Biomedical subjects

A Sémont

Publications and source records attributed to A Sémont.

10 recordsLinked to original sources

PubMed2000

Regulation of central corticosteroid receptors following short-term activation of serotonin transmission by 5-hydroxy-L-tryptophan or fluoxetine.

Alterations of the hypothalamic-pituitary-adrenal (HPA) axis function characterized by a decreased negative feedback capacity are often associated with affective disorders and are corrected by treatment with antidepressant drugs. To gain a better understanding of the effects of the antidepressant drug fluoxetine, a specific serotonin (5-HT) reuptake inhibitor, on central corticosteroid receptors, the effects of short-term activation of serotonin transmission on central corticosteroid receptor expression were analysed in adrenalectomized (ADX) rats either supplemented or not with corticosterone. Serotonin transmission was stimulated either by a single injection of the 5-HT precursor, 5-hydroxy-L-tryptophan (5-HTP), or by a 2-day treatment with fluoxetine. In ADX rats, administration of 5-HTP decreased hippocampal mineralocorticoid (MR) and glucocorticoid (GR) receptor numbers 24 h later, while their respective mRNAs were unchanged and these effects of 5-HTP were mediated by 5-HT2 receptors. In the hypothalamus, GR mRNAs and binding sites decreased 3 h and 24 h after 5-HTP, respectively. By contrast, fluoxetine treatment increased hippocampal MR and GR mRNAs and MR binding sites while GR number remained unchanged. In ADX rats supplemented with corticosterone, 5-HTP and fluoxetine treatment had the same effects on corticosteroid receptors compared to those observed in non supplemented ADX rats: 5-HTP decreased hippocampal MR and GR and hypothalamic GR while fluoxetine treatment increased hippocampal MR. These results show that short-term stimulation of 5-HT transmission by 5-HTP decreases hippocampal and hypothalamic corticosteroid receptor numbers through a corticosterone-independent mechanism. It is hypothesized that the delayed maximal increase in extracellular 5-HT contents after fluoxetine treatment, due to negative feedback regulations induced by the activation of 5-HT1A and 5-HT1B autoreceptors, is not the primary cause for the delayed normalization of corticosteroid receptor numbers that regulates the HPA axis functioning.

5-Hydroxytryptophan↗

PubMed2000

The effects of serotonin on glucocorticoid receptor binding in rat raphe nuclei and hippocampal cells in culture.

The raphe-hippocampal serotonin (5-HT) system is involved in the regulation of the hypothalamus-pituitary-adrenal axis. The purpose of this study was to determine and compare the roles of 5-HT in the regulation of glucocorticoid receptor (GR) binding in the raphe nuclei and in the hippocampus. The effects of 5-HT, 5-HT agonists, and the 5-HT reuptake inhibitor citalopram on GR binding sites were studied in primary cultures of the fetal raphe nuclei and the hippocampus. Exposure of hippocampal cells to 5-HT, (+/-)-2,5-dimethoxy-4-iodoamphetamine (DOI; a 5-HT2 agonist), or citalopram resulted in an increase in number of GR binding sites. The effect of DOI was blocked by ketanserin (a 5-HT2 antagonist). Specific and saturable GR binding was found in raphe cells. Exposure of raphe cells to 5-HT, (+/-)-8 hydroxy-2-(di-n-propylamino)tetralin (8-OH-DPAT; a 5-HT1A agonist), or citalopram induced a significant decrease in number of GR binding sites. The effect of 8-OH-DPAT was reversed by WAY 100135 [N-tert-butyl-3-[1-[1-(2-methoxy)phenyl]piperazinyl]-1-phenylpropiona mide; a 5-HT1A antagonist]. These results show that the regulation of GRs during fetal life is structure-dependent and involves different 5-HT receptor subtypes. Moreover, the regulation of hippocampal GRs by citalopram suggests an action of antidepressants independent of their effects on monoamines.

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

PubMed1999

Identification and role of serotonin 5-HT1A and 5-HT1B receptors in primary cultures of rat embryonic rostral raphe nucleus neurons.

Autoregulatory mechanisms affecting serotonin [5-hydroxytryptamine (5-HT)] release and synthesis during the early period of development were investigated in dissociated cell cultures raised from embryonic rostral rat rhombencephalon. The presence of 5-HT1A and 5-HT1B receptors in serotoninergic neurons was assessed using binding assays. The involvement of 5-HT1A and 5-HT1B receptors in the control of the synthesis and release of [3H]5-HT was studied using biochemical approaches with several serotoninergic receptor ligands. A mean decrease of 30% in [3H]5-HT synthesis and release was observed in the presence of 5-HT (10(-8) M), the 5-HT1A agonist 8-hydroxy-2-(di-n-propylamino)tetralin (8-OH-DPAT), the 5HT1B/1A agonist 5-methoxy-3-(1,2,5,6-tetrahydro-4-pyridinyl)-1H-indole (RU 24969), the 5-HT1B agonist 3-(1,2,5,6-tetrahydropyrid-4-yl)pyrrolo[3,2-b]pyrid-5-one (CP-93,129), and the 5-HT(1D/1B) agonist sumatriptan. Inhibition of 5-HT synthesis and release induced by 8-OH-DPAT was blocked by chiral N-tert-butyl-3-[1-[1-(2-methoxy)phenyl]piperazinyl]-1-phenylpropionam ide dihydrochloride quaternary-hydrate (WAY 100135) (10(7) M) or methyl 4-[4-[4-(1,1,3-trioxo-2H-1,2-benzoisothiazol-2-yl)butyl]-1-p iperazinyl]-1Hindole-2-carboxylate (SDZ 216-525) (10(-7)M), and that of CP-93,129 was blocked by methiothepin (10(-7) M). Paradoxically, extracellular levels of [3H]5-HT increased in the presence of 8-OH-DPAT and RU 24969 at 10(-6) M. 5-HT uptake experiments showed that these two agonists interacted with the 5-HT transporter. 5-HT1 binding sites (620 fmol/mg of protein) and 5-HT1A (482 fmol/mg of protein) and 5-HT1B (127 fmol/mg of protein) receptors were detected in 12-day in vitro cell cultures. Experiments carried out with tetrodotoxin suggested that 5-HT1A receptors are located on nerve cell bodies, whereas 5-HT1B receptors are located on the nerve terminals. We concluded that autoregulatory mechanisms involving 5-HT1A and 5-HT1B autoreceptors are functionally mature in cells from rostral raphe nuclei during the early period of development.

Animals↗

PubMed1999

Regional serotonin metabolism under basal and restraint stress conditions in the brain of transgenic mice with impaired glucocorticoid receptor function.

Transgenic (TG) mice deficient in glucocorticoid receptors (GR) were used in order to study the effects of a reduced GR function on adrenocorticotropin hormone and corticosterone plasma levels and on serotonin metabolism in different brain areas under basal resting conditions, after a 30-min restraint stress and 60 min after the end of the restraint stress. There was no difference in basal or stress-induced levels of either adrenocorticotropin hormone or corticosterone in control and TG mice, but the return of adrenocorticotropin hormone to basal values after the end of the stress was delayed in TG mice. Under basal conditions, the ratio 5-hydroxyindoleacetic acid/5-hydroxytryptamine was decreased only in the hippocampus of TG mice compared to controls. In the brain stem, the ratio 5-hydroxyindoleacetic acid/5-hydroxytryptamine increased compared to basal values after a 30-min restraint stress and values were still high 60 min after the end of the restraint stress in both control and TG mice. In the hippocampus, the ratio 5-hydroxyindoleacetic acid/5-hydroxytryptamine increased at the end of the stress and returned to basal levels 60 min later in control mice, whereas there was no change at the end of the stress but an increase 60 min later in TG mice. Finally there was no change in serotonin metabolism in the cortex, striatum or hypothalamus in either group or situation. Our results support the hypothesis of a tonic activation of serotonin turnover by corticosterone through GR in the mouse hippocampus. Moreover, stress-induced stimulation of serotonin metabolism in the brain stem and hippocampus appears to be delayed in TG mice compared to control mice. These results are particularly relevant for mood disorders such as depression where alterations of serotoninergic transmission might be secondary to an impairment of GR functions.

Adrenocorticotropic Hormone↗

PubMed1999

Eye movements during torso rotations in labyrinthine-defective subjects.

The aim of this study was to examine whether the chronic loss of vestibular function modifies perceptual and oculomotor responses during torso rotations in darkness. Subjects (4 patients with complete vestibular loss and 7 healthy volunteers) were seated on a rotating chair. Stimuli consisted of sinusoidal chair rotations (+/-30 degrees, 0.1 Hz and 0.011 Hz). We used 2 conditions: space stationary head (neck stimulation) and space stationary head and shoulders (torso stimulation). Horizontal eye deviations and slow component of eye movements were analysed. The results showed that eye movements and perception of head motion in space during neck stimulation were similar to those during torso stimulation both in normal and labyrinthine-defective (LD) subjects. During low-frequency chair rotations (0.011 Hz) all subjects perceived illusory head or head and shoulder rotation in space (as if the lower part of the body was stationary relative to the room) and shifted their gaze in the direction of illusory head rotation. In these conditions there was no significant difference in eye movements between normal and LD subjects. During higher frequency chair rotations (0.1 Hz), LD subjects had significantly larger eye deviations as well as increases in the gain of the slow component of eye movements relative to normals. In these conditions patients mostly perceived illusory head or head and shoulder rotation in space while normal subjects mainly perceived the head as stationary in space. The results indicate that 1) neck and torso rotations can evoke similar ocular responses in LD subjects, 2) the chronic loss of vestibular function modifies the representation of axial body segment motion relative to space.

Aged↗

PubMed1995

Modification of parameters in vertical optokinetic nystagmus after repeated vertical optokinetic stimulation in patients with vestibular lesions.

Eye movements were recorded in patients with unilateral and bilateral vestibular lesions after upward and downward optokinetic (OK) stimulation before and following 6 weeks' repeated exposure to OK stimulation. In control subjects there was no asymmetry between upward and downward slow-phase velocity (SPV). Before training, less subjects showed that upward and downward SPV was significantly lower than that of controls. There was no asymmetry between upward and downward SPV. After training, in unilateral cases, the values of both upward and downward SPV recovered to the control range. In bilateral cases, the downward SPV values returned to the control range, whereas the values of upward SPV exceeded the control range. The frequencies of both upward and downward OKN in controls were about 3.0 Hz. In unilateral and bilateral cases, before and after training, the OKN frequencies approximated 3.0 Hz, showing no significant differences. The recovery of the SPV in unilateral and bilateral cases after training suggests that OK stimulation acts to stabilize the body and consequently to provoke pronounced OKN, due to eye-head-body co-ordination. The asymmetry of SPV after training in bilateral cases might be a result of the lack of otolith function.

Adult↗

PubMed1995

Videonystagmoscopy: its use in the clinical vestibular laboratory.

Vestibular function of a population including labyrinthine-defective patients and a control group of age-matched normal healthy volunteers was evaluated using videonystagmoscopy. This device is made of one or two CCD infra-red cameras mounted on diving glasses and allows observation of ocular movements on a video monitor and/or recording on a videotape. Eye movements are observed after rotations in a Bárány chair and during passive head tilts. With this simple and non-invasive test, a screening of vestibular function at bedside or during ENT clinical investigations can be performed. A further study with videonystagmography to quantify these results being prepared.

Humans↗

PubMed1994

Repeated optokinetic stimulation in conditions of active standing facilitates recovery from vestibular deficits.

Successful results obtained by training sessions using optokinetic (OK) stimulations in order to rehabilitate patients with balance disorders motivated this study. The purpose of the study was to measure eye movement parameters and body stabilization during OK stimulation before and after the rehabilitation program. Two populations of patients were studied: bilateral and unilateral labyrinthine-defective patients. Before training, the OK nystagmus (OKN) showed irregularities of the slow-phase velocity (SPV) as well as a reduced number of beats (frequency) when compared with a control group of age-matched healthy volunteers. After training, the SPV became more regular (decrease in SD) and the frequency was similar to the control group's (3 Hz). Body stabilization was measured by dynamic posturography (Equitest) at the beginning and at the end of the training program. At the end of the training program, the patients were asymptomatic and there was a significant correlation between the Equitest results and the modification of the OKN parameters.

Adult↗

PubMed1989

[Benign paroxysmal positional vertigo and provocative maneuvers].

Main features of the benign paroxysmal positional vertigo (B.P.P.V.) are: latency before the onset of vertigo, nystagmus of the rotatory type beating toward the lower ear, nystagmus tires out, nystagmus gets inverted when the head is brought back to orthostatism, nystagmus is reproducible as many times as the position is taken. B.P.P.V. is due to a deposit of heavy material on the cupula of the posterior semi circular canal. In this unusual condition, the cupula moves under the effect of gravity acceleration. The goal of the treatment is to free the cupula. The manoeuvre consists after determination of the position that elicits the vertigo to move the whole head and body together of the patient to a 180 degree opposite position in which the addition to the endolymph flow forces and weight forces of the material will unstick it from the cupula. The positive result of the manoeuvre is instantly proved by the arising of a rotatory nystagmus beating again toward the sick ear. In other words it is not the inversion of the primary nystagmus but a nystagmus beating the same direction. This is explained by the dynamic of the cupula: in the prime position the density modified cupula moves toward the canal. At the end of the manoeuvre when the velocity of the head is zero, the cupula has to support different forces. First the addition of the endolymph flow forces and the inertia of the heavy material makes the cupula move toward the ampulla. Secondly when the superficial tension forces are too high the heavy material unstick from the cupula and it goes back to its normal position. En this very moment the cupula moves toward the canal. The results are of more than 90% positive in one ore two sessions 4,2% of recurrence. The manoeuvre is unsuccessful in spontaneous nystagmus revealed by a position, in torsional nystagmus as in fistulas or in central position nystagmus.

Humans↗

PubMedDate not supplied

Assessment of vestibular function by videonystagmoscopy.

Videonystagmoscopy has been used to subjectively observe the responses of the vestibular system in a population of patients with vestibular deficits. These results were compared with those of a control group of healthy, age-matched volunteers. The videonystagmoscopy device is made of one or two CCD cameras mounted on lightproof goggles, allowing a subjective observation of ocular movements on a video monitor. The eye movements, as well as the position of the head in space, can be recorded on videotape. The eyes are illuminated by infrared light emitting diodes placed on each side of the camera lens. The subjects are seated on a manually driven Barany chair. Subjects went through a protocol of passive roll head tilt on each side, followed by a slow, whole body rotation of 180 degrees amplitude, clockwise and counterclockwise, and then a head shaking test (HST). The eyes were subjectively observed, and we focussed on: torsional eye movements during head tilt, nystagmus when the rotation had stopped, and nystagmus induced by HST. With this simple and noninvasive examining procedure, screening of vestibular function at the bedside or during E.N.T. clinical investigations is possible.

Computer Terminals↗