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Biomedical subjects

F Chaouloff

Publications and source records attributed to F Chaouloff.

At least 19 recordsLinked to original sources
PubMed1995

Cortical [3H]ketanserin binding and 5-HT2A receptor-mediated behavioral responses in obese Zucker rats.

Past studies have indicated that genetically obese Zucker (fa/fa) rats are hypercorticoid, and that this neuroendocrine alteration plays a key role in the syndrome. In keeping with the proposal that glucocorticoids may upregulate central 5-HT2A receptors, we have studied the effects of acute and repeated 5-HT2A receptor stimulation by 1-(4-iodo-2,5-dimethoxyphenyl)-2-aminopropane (DOI) in lean and obese Zucker rats. Acute injection of DOI (2 mg/kg, SC) elicited a lower number of head shakes in obese rats compared to that measured in lean rats. Conversely, neither DOI-elicited decreases in food intakes and body weights nor cortical [3H]ketanserin binding were affected by obesity. In rats repeatedly pretreated with DOI, biochemical and functional indices of 5-HT2A receptor downregulation failed to reveal an effect of obesity. It is suggested that 5-HT2A receptor-mediated functions, but not their downregulation, may be differentially affected in the hypercorticoid obese Zucker rat.

Amphetamines↗
PubMed1995

Regulation of 5-HT receptors by corticosteroids: where do we stand?

Twenty five years ago, experimental procedures such as adrenalectomy and corticosteroid administration (to intact rats) allowed the recognition of direct and indirect controls of central 5-HT synthesis rate by corticosteroids. These effects indicated that the activity of the hypothalamo-pituitary-adrenal (HPA) axis, whether under basal conditions or during stress, is endowed with a modulatory action upon serotonergic neurons. Nowadays, in situ hybridisation, in vitro autoradiography, and radioligand binding on the one hand, and electrophysiological, behavioural, and neuroendocrinological responses on the other hand, are tools that allow the analysis of direct corticosteroid effects upon 5-HT receptors. Among the dozen of 5-HT receptors identified so far, four receptors (namely the 5-HT1A, 5-HT1B, 5-HT2A, and 5-HT2C receptors)--and the 5-HT uptake system--have been the focus of studies aimed at detecting corticosteroid modulatory effects. The results that are reviewed herein indicate that hippocampal 5-HT1A receptors are under the tonic inhibitory control of corticosterone. This control is directly exerted at the level of the 5-HT1A receptor gene, essentially through mineralocorticoid receptors; as well, electrophysiological findings bring support for an additional modulation of hippocampal 5-HT1A receptor-mediated functions by indirect (ie 5-HT1A receptor gene-independent) genomic actions of corticosteroids. In keeping with the respective effects of stressful stimuli and psychotropic drugs upon the HPA axis and central serotonergic systems, it is likely that these corticosteroid-5-HT1A receptor interactions in the hippocampus have consequences in the pathophysiology of mood disorders. However, because the data regarding a corticosteroid control of other 5-HT receptors are either scarce and contradictory (eg 5-HT1B, 5-HT2A, 5-HT2C receptors and 5-HT uptake systems) or lacking, it is at the present time unknown whether corticosteroids exert other effects on 5-HT receptor-mediated functions, including those related to homeostasis.

Adrenal Cortex Hormones↗
PubMed1994

Paradoxical differences in animal models of anxiety among the Roman rat lines.

The Roman high-avoidance (RHA) and low-avoidance (RLA) rat lines have been selected upon their divergent active avoidance behaviours. On the basis of open-field behavioural analyses, it has been suggested that RLA rats display more emotionality than RHA rats. Herein, we have analysed the behaviours of male RHA and RLA rats in three tests putatively related to anxiety, namely the elevated plus-maze, the black/white box, and the social interaction test. In the elevated plus-maze, neither the number of total arm entries nor the percent number of open arm entries were different between the Roman lines. Alternatively, RLA rats spent more time on the open arms, compared to RHA rats. In the black/white box, both the latency to enter the black compartment, the number of shuttles, the time spent in the white compartment, and the general activity in the white compartment were higher in RLA rats, compared to their RHA counterparts. Lastly, socially isolated RHA and RLA behaved similarly when exposed to a social interaction test. It is suggested that under particular experimental conditions male RLA rats display less anxiety than male RHA rats, and that the open-field test may provide indices of activity rather than indices of anxiety.

Animals↗
PubMed1994

Influence of physical exercise on 5-HT1A receptor- and anxiety-related behaviours.

Treadmill exercise (1 h at 20 m/min) has been shown to increase brain serotonin (5-HT) synthesis/metabolism in 4-day trained rats. This work has analysed whether these changes are associated with (5-HT-dependent or -independent) alterations in pre- and postsynaptic 5-HT1A receptor-mediated behaviours; in addition, the controversial hypothesis that exercised rats are less anxious than sedentary rats was tested in the elevated plus-maze and the social interaction models. Acute administration of the 5-HT1A receptor agonist 8-hydroxy-2-(di-n-propylamino)tetralin (8-OH-DPAT; 0.125-0.5 mg/kg) triggered hyperphagia, forepaw treading, and flat body posture, the amplitude of which were not affected by training or acute exercise. In the elevated plus-maze, training, but not acute exercise, reduced the number of total arm entries. In the social interaction test, trained and acutely exercised rats displayed increased locomotion and decreased defecation, compared to resting rats, but social interaction and rearings were not affected. It is suggested that the aforementioned effects of acute exercise upon 5-HT synthesis/metabolism in short-term trained rats are not associated with changes in 5-HT1A receptor- and anxiety-related behaviours.

8-Hydroxy-2-(di-n-propylamino)tetralin↗
PubMed1994

Failure to find behavioural differences between lean and obese Zucker rats exposed to novel environments.

Past studies have evidenced a key role for hypercorticism in the obesity syndrome of the Zucker (fa/fa) rat. Here, the hypothesis that obesity-related hypercorticism is associated with increased anxiety/emotionality was tested in the elevated plus-maze, the black/white box, and the open field. In the elevated plus-maze, none of the parameters examined (open arm entries, time in open arms, total number of entries) differed between lean (Fa/?) and obese (fa/fa) rats. In addition, neither the behaviours measured in the black/white box (latency to enter the black compartment, number of transitions, time spent in the white compartment, locomotion, rearing) nor those measured in the open field (locomotion, rearing, grooming, defecation) were affected by obesity. This study suggests that obesity-related hypercorticism in fa/fa rats is not associated with indices of emotionality and anxiety, at least those analysed by means of the tests used here.

Adrenocortical Hyperfunction↗
PubMed1993

Chronic treatment with an anxiolytic dose of the 5-HT1A agonist ipsapirone does not alter ipsapirone acute neuroendocrine effects.

We recently reported that chronic administration of the 5-HT1A receptor agonist, ipsapirone (0.5 milligrams in drinking water for 3 weeks), has anxiolytic activity in the rat. Herein, we investigated whether this treatment promotes tachyphylaxis to the acute neuroendocrine effects of ipsapirone. Rats chronically treated with ipsapirone displayed a 7% decrease in body weights, compared to vehicle-pretreated rats, thereby confirming previous observations. On the other hand, ipsapirone pretreatment did not affect basal plasma levels of adrenocorticotropin (ACTH), corticosterone, prolactin, aldosterone, and renin activity, nor did it affect their respective rises following an acute ipsapirone (50 mg/kg PO) challenge. Moreover, ipsapirone pretreatment did not affect the increase in plasma prolactin levels elicited by the dopaminergic receptor antagonist haloperidol. These results suggest that neither the 5-HT1A receptors nor the catecholamine receptors that mediate ipsapirone acute neuroendocrine effects develop tolerance to stimulation upon sustained ipsapirone treatment.

Adrenocorticotropic Hormone↗
PubMed1993

Are 5-HT1A autoreceptors involved in the inhibitory effect of ipsapirone on cold-elicited thyrotropin secretion?

Administration of the serotonin (5-HT)1A receptor agonist ipsapirone has been shown to decrease cold-elicited thyrotropin (TSH) secretion. We have analyzed (1) the influence of 5-HT1A receptors and ipsapirone metabolism into 1-(2-pyrimidinyl)-piperazine (1-PP, an alpha 2-adrenoceptor antagonist) on the effect of ipsapirone on TSH release, and (2) the interaction between the corticosterone-releasing effect of ipsapirone and its inhibitory influence on TSH release. Pretreatment with proadifen (50 mg/kg, 5 h before ipsapirone), i.e. an inhibitor of ipsapirone metabolism into 1-PP, did not affect ipsapirone-induced inhibition of cold-elicited TSH secretion. Pretreatment (15 min before ipsapirone) with the 5-HT1/5-HT2 receptor antagonist metergoline 2 mg/kg) or with the 5-HT1A receptor blocker (-)-pindolol (5 mg/kg) increased baseline and cold-elicited TSH release but the inhibitory influence of ipsapirone on cold-elicited TSH release was alleviated by (-)-pindolol pretreatment only. Cold exposure increased corticosterone release, an effect which was insensitive to (-)-pindolol pretreatment. Lastly, pretreatment with the 5-HT synthesis inhibitor p-chlorophenylalanine prevented the immediate inhibitory effect of the selective 5-HT1A receptor agonist 8-hydroxy-2-(di-n-propylamino)tetralin (8-OH-DPAT) upon cold-induced TSH release, but it amplified the late release of TSH in cold-exposed 8-OH-DPAT-injected rats. These results suggest that presynaptic 5-HT1A receptors mediate ipsapirone-induced inhibition of cold-elicited TSH release, an effect which may be partially opposed by postsynaptic 5-HT1A receptor stimulation.

8-Hydroxy-2-(di-n-propylamino)tetralin↗
PubMed1992

Effects of cold stress on some 5-HT1A, 5-HT1C and 5-HT2 receptor-mediated responses.

The purpose of the present study was to analyze the influence of stress (24-h cold exposure) on presynaptic 5-HT1A receptors, and on postsynaptic 5-HT1A, 5-HT1C and 5-HT2 receptors. Cold exposure for 24 h affected neither pargyline-induced decreases in 5-hydroxyindoleacetic acid (5-HIAA) levels in midbrain and rest of brain, nor plasma glucose and corticosterone levels. Treatment with the 5-HT1A receptor agonist, 8-hydroxy-2-(di-n-propylamino)tetralin (8-OH-DPAT; 0.5-1 mg/kg), 3-5 h after the end of cold exposure triggered less intense flat body posture and forepaw treading in cold-exposed rats than in controls. On the other hand, 15- and 30-min plasma glucose responses to 8-OH-DPAT (0.25-0.5 mg/kg, 3-5 h after cold) or to the alpha 2-adrenoceptor agonist, clonidine (0.025 mg/kg), were not affected by cold, while the 15-min, but not the 30 min, plasma corticosterone response to 8-OH-DPAT was slightly amplified in cold-exposed rats. Cold exposure affected neither the inhibitory effect of 8-OH-DPAT (0.25-0.5 mg/kg, 3-5 h after cold) on midbrain 5-HIAA levels, nor the hypothermic effect of 8-OH-DPAT (0.5-1 mg/kg, 3-5 h after cold). Lastly, the hypoactivity elicited by the 5-HT1C receptor agonist, m-chlorophenyl-piperazine (1.5-3 mg/kg, 3-5 h after cold), or head shakes elicited by the 5-HT2 receptor agonist, 1-(2,5-dimethoxy-4-iodophenyl)-2-aminopropane (1-2 mg/kg, 3-5 h after cold), were of similar intensities in control and in cold-exposed rats.

8-Hydroxy-2-(di-n-propylamino)tetralin↗
PubMed1992

The 5-HT2 receptor agonist 1-(2,5-dimethoxy-4-iodophenyl)2-aminopropane increases brain tryptophan levels in the rat.

Earlier studies have indicated that the sympathoadrenal system and the corticotropic axis control brain levels of tryptophan (Trp), the precursor of 5-hydroxytryptamine (5-HT). We investigated the effects of 5-HT receptor agonists known to activate the sympathoadrenal system and/or the corticotropic axis on plasma and brain Trp levels. Neither the 5-HT1A receptor agonist 8-hydroxy-2-(di-n-propylamino)tetralin (8-OH-DPAT, 0.5 mg/kg s.c.), nor the 5-HT1C receptor agonist 1-(3-chlorophenyl)piperazine (mCPP, 2.5 mg/kg s.c.) affected plasma and brain Trp levels. The 5-HT2 receptor agonist 1-(2,5-dimethoxy-4-iodophenyl)2-aminopropane (DOI, 0.5-2 mg/kg s.c.) increased brain Trp levels, an effect which was significant for the two highest doses used (1.5-2 mg/kg s.c.).

8-Hydroxy-2-(di-n-propylamino)tetralin↗
PubMed1992

Mechanisms involved in the hyperglycemic effect of the 5-HT1C/5-HT2 receptor agonist, DOI.

Previous experiments have indicated that 5-HT2 receptors and catecholaminergic systems mediate the rise in plasma glucose levels elicited by acute administration of the 5-HT1c/5-HT2 receptor agonist, 1-(2,5-dimethoxy-4-iodophenyl)-2-aminopropane (DOI). On this basis, we investigated the location of these serotonin receptors and the nature of this catecholaminergic involvement. Administration of DOI (0.4 mg/kg i.v.) to conscious rats (bearing jugular catheters) elicited a rapid rise in plasma glucose which was associated with a decreased insulin response to a glucose bolus (300 mg/kg i.v.). Pretreatment with the peripherally acting 5-HT1c/5-HT2 receptor antagonist, BW 501C67 (0.5 mg/kg i.v. 10 min beforehand) prevented the rise in plasma glucose triggered by the peripherally acting 5-HT1c/5-HT2 receptor agonist, alpha-methyl-5-HT (0.75 mg/kg i.v.), but amplified the rise elicited by DOI. Pretreatment with chlorisondamine (1 mg/kg i.v. 10 min beforehand) or adrenalectomy 20 h beforehand prevented the DOI-induced hyperglycemia. On the other hand, pretreatment with dexamethasone (0.35 mg/kg s.c. 2 h and 20 min beforehand) did not affect the DOI-induced hyperglycemia. It is concluded that the hyperglycemic effect of DOI administration is mediated by centrally located 5-HT2 receptors and, in turn, adrenal epinephrine release.

Adrenalectomy↗
PubMed1992

Influence of the novel antidepressant tianeptine on neurochemical, neuroendocrinological, and behavioral effects of stress in rats.

Tianeptine is a novel tricyclic agent that activates the neuronal uptake of serotonin (5-hydroxytryptamine, 5-HT). Taking into account the antidepressant effect of tianeptine in animals and humans, we have measured the influence of a pretreatment with tianeptine (10 mg/kg IP 1 hr beforehand) on some consequences of a single 2-hr restraint stress session in male rats. Thus, we have analyzed (1) 5-HT metabolism in various brain regions and plasma glucose (an index of sympathoadrenal activity) and corticosterone levels at the end of stress, and (2) open field scores 18-19 hr after immobilization in saline- or tianeptine-pretreated rats. Tianeptine was found to leave unaltered stress-induced increases in cortical, hippocampal, hypothalamic, midbrain, and striatal serotonergic metabolism. Similarly, stress-elicited elevations in plasma glucose and corticosterone levels were not affected by tianeptine pretreatment. On the other hand, tianeptine pretreatment reversed stress-induced deficit in exploratory activity. To test whether the latter positive effect of tianeptine was associated with changes in plasma glucose and corticosterone levels during the early phase of stress, we have measured plasma glucose and corticosterone levels (at 0, 5, 15, 30, and 60 min) in resting and stressed (catheterized) rats. The results indicated that tianeptine pretreatment did not alter plasma glucose and corticosterone early responses to stress. Although this study confirmed the antidepressant effect of tianeptine, the neurochemical and neuroendocrinological mechanisms underlying this positive effect remain to be determined.

Animals↗
PubMed1992

Differential effects of the novel antidepressant tianeptine on L-5-hydroxytryptophan (5-HTP)-elicited corticosterone release and body weight loss.

Biochemical and behavioural experiments have indicated that the novel antidepressant tianeptine stimulates 5-hydroxytryptamine (5-HT) reuptake. The present study has explored the influence of acute tianeptine pretreatment upon corticosterone release and body weight loss following L-5-hydroxytryptophan (5-HTP) administration in conscious rats. Administration of 5-HTP (20 mg/kg i.v.) increased plasma corticosterone levels to a similar extent in rats pretreated either with saline or tianeptine (10 mg/kg i.p., 60 min beforehand). Besides, prior administration of benserazide (50 mg/kg i.p., 30 min beforehand), an inhibitor of peripheral aromatic L-amino acid decarboxylase, prevented 5-HTP-induced corticosterone release in both saline- and tianeptine-pretreated rats. However, combined administration of benserazide and 5-HTP decreased overnight body weight in saline-, but not in tianeptine-pretreated rats. These results suggest that tianeptine preferentially activates 5-HT reuptake in central serotonergic neurones.

5-Hydroxytryptophan↗
PubMed1992

Central 5-hydroxytryptamine2 receptors are involved in the adrenal catecholamine-releasing and hyperglycemic effects of the 5-hydroxytryptamine indirect agonist d-fenfluramine in the conscious rat.

Stimulation of either the 5-hydroxytryptamine (5-HT)1A, the 5-HT1C or the 5-HT2 receptor subtype triggers adrenal catecholamine release and hyperglycemia. Nonetheless, the identity of the serotonergic receptors that mediate the effects of 5-HT release upon the sympathoadrenal system (and on plasma glucose) is still unknown. Thus, we have examined the effects of the 5-HT uptake inhibitor and releaser d-fenfluramine (d-Fen) on plasma epinephrine (EPI), norepinephrine (NE) and glucose levels in conscious rats. Acute administration of d-Fen (1-8 mg/kg i.v.) promoted early increases in plasma EPI and glucose levels, whereas increases in plasma NE levels were less marked. The effects of a 4-mg/kg dose of d-Fen were then evaluated. Prior adrenalectomy prevented d-Fen-induced hyperglycemia but not d-Fen-induced increases in plasma NE levels. Pretreatment (15 min beforehand) with either the 5-HT1C/5-HT2 receptor antagonist LY 53857 (0.3 mg/kg i.v.) or the 5-HT2 receptor/alpha-1 adrenoceptor antagonist ketanserin (0.3 mg/kg i.v.) markedly diminished the EPI-releasing effect of d-Fen. Pretreatment with the 5-HT1C receptor agonist/5-HT2 receptor antagonist m-chlorophenylpiperazine (1 mg/kg i.v.) tended to decrease the EPI-releasing effect of d-Fen, whereas that with the peripheral 5-HT1C/5-HT2 receptor antagonist BW 501C67 (0.5 mg/kg i.v.) did not alter the EPI-releasing effect of d-Fen. In addition, pretreatment with either LY 53857 or ketanserin prevented the hyperglycemic effect of d-Fen.(ABSTRACT TRUNCATED AT 250 WORDS)

Adrenal Glands↗
PubMed1991

[Behavioural adaptation to stress. Improvement by tianeptine].

The aim of this study was to analyse the behaviour effects of tianeptine, an activator of the serotonin neural recapture, in three animal models of depression: immobilization stress, acquired resignation and obligatory swimming. Acute or chronic administration of tianeptine provoked effects comparable to those of the classic antidepressants (tricyclic or atypic). Tianeptine decreased or prevented exploration inhibition induced by immobilization stress, the number of escape failures occurring in a session of adverse and uncontrollable shocks and immobility time following obligatory swimming in a confined space. The relationship between these positive effects of tianeptine and the serotonin system are discussed.

Animals↗
PubMed1991

Buspirone, ipsapirone and 1-(2-pyrimidinyl)-piperazine decrease cold-induced thyrotropin secretion in rats.

The aim of this study was to analyse the effects of the 5-HT1A receptor-related antidepressants/anxiolytics, buspirone and ipsapirone (1-10 mg/kg i.v.), and those of their common metabolite, the alpha 2-adrenoceptor antagonist, 1-(2-pyrimidinyl)-piperazine (1-PP, 1-10 mg/kg i.v.), on cold-induced thyrotropin (TSH) secretion in conscious catheterised rats. The effects of the centrally acting 5-HT1A receptor agonist, 8-hydroxy-2-(d-n-propylamino)tetralin (8-OH-DPAT, 0.1-1 mg/kg i.v.), and of the peripherally acting 5-HT1A receptor agonist, N,N-dipropyl-5-carboxamidotryptamine (DP-5-CT, 0.1-1 mg/kg i.v.), were also included in this study. Buspirone, ipsapirone, and 1-PP dose dependently decreased cold-induced TSH secretion throughout the 90 min of analysis. However, the preventive effect of 1-PP was reached with a lower dose (3 mg/kg) than that needed for the parent compound (10 mg/kg). 8-OH-DPAT administration diminished but did not prevent cold-induced TSH secretion, while only the highest dose of DP-5-CT diminished secretion (1 mg/kg). Lastly, the TSH-releasing hormone (TRH)-induced TSH secretion was left unaffected by either buspirone or ipsapirone pretreatment (10 mg/kg), but was diminished by 1-PP pretreatment (3 mg/kg). These data suggest that both central 5-HT1A receptors and alpha 2-adrenoceptors mediate the effects of azapirones on cold-induced TSH secretion.

8-Hydroxy-2-(di-n-propylamino)tetralin↗
PubMed1991

Repeated treatment with the 5-HT1A receptor agonist, ipsapirone, does not affect 8-OH-DPAT- and stress-induced increases in plasma adrenaline levels in the rat.

The aim of this study was to investigate whether 5-HT1A receptor-mediated adrenal catecholamine release undergoes rapid desensitisation. Thus, we measured plasma adrenaline either following the acute administration of the 5-HT1A receptor agonist, 8-hydroxy-2-(di-n-propylamino)tetralin (8-OH-DPAT, 0.3 mg/kg i.v.), or during immobilisation stress, in rats pretreated repeatedly with saline or with the 5-HT1A receptor agonist, ipsapirone (10 mg/kg i.p., t.i.d. for 7 days). Plasma corticosterone and glucose were measured concomitantly. Neither body weight nor basal plasma adrenaline and corticosterone levels were significantly affected by ipsapirone treatment. Conversely, the latter diminished basal plasma glucose levels. While the 8-OH-DPAT-induced elevations in plasma adrenaline remained unaffected by ipsapirone, the 8-OH-DPAT-induced elevations in plasma corticosterone and glucose tended to be diminished by ipsapirone. Ipsapirone treatment modified the kinetics, but not the amount of adrenaline released by stress. On the other hand, stress-induced activation of the corticotropic axis was amplified by ipsapirone. Lastly, ipsapirone treatment again tended to diminish the hyperglycemic response to stress. These results indicate that (i) 5-HT1A receptor-mediated activation of adrenaline release is not desensitised by short-term ipsapirone treatment, (ii) the anxiolytic/antidepressant effect of ipsapirone may not be explainable in terms of tolerance to some neuroendorinological consequences of stress.

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