed on the DRN do not consistently demonstrate the high density of serotoninergic varicosities in the DRN. In addition, two types of 5-HT axonal varicosities, characterized by their synaptic or non-synaptic junctions, are present in the brain. The concept that the quantities of 5-HT released could vary from one type compared to the other is discussed.

Animals↗
PubMed1980

Dopamine released from dendrites in the substantia nigra controls the nigral and striatal release of serotonin.

Using push--pull cannulae, the release of endogenously synthesized [3H]serotonin was estimated in both substantia nigra and caudate nuclei of 'encéphale isolé' cats. The unilateral nigral application of dopamine (10(-7) M) reduced [3H]serotonin release in ipsilateral structures whereas alpha-methylparatyrosine (10(-4) M) induced opposite effects. Both treatments decreased [3H]serotonin release in the contralateral caudate nucleus but not in the contralateral substantia nigra. As a working hypothesis it is suggested that the effects observed are related to changes in the activity of nigroraphe neurons regulated by dopamine release from dendrites of the nigrostriatal dopaminergic neurons. However it cannot yet be excluded that the local changes in [3H]serotonin release induced by the nigral application of dopamine or alpha-methylparatyrosine result from presynaptic modulation.

Animals↗
PubMed1980

Decreased convulsant potency of picrotoxin and pentetrazol and enhanced [3H]flunitrazepam cortical binding following stressful manipulations in rats.

Various stressful manipulations in rats (cold-water swim, electric foot-shock administration, imparied access to food reward) were found to reduce the convulsant potency of drugs which interfere with GABA or benzodiazepine central processes. The convulsant threshold dosages of picrotoxin (0.4 mg/ml) or pentetrazol (10 mg/ml) administered after the stress by infusion (0.2 ml/min) via a vein of the tail were enhanced. The onset of generalized seizures induced by isoniazid (800 mg/kg) or by thiosemicarbazide (64 mg/kg) i.p. was delayed after cold-water swim. However, convulsant threshold dosages of bemegride or strychnine perfused at 2 and 0.2 mg/ml respectively were not changed by stress. Cold-water swim increased the number of cortical (but not cerebellar) [3H]flunitrazepam binding sites (+ 24%) but failed to alter cortical [3H]muscimol binding. This post-stress enhancement of binding sties, although suppressed by bicuculline (10(-4) M) seems not to be dependent on GABAergic mechanisms. Indeed cold-water stress did not reduce the ability of muscimol (10(-6) and 10(-5) M) and GABA (5 x 10(-6) and 5 x 10(-5) M) to increase flunitrazepam binding. Finally, this post-stress enhancement of benzodiazepine binding was not found to be paralleled by changes in the protective effects of diazepam against picrotoxin- or pentetrazol-induced seizures.

Animals↗
PubMed1977

Daily variations of various parameters of serotonin metabolism in the rat brain. I. Circadian variations of tryptophan-5-hydroxylase in the raphe nuclei and the striatum.

Daily changes in tryptophan-5-hydroxylase (TrH) activity have been studied in six different 5-HT-containing cell groups (B3, B4, B5, B6, B7, B8,) in the brain stem of rats maintained in a regular cycle of 12 h of light and 12 h of darkness. Significant circadian alternations of TrH activity were observed in most of the raphe nuclei tested, although the changes were not identical from one structure to another. The striatum showed daily variations in TrH activity in opposite phase to the nucleus raphe dorsalis which projects specific terminals into this area. Monoamine oxidase (MAO) activity was simultaneously estimated in these nuclei but did not exhibit and significant rhythm, suggesting a specific regulation of TrH. Total protein levels were also subject to daily changes.

Animals↗
PubMed1977

Daily variations of various parameters of serotonin metabolism in the rat brain. II. Circadian variations in serum and cerebral tryptophan levels: lack of correlation with 5-HT turnover.

Rats submitted to regular 12 h cycles of light and darkness for three weeks were sacrificed at various times of the day. 5-HT, 5-HIAA and tryptophan levels were estimated in the fronto-parietal cerebral cortex. Tyrosine and free and total tryptophan levels in serum were estimated in parallel. Significant circadian variations in 5-HT and 5-HIAA levels were found in cerebral tissues. The peaks of 5-HIAA levels were dectected during the lignt and dark periods respectively, the maximal fluctuations being seen between 17.00 h and 21.00 h, two times separating the light off. Important significant circadian variations in free and total serum tryptophan levels were also observed. In both cases, the maximal levels were found during the middle of the dark phase after the peak of 5-HIAA levels. The circadian rhythm of tyrosine levels in serum was in opposite phase with that of tryptophan (free or total). The diurnal changes in tryptophan content in cerebral tissues seemed thus related to those found in serum. Taking in consideration results obtained in previous studies 16,17 carried out in similar experimental conditions, it was concluded that the parallel increase in serum free tryptophan and in tissues 5-HIAA levels seen during the night were not related to a stimulation of 5-HT turnover. Indeed 5-HT synthesis is minimal at this time16.

Amino Acids↗
PubMed1977

Characteristics of tryptophan binding in the serum of the newborn rat.

During the very first period of postnatal life, tryptophan is almost entirely free in the serum of rats. This situation is in sharp contrast with the well-known ability of serum albumin to bind the essential amino acid in the adult. Three main factors accounted for the relative lack of binding during the early postnatal life when compared to the adult: (1) the lower concentration of serum albumin, the binding protein; (2) the inhibition of binding by nonesterified fatty acids, which were at a high level in the serum of young rats until weaning, and (3) the decreased number of available binding sites for tryptophan on the defatted serum albimin, whereas the apparent association constant of tryptophan binding to serum albumin was similar in newborn and adult. Since immunological characterization of newborn and adult serum albumins did not reveal a specific fetal serum albumin, we suggest that discrete changes at the association site for tryptophan are sufficient to induce large alteration in the binding capacity of the protein. In contrast to the situation observed in adult rats, serotonin synthesis in the brain of newborn animals is therefore not dependent on the equilibrium between bound and free tryptophan in serum.

Age Factors↗
PubMed1976

In vivo release of 5-HT in the lateral ventricle of the rat: effects of 5-hydroxytryptophan and tryptophan.

The in vivo release of 5-HT was examined in the rat brain. For this purpose, the left lateral ventricle was perfused at a constant rate with an artificial CSF for several hours in animals anaesthetized with halothane. 5-HT was estimated in serial 1-h collected fractions. The amine was first isolated by adsorption on a Sephadex G-10 column and then assayed using the radioenzymatic method of Saavedra et al.37, slightly modified to improve its sensitivity. The quantity of 5-HT released spontaneously during the first hour fraction was 296 pg, it was lower (99 pg/h) in the following fractions. 5-HT released into the CSF may in great part originate from serotoninergic terminals localized in structures surrounding the ventricle. This was suggested by experiments in which exogenous [3H]5-HT or [3H]tryptophan were perfused through the lateral ventricle during a few hours. [3H]5-HT taken up or synthetized was mainly localized in structures surrounding the ventricular space. The acute injection of 5-hydroxytryptophan (100 mg/kg) induced an immediate important and long lasting increase of 5-HT release. In contrast the acute injection of tryptophan (100 mg/kg) led to a transient and moderate elevation of 5-HT release which was only detected during the second hour of perfusion. Curiously a similar pattern of transmitter release was observed following the constant intravenous infusion of the amino acid (70 mg/kg/h) except that the increase in 5-HT release was much more pronounced during the second hour than after the acute injection. Parallel experiments were made to determine the time course of the changes of free and total tryptophan levels in plasma and of those of tryptophan, 5-HT, and 5-hydroxyindoleacetic-acid (5-HIAA) in brain tissues, induced by the acute and long term administrations of tryptophan. Moreover the rate of 5-HT synthesis was estimated using the monoamine oxidase inhibition method 2 and 5 h after both tryptophan treatments in halothane anaesthetized rats. 5-HT levels and the synthesis rate of the transmitter were increased at 2 h (when both tryptophan treatments stimulated 5-HT release). Despite the presence of high tryptophan levels in plasma and tissues and of high 5-HT and 5-HIAA levels in tissues, the synthesis rate of 5-HT (as the 5-HT release) was similar to that of controls 5 h after the onset of tryptophan infusion. These results suggest that some relationships occurred between the changes in 5-HT SYNTHESIs and release after the first hour of perfusion. The absence of effects of tryptophan treatments on 5-HT release during the first hour of perfusion are also discussed.

5-Hydroxytryptophan↗
PubMed1976

The effects of quipazine on 5-HT metabolism in the rat brain.

Since quipazine is a potent 5-HT agonist in peripheral organs, its possible stimulatory effects on serotoninergic receptors in the rat brain were investigated. Quipazine administration (10 mg/kg, i.p.) induced a significant decrease in the synthesis and turnover rates of serotonin in the brain stem as well as in the forebrain. It is not likely that these changes were mediated by a negative feed-back mechanism triggered by a direct action of quipazine on central 5-HT postsynaptic receptors. Indeed, in contrast to LSD and 5-methoxy-N,N-dimethyltryptamine, this compound failed to activate the 5-HT sensitive adenylate cyclase in colliculi homogenates of newborn rats. However, quipazine exerted direct effects on serotoninergic terminals. It inhibited competitively the reuptake process in synaptosomes (Ki=1.38 X 10(-7) M) and stimulated the K+ evoked release of newly synthesized 3H-5-HT in slices of the brain stem. Injected in vivo in a dose which affected 5-HT uptake and release, quipazine did not modify MAO activity. However, this activity was non-competitively inhibited by high concentratin of the drug in vitro (Ki=3.0 X 10(-5) M). These actions are very likely indirectly responsible for the stimulation of central 5-HT receptors.

Adenylyl Cyclases↗