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Biomedical subjects

J M Gaillard

Publications and source records attributed to J M Gaillard.

At least 19 recordsLinked to original sources
PubMed1992

The EEG of the sleep onset period in insomnia: a discriminant analysis.

A period of rapid change in the wave components of the electroencephalogram (EEG) marks the transition from wake to sleep. Twenty-six insomniac and 28 control nights were studied in a discriminant analysis to determine whether this transitional state is modified in any way in subjects diagnosed for psychophysiological insomnia. A discriminant function was derived based on 20 insomniac and 22 normal nights. All 42 nights were correctly classified by this function. The sleep onset period, extending on the average over about 3 minutes, was characterized essentially by the beta and delta components of the EEG signal and by an activity index given by the ratio beta/delta, measured at the temporal lobe sites. Other variables included the subject's age and the magnitude of the changes occurring in the difference between activities in the right and left hemispheres. The variables contributing most to the discrimination were the activity index and beta, especially at the transitions from wake to stage 1 and from stage 1 to stage 2. The contribution of delta to the discrimination was less, but extended further in time to include stage 2 sleep. A test on the remaining six insomniac and six control nights gave a 75% classification accuracy, thus validating the derived discriminant function.

Adolescent↗
PubMed1992

Platelet membrane alpha 2-adrenergic receptors in depression.

The platelet membrane was used as a model system to examine alpha 2-adrenergic receptors in 30 depressed patients and 30 healthy control subjects. The number of binding sites and their affinity for 3H-UK 14304 (5-bromo-6-(2-imidazoline-2-ylamino)-quinoxaline), a potent, highly selective alpha 2-adrenergic receptor agonist, was measured. Plasma magnesium and free 3-methoxy-4-hydroxyphenylglycol (MHPG) concentrations were assayed in the same sample. A decreased agonist-receptor affinity was found in depressed patients, whereas receptor density was not significantly altered compared with that in control subjects. In bipolar depressed and dysthymic patients, there was a tendency toward a higher density of alpha 2-adrenergic receptors. This trend was not apparent in unipolar, recurrent depressed subjects. Moreover, a positive correlation between Bmax and Kd values was observed in patients but not in control subjects--a finding that suggests that a compensatory phenomenon occurs in depression. After the patients were treated with antidepressant drugs, an increased affinity (decrease in Kd) was observed, together with a decrease in binding sites. Plasma magnesium concentrations were higher in drug-free depressed patients than in control subjects. In addition, magnesium concentrations were negatively correlated with the density of alpha 2-adrenergic receptor binding sites in depressed patients, both before and during treatment. Lastly, a trend toward a negative correlation between plasma MHPG concentration and the number of binding sites was also observed. These results suggest a complex multifactorial regulation of alpha 2-adrenergic receptors, which are probably hyposensitive in depressive syndromes.

Adrenergic alpha-Agonists↗
PubMed1992

Decrease in epinephrine-induced attenuation of platelet adenylate cyclase activity in depressed patients: relation with plasma electrolytes.

We have measured the alpha 2-adrenoceptor-mediated inhibition of platelet membrane adenylate cyclase in depressed patients and control subjects. The results showed a decrease in the forskolin-stimulated adenylate cyclase inhibition of depressed patients compared to the healthy subjects. This suggests a subsensitivity of alpha 2-adrenoceptor in depression. However, this subsensitivity was not correlated to the severity of depression as both severely and moderately depressed patients exhibited the same percent of adenylate cyclase inhibition. The antidepressant drugs treatment induced an increase in the percent of adenylate cyclase inhibition with a trend towards the control values. However, this increase did not equal control value, and moreover both remitted and unremitted patients presented a similar change in their alpha 2-adrenoceptor-mediated adenylate cyclase inhibition. This result raises the question about a simple and direct relation between the clinical status of depression and the power of alpha 2-adrenoceptor-mediated adenylate cyclase inhibition. Plasma magnesium and sodium yielded correlations to this alpha 2-adrenoceptor-mediated adenylate cyclase inhibition suggesting a relation between the platelet adrenergic function and plasma electrolytes.

Adenylyl Cyclase Inhibitors↗
PubMed1992

Evolution of blood magnesium, sodium and potassium in depressed patients followed for three months.

No consensus has been obtained about blood electrolyte status, especially about magnesium, in affective disorders. This is mainly due to the lack of information about the distribution of the patients in clinical subgroups, sex, type of treatment and about the severity of their illnesses. Most of these studies concerned treated patients. We confirmed in this study that drug-free depressed patients have higher erythrocyte and plasma magnesium than controls, as shown in previous reports. Significant differences are observed in as shown in previous reports. Significant differences are observed in patients for sex and between clinical subgroups. Low plasma potassium levels are described in both male and female depressed patients. The erythrocyte magnesium level tends to normalize in parallel with clinical improvement, depending on sex and clinical subgroup, and seems then to be related to the intensity of the depression. Plasma magnesium in male and female patients, except for female unipolars, remains higher than controls in all conditions and might be related to the diagnosis of affective disorders.

Adult↗
PubMed1991

A study of the interrupted REM episode.

Brief interruptions of REM sleep are considered to be part of the REM episode. The maximum allowable duration of such an interruption, which is used to define the end of the REM episode, is currently a matter of debate. Making measurements on individual REM cycles, inter-REM interval analysis was carried out to determine whether the generally adopted 15 minute empirical rule for this maximum needs to be extended to 25 minutes as suggested by several including Kobayashi et al. Our results show that there is no reason to alter the 15 minute rule and that measurements which do not take into account the time-of-night effect may be misleading. The proportion of interrupted REM episodes observed in our population of healthy adults is high. We have therefore also examined in some detail the phenomenology of the temporal evolution of the structure and content of the interrupted REM episodes. Both showed a definite change over the night: the interruptions in the earlier episodes tend to return the system to slow wave sleep while those in the later episodes tend to return it to wake. It is hypothesized that these interruptions reflect a measure of REM sleep pressure and its interaction with both slow wave sleep and wake pressures.

Adolescent↗
PubMed1991

Hypnotic action of flunitrazepam is reversed by proglumide in rats.

1. Caerulein, an analogue of cholecystokinin (CCK-8), like CCK-8, has been shown to produce hypnotic effects similar to those of benzodiazepine (flunitrazepam). 2. Proglumide antagonizes the action of CCK-8 and of its analogue. 3. The aim of the present study was to demonstrate whether proglumide would affect the potent hypnotic action of flunitrazepam in rats. 4. The association of proglumide with flunitrazepam suppress the increase of total sleep time and slow wave sleep seen after flunitrazepam alone. Proglumide alone has no effect on sleep stages. The authors report here for the first time that the hypnotic action of flunitrazepam is antagonized by proglumide in rat.

Animals↗
PubMed1990

Effects of moclobemide on sleep in healthy human subjects.

Ten healthy, normal subjects (5 male and 5 female) aged 20-28 years participated in this experimental study of the effect of moclobemide on sleep. The design consisted of 2 sessions of 5 nights each, comprising 1 adaptation night, 2 nights on placebo and 2 inputs of moclobemide 4 mg/kg (session B). The 2 sessions were separated by at least 15 days and their order was balanced and randomized. During the last 4 nights of each session, sleep parameters were recorded throughout the night according to standard procedures. Moclobemide at a dose of 4 mg/kg induced moderate changes in the sleep-wake balance: a significant increase in stage 1 on the second drug night, a slight increase in stage 2 and a significant decrease in paradoxical sleep on the 2 drug nights. There was also a moderate reduction in the number of rapid eye movements (REM) during paradoxical sleep, but the number of cycles and latency to paradoxical sleep were unchanged, as well as all other sleep parameters measured. With 6.5 mg/kg, the changes were more pronounced: total sleep time was diminished, but this was significant only on the second and third nights. Transient awakenings increased significantly on the first drug night, and wakening latency decreased. The only modification of orthodox sleep was an increase in the percentage of stage 2 on the first drug night, whereas slow-wave sleep was unchanged. Paradoxical sleep was reduced on the first 2 drug nights, but tolerance appeared on the third night. The decrease in paradoxical sleep was exacerbated in the last part of the night. REM were decreased during paradoxical sleep.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1979

Involvement of pre- and postsynaptic receptors in catecholaminergic control of paradoxical sleep in man.

In an attempt to clarify the roles of pre- and postsynaptic catecholaminergic (CA) receptors in the regulation of paradoxical sleep (PS) in man, the effects of various doses of chlorpromazine (CPZ) and clonidine (CLN) have been investigated. The action of CPZ was biphasic, small doses enhancing and larger doses depressing the production of PS. However, the effect of CLN was monophasic, showing no modification after small doses, and a decrease in production of PS after moderate doses. In addition, a small dose of CLN, ineffective by itself, completely abolished the effect of a small dose of CPZ. These observations can be explained by preferential blockade of presynaptic alpha-receptors by a small dose of CPZ. They show, too, that it is possible to investigate in man the functional consequences of pharmacological manipulation of pre-synaptic receptors on cerebral CA neurons.

Adult↗
PubMed1979

[The physiology of sleep and the physiopathology of insomnia].

After a review of the semiology and organization of normal sleep, the neuronal structures presently accepted as participating in sleep mechanisms are discussed. During a series of experiments designed to define the physiopathological role of slow wave sleep in chronic insomnia, we recorded in our laboratory normal subjects of both sexes and insomniacs whose predominant disorders was sleep maintenance. Sleep modifications as a function of aging chiefly involve stage 4, which is reduced by about one half between the ages of 19 and 30. Analyzing a large group of normal and insomniac subjects, it is possible to show a statistical association between very low values of slow wave sleep and short and fragile total sleep. This association cannot be explained simply by an increase in waking pressure. Comparison of a group of 16 insomniacs with 16 age and sex matched normal subjects shows in the insominacs a deficiency of production of slow wave sleep (stages 3 and 4), most probably linked to a disturbed waking/sleep balance, whereas the other parameters of sleep, especially paradoxical stage, remain unmodified. These results are consistent with the hypothesis of a physiopathological role of slow wave sleep deficiency in chronic primary insomnia; on the other hand, slow wave sleep may possibly be responsible for sleep induction and maintenance, playing the role of a physiological hypnogenic mechanism.

Adult↗
PubMed1979

Distribution of tryptophan in erythrocytes, leukocytes and thrombocytes, and its binding to plasma albumin.

The extended theory about a dysfunction of the serotoninergic system in depression and schizophrenia includes the hypothesis of a disturbance in the transport systems of tryptophan and tyrosine from blood to brain. It would be interesting to know if blood cells may be used as a model for the central transport mechanisms of these amino acids. After an oral load, the in vivo distribution of L-tryptophan (50 mg/kg) was studied in the blood plasma, in the different blood cells and its binding to plasma albumin, in six healthy, seven schizophrenic and two depressive subjects. In all the compartments studied, tryptophan reached a peak, 1--2 hours after the load. Before and after the load, the variation of the tryptophan concentration in the erythrocytes was parallel to the plasma free tryptophan, whereas the uptake of this amino acid was higher in leukocytes and thrombocytes than in erythrocytes. However, this model does not show differences between schizophrenic and normal subjects with regard to the transport of tryptophan and tyrosine in these cells.

Biological Transport, Active↗
PubMed1979

The influence of oral tryptophan on cortical evoked responses in normals and schizophrenics.

The cortical evoked responses to sensory stimulation were studied in order to evaluate the central effects of oral tryptophan in normals and schizophrenics. In the first study, seven volunteer male students were tested during four experimental sessions. Visual evoked responses to flashes were recorded at occiput and vertex, before and 1 1/2 hours after the ingestion of 35 mg/kg tryptophan in apple purée with 50 g glucose or placebo. Some significant modifications of evoked responses were observed after tryptophan ingestion: a decrease of amplitude and an increase of variability. The latencies were rather stable, presenting only minor modifications. From these results, corroborated by some data from literature, it may be supposed that tryptophan induces a decrease of arousal. In the second study, seven chronic schizophrenics and 6 volunteer controls were tested, using an analogous experimental design, however with some modifications: the tryptophan dose was increased to 50 mg/kg and administered in 200 ml of milk, instead of apple purée with glucose. The modifications of evoked responses recorded in the preceding study were no longer found. Probably, the substitution of milk for glucose resulted in an alteration of the transport of tryptophan across the blood-brain barrier. The blood parameters were rather similar in the two studies; therefore, the central effects of tryptophan did not parallel its blood levels.

Administration, Oral↗
PubMed1979

Blood-brain movements of tryptophan and tyrosine in manic-depressive illness and schizophrenia.

In order to investigate possible disturbances of the blood-brain transport mechanisms of monoamine precursors in manic-depressive illness and schizophrenia, we have measured the brain arterio-venous difference of DOPA, or 5-HTP, or tyrosine and tryptophan in 36 patients, during the infusion of either L-DOPA or L-5-HTP. The infusion lasted for 30 min, and blood was sampled during and immediately after the infusion, simultaneously in the femoral artery, the jugular vein and a vein of the arm. During the infusion of L-DOPA, manic patients have a higher extraction of L-DOPA than depressive patients and controls. During the infusion of L-5-HTP, pdpressive patients have a higher brain extraction of 5-HTP than manic or schizophrenic patients. In depressive patients, a small uptake of tryptophan correlated with a large outflow of tyrosine was observed. The opposite was seen in manic patients, with an outflow of tryptophan correlated with an uptake of tyrosine. In schizophrenics, there was an outflow of tryptophan and random variations of tyrosine. These brain arterio-venous differences were not correlated with arterio-venous differences for peripheral tissues. Taken together, these results are compatible with a disturbance of the blood-brain transport of amino acids precursors of monoamines in manic-depressive illness and schizophrenia.

Adult↗
PubMed1979

[Biological approach to depressive conditions: study of sleep (author's transl)].

Sleep disturbances are common in depressive states, and have been recently precised. Apart from insomnia, alterations of the organization of sleep and especially a shortening of paradoxical sleep latency, as well as modifications of slow wave sleep, have been reported. The main effect of classical antidepressant drugs is a marked decrease or a complete abolition of paradoxical sleep. However, some antidepressant drugs do not affect paradoxical sleep, and other drugs, devoid of antidepressant properties, depress markedly the production of paradoxical sleep. The investigation of the modifications of sleep in depressive states, as well as of the effect of antidepressant drugs, may contribute to a better understanding of the physiopathology of these diseases.

Antidepressive Agents↗
PubMed1978

Biphasic effect of chlorpromazine on rat paradoxical sleep: a study of dose-related mechanisms.

The experiments reported here investigated the effect of chlorpromazine (CPZ) alone or after inhibition of catecholamine (CA) synthesis on paradoxical sleep (PS) in the rat. The dose--response curve for CPZ was biphasic with enhancement of PS after low doses, and depression of PS after higher doses. In contrast, low doses of CPZ after inhibition of CA synthesis markedly decreased PS. This decrease was greater after tyrosine hydroxylase inhibition than after dopamine-beta-hydroxylase inhibition. These results support the view that low doses of CPZ produce increased activity in brain CA synapses, and that both dopamine and noradrenaline participate in the control of PS in the rat.

Animals↗
PubMed1978

Chronic primary insomnia: possible physiopathological involvement of slow wave sleep deficiency.

This study was designed to compare the sleep of a carefully selected group of patients with chronic primary insomnia toage- and sex-matched controls, in order to investigate the possible physiopathological role of slow wave sleep deficiency in this disturbance. In addition, the effect of age on normal sleep was studied in a group of 40 normal subjects. Sleep was recorded in the laboratory and automatically scored with an electronic system already described. The general trends of sleep stages were computed. Aging in normal subjects was characterized by a sharp decrease of stage 4, but a good stability of stage 3. Insomniacs' sleep showed a sleep-waking imbalance and a marked deficiency in stages 3 and 4. This deficiency seems to be similar to the age effect in normals, but more accentuated; it cannot be attributed merely to increased pressure of wakefulness. We suggest that slow wave sleep is involved in sleep induction and maintenance, and that its deficiency is linked to the fragility of sleep in chronic primary insomnia.

Adult↗
PubMed1978

[Uptake of tryptophan and tyrosine in some cases of manic depressive psychosis and schizophrenia (author's transl)].

The uptake of tryptophan and tyrosine by the brain has been studied in 6 manic-depressive patients and in 8 schizophrenics. In an attempt to saturate the blood-brain transport mechanisms, this uptake has been evaluated by measuring the arteriovenous differences (arterial plasma-internal jugular plasma) of these two amino acids before and after perfusion with L-dopa and L-5-HTP. Considering a positive difference as an uptake and a negative one as an outflow, results show (1) in melancholia an uptake of tryptophan and an outflow of tyrosine; (2) in mania an uptake of tyrosine and an outflow of tryptophan, and (3) in schizophrenia an outflow of tryptophan accompanied with either an uptake or an outflow of tyrosine. In addition, the kinetics of tryptophan binding to plasma proteins and the ratio of tryptophan/tyrosine uptake are different in manic-depressive illness and in schizophrenia. These results support the view that a disturbance in the blood-brain transport mechanisms of tryptophan and tyrosine could be involved in the physiopathology of manic-depressive illness and schizophrenia.

Bipolar Disorder↗