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C Burlet

Publications and source records attributed to C Burlet.

At least 19 recordsLinked to original sources
PubMed1998

Neuropeptide Y release in the paraventricular nucleus of Long-Evans rats treated with leptin.

Neuropeptide Y (NPY) and leptin are actually two of the most potent peptides involved in the regulation of food intake with their respective stimulatory and inhibitory actions. The infusion of each peptide has a significant influence on the mRNA expression of the other in the adipose tissue for leptin and in the arcuate nucleus of the hypothalamus for NPY. To confirm this functional interaction, we measured the in vivo release of hypothalamic neuropeptide Y in awake fasted and refed Long-Evans rats after intraperitoneal (I.P.) injection of leptin. For this purpose, we used the push-pull perfusion technique with the cannula placed above the right paraventricular nucleus. I.P. leptin significantly inhibited food intake during the two hours of food access (-50%; p < 0.02). NPY release was not modified by leptin alone. But, when food was present, it slightly but significantly increased (p < 0.03 or less) and remained at a sustained level in the leptin-treated rats whereas it decreased in the control saline-injected group (p < 0.04). Thus, leptin did not acutely regulate NPY release and other food-related factors are probably involved as mediators of its anorexigenic effects.

Animals↗
PubMed1998

Behavioral deficits in monosodium glutamate rats: specific changes in the structure of feeding behavior.

We studied the feeding rhythms and feeding patterns of adult Long-Evans rats treated with monosodium glutamate (MSG) in their early post-natal period. This treatment is known to induce neuronal degeneration in the arcuate nucleus (ARC), a major hypothalamic site implicated in the regulation of feeding. Neonatal rats were treated intraperitoneally with MSG or saline (controls) alone on the first days of life. At age of 6 months, male control and male MSG rats were placed in our automatic feeding system, and the structure of feeding behavior and diurnal feeding rhythms were analysed. On a 24 hours basis, MSG rats ate less than control rats (-24%). This hypophagia resulted from a mild diurnal hyperphagia (+6%) and a pronounced nocturnal hypophagia (-34%). This hypophagia was the main consequence of a decrease of meal size in MSG rats (-37%) and was associated with an increase in meal duration (+52%). It was also associated with a total disappearance of the two feeding peaks that normally occur at light and dark onset in the rat (-90% 2 h after dark onset and -49% 2 h before light onset). These results indicate that neonatal treatment with MSG induces important changes in feeding patterns and feeding rhythms in the adulthood. These changes might be related to the disappearance of neurotransmitters located in the arcuate nucleus.

Animals↗
PubMed1997

Arginine vasopressin (AVP) depletion in neurons of the suprachiasmatic nuclei affects the AVP content of the paraventricular neurons and stimulates adrenocorticotrophic hormone release.

Arginine vasopressin (AVP) produced in the hypothalamic suprachiasmatic nuclei (SCN) plays a role in establishing neuroendocrine rhythms and, in particular, in regulating the corticotrope axis rhythm. It has recently been shown that AVP from SCN inhibits corticosteroid release. In order to investigate the influence of suprachiasmatic AVP on the different peptidergic systems through the hypothalamus, SCN neurons containing AVP were functionally lesioned by using toxins associated with a cytotoxic monoclonal antibody (MAb) raised against AVP. Six days later, the AVP contents and AVP mRNA were measured in different hypothalamic and extrahypothalamic sites. Adrenocorticotrophic hormone (ACTH) concentration was also measured in plasma. Microinjection of the AVP-MAb/toxin mixture into SCN brought about a significant decrease in the AVP expression in SCN. This is demonstrated by the decrease in the AVP immunoreactive content (24%, P < 0.01) and the decrease of AVP hybridized mRNA (33%, P < 0.01). This points to the efficiency of the microinjection in decreasing the production of AVP in the injection area. Modifications of the AVP contents in the two subdivisions of the hypothalamic paraventricular nucleus (PVN) were also observed. AVP contents decreased in the parvocellular subdivision (pPVN); this is coherent with the AVP depletion in SCN since pPVN is the major site of the SCN hypothalamic efferences. AVP content and AVP mRNA increased in the magnocellular subdivision (mPVN); this also confirms the difference in AVP synthesis regulation according to the PVN subdivisions. The microinjection did not modify AVP expression in supraoptic nuclei or oxytocin (OT) immunoreactive content in the main hypothalamic OT containing sites. Plasma ACTH values were double (P < 0.02) the values measured under non-specific IgG treatment 10 hr after lights on. This probably resulted from the stimulation of the hypothalamo-pituitary-adrenal system since corticotrophin-releasing hormone (CRH) mRNA increased simultaneously by 24% (P < 0.05) in the PVN and the immunoreactive CRH content of the median eminence significantly decreased (26%, P < 0.05). Overall, our data confirm that AVP produced in the SCN inhibits the CRH-adrenocorticotrope axis in normal conditions, probably because of SCN projections of AVP neurons on the PVN.

Adrenocorticotropic Hormone↗
PubMed1997

Dietary preferences in monosodium glutamate-lesioned rats: age-variable influence of hypothalamic neuropeptide Y.

In this study, we measured hypothalamic neuropeptide Y (NPY) and the food preference in weanling and adult monosodium glutamate (MSG)-lesioned and control rats. The MSG lesion was induced by three subcutaneous injections (4 g/kg body wt) during the first week of life of the rats. All treated and control weanling rats strongly preferred a high carbohydrate (HC) diet to a high fat (HF) diet. Adult control rats ate 60% more HF diet (P < 0.001) and 25% less HC diet (P < 0.01) than MSG-treated rats. At weaning and in adulthood, NPY concentrations in MSG-rats were markedly lower in the arcuate and paraventricular nuclei (P < 0.01 or less) than in control rats. The MSG treatment did not affect carbohydrate preference observed at weaning. It was associated with a limited development of fat appetite in adulthood. NPY could influence the dietary preferences more in adulthood, likely when all neuropeptidergic systems are mature.

Age Factors↗
PubMed1997

Physiological regulation of hypothalamic neuropeptide Y release in lean and obese rats.

The paraventricular nucleus (PVN) of the hypothalamus is an important site for the regulation of feeding behavior. Neuropeptide Y (NPY) injected into this nucleus strongly stimulates food intake. In the current study we measured NPY release in the PVN of unrestrained rats through the push-pull technique. The rats were placed in their habitual environment and conditions of life. NPY release was augmented by > 40% (P < 0.01) in Long-Evans rats deprived of food for 12 h. It returned to the baseline as measured in ad libitum-fed rats 90 min after food access. Its stimulation by 55 mM KCl in refed animals indicated that the whole stock of NPY was not used during a short fast. During the light-dark transition, when feeding behavior is initiated. NPY release in lean Zucker rats showed a peak 20 min after lights off and then declined. It corresponded well with the first feeding episodes. In the obese Zucker rats, this peak was absent. NPY release was totally anarchic but at a high level. The feeding behavior of the obese rats was not as time delimited as in the lean rats. This study performed in very physiological conditions therefore indicates that NPY release could drive feeding behavior in the normal life. Its dysregulation in obese rats could participate in overeating and absence of feeding rhythm measured in these rats and speed up the development of their obesity.

Animals↗
PubMed1997

Relationship between blood pressure and renin, angiotensin II and atrial natriuretic factor after renal transplantation.

The objective of the study was to assess the evolution of renin, angiotensin II, atrial natriuretic factor (ANF) and blood pressure (BP) in the first trimester following renal transplantation in man Thirty-two recipients were investigated for 3 months post-transplantation. Twenty had a history of hypertension with moderate cardiac hypertrophy. Thirty-one retained their native kidneys. Five kidney donors had a history of mild hypertension. The recipients were perioperatively volume-expanded with 0.9% saline and diuresis was maintained for 48 h with furosemide and dopamine. The sodium intake was 25 mEq/24 hours. Prophylactic immunosuppressive therapy was antilymphocyteglobulins (25 cases), or anti-LFA1 (7 cases) and maintenance therapy was cyclosporine-prednisone (8 cases), or cyclosporine-prednisone-azathioprine (24 cases). Mean BP, serum creatinine, urinary sodium excretion (UNA) and hormonal (renin, angiotensin II and ANF) parameters were collected every other day for the first week after transplantation and then twice monthly. Twenty (62.5%) patients developed hypertension and hypertension was more frequent in patients with a delayed graft function, than in patients with immediate good graft function (10/20 vs. 4/12, p < 0.05%). Both hypertensive (group HBP) and normotensive (group NBP) patients had similar very low renin and angiotensin II plasma levels, after an initial early peak. Analysis of covariance with multiple regression analysis showed that in the HBP patients, BP was negatively correlated with UNA (p = 0.02) and positively with plasma ANF (p < 0.01). The normal BP patients also showed a correlation between BP and UNA, although it was limit of statistical significance (p = 0.05); there was no correlation between ANF and BP. We conclude that the RAS is rapidly depressed after renal transplantation and does not interfere with BP regulation. The hypertension in the early stage of post-transplantation varies inversely with the urinary sodium excretion. The defective sodium excretion, which dominates the effect of the low sodium diet, results in volume overload, increased ANF and volume-dependent hypertension.

Adult↗
PubMed1996

Enhanced feeding response to neuropeptide Y in hypothalamic neuropeptide Y-depleted rats.

Monosodium glutamate is neurotoxic for the arcuate nucleus and more generally for all circumventricular organs when injected in newborn rats. Neuropeptide Y, a potent stimulator of food intake, is mainly synthesized in the arcuate nucleus. In the present experiment, we determined the hypothalamic status and the feeding response to intracerebroventricular neuropeptide Y in adult rats neonatally treated with monosodium glutamate. Marked neuropeptide Y decreases were measured in the arcuate nucleus and in the paraventricular nuclei in monosodium glutamate-treated rats (-40%; P < 0.01). Adult rats neonatally treated with monosodium glutamate weighed significantly less (-8%; P < 0.01) and ate less (-10%; P < 0.01) than the control rats. Neuropeptide Y injections in a lateral brain ventricle stimulated food intake in control and monosodium glutamate-treated rats in a dose-dependent manner (P < 0.001). Whatever the time after drug injection (2, 4, 6 and 8 h) and the injected dose (0.5, 1 and 5 micrograms), feeding responses were always greater in monosodium glutamate-treated rats (about 2 times greater starting with the lowest dose (0.5 microgram): 9.3 +/- 1.0 (monosodium glutamate) vs. 5.3 +/- 0.7 (control) g/2 h, P < 0.01). Calculated minimal effective doses were also always smaller in monosodium glutamate-treated rats than in control animals (P < 0.01). Neuropeptide Y increased meal duration, meal size and decreased latency to initiate feeding in monosodium glutamate-treated rats (P < 0.01) and control rats (P < 0.01). For each dose of neuropeptide Y, effects were more pronounced on meal size (+70%) and meal duration (+25%) in monosodium glutamate-treated rats than in control rats. Therefore, monosodium glutamate-treated rats were more sensitive to exogenous neuropeptide Y. Decreased food intake in the monosodium glutamate-treated rats was associated with a decrease in neuropeptide Y concentrations in the arcuate-paraventricular axis. This confirms the functional role of this peptidergic pathway in eating behavior.

Animals↗
PubMed1996

Consequences of coronary occlusion on changes in regional interstitial myocardial neuropeptide Y and norepinephrine concentrations.

An attempt to determine the consequences of prolonged ischemia on simultaneous regional changes in norepinephrine (NE) and neuropeptide Y (NPY) interstitial myocardial concentrations in a pig model in vivo was made. The aim of the authors was to investigate further the mechanism of the major NE release previously observed in perfused hearts preserved using a Langendorff technique. Regional myocardial ischemia was induced by ligation of the left anterior descending coronary artery (LAD) in ten anesthetized pigs. NE and NPY release was studied using interstitial microdialysis, a technique initially used to monitor neurotransmitter kinetics in brain dialysate samples. Four dialysis probes were implanted into the left ventricular wall of the beating heart. Two were implanted into the ischemic region (LAD) (for NE and NPY determinations, respectively) and the remaining two into the non-ischemic left circumflex coronary artery region (LCX). Dialysate NE and NPY concentrations, as indices of interstitial myocardial NE and NPY concentrations, were measured by HPLC and RLA, respectively. A slight but significant increase in NPY levels was observed in both territories (LAD: from 190 +/- 27 to 349 +/- 62 pmol/l, LCX: 146 +/- 30 to 257 +/- 52 pmol/l) suggesting moderate stimulation of cardiac sympathetic nerve activity following LAD occlusion. On the contrary, a marked but progressive increase in NE release was observed in the ischemic region (from 8.8 +/- 1.0 to 251.4 +/- 44.8 nmol/l), when NE levels in the non-ischemic region remained stable (from 10.3 +/- 2.1 to 11.0 +/- 1.9 nmol/l). These results demonstrate the utility of regional in-vivo myocardial NE and NPY monitoring using microdialysis. The strong and sustained NE accumulation occurring in the ischemic region is consistent with the hypothesis of a local non-exocytotic metabolic NE release in case of prolonged myocardial ischemia, when exocytotic release remain only minimal as attested by the slight increase in NPY observed.

Animals↗
PubMed1996

Nitric oxide mediates hyperphagia of obese Zucker rats: relation to specific changes in the microstructure of feeding behavior.

The presence of a nitric oxide synthetase (NOS) was demonstrated in the rat brain. It has been demonstrated recently that NOS-inhibitors reduce food intake in mammals and this suggest that nitric oxide (NO) might be a physiological mediator involved in the mechanisms controlling feeding behavior. Actually, there is no information about the acute central and peripheral effects of NOS-inhibitors on feeding behavior in obese and lean Zucker rats. That is why we investigated the acute dose-dependent activity of NG-Nitro-Arginine-Methyl-Ester (L-NAME) on food intake and feeding behavior in these rats. When given peripherally in the obese rats, L-NAME produced a dose-dependent decrease in food intake (p<0.001). The calculated MED and the ED 50 were 0.50 mg/kg IP and 3.46 mg/kg IP, respectively. These effects could not be reproduced in the lean Zucker rats whatever the dose used (p=0.59). The anorectic properties of L-NAME were very well translated into the microstructure of the feeding behavior. Time spent to eat (p<0.001), meal duration (p<0.01) and meal number (p<0.01) were reduced in the obese rats. Interestingly, L-NAME produced the same effects in the lean rats, but meal size increased in a compensatory manner. Central administration of L-NAME reproduced the same effects in the obese rats, but lean rats still remained insensitive. Central aminergic and/or peptidergic defects associated with the expression of hyperphagia might explain the differences observed between these lean and the obese animals. These results indicate a role of nitric oxide in the expression of hyperphagia and show that it might be a physiological mediator involved in the mechanisms controlling feeding behavior.

Animals↗
PubMed1996

Opposite influence of carbohydrates and fat on hypothalamic neurotensin in Long-Evans rats.

Neurotensin inhibits food intake when injected in the central nervous system and is released after fat ingestion. The aim of the present study was to measure it in different brain areas and to determine if it is involved in the long-term variations in food intake induced by the ingestion of a high-fat (HF) diet. We compared the results with those obtained with 2 low-fat [high-carbohydrates (HC)] diets and a well-balanced diet. For this purpose, weanling male Long-Evans rats were fed ad libitum for 14 weeks either on a control diet, a HF diet or a HC diet. The rats with the HC (high-starch) diet were divided into 2 subgroups: the first (HC) drank water and the second (HCS) drank a 25% sucrose solution. During the last week of the experiment, energy intake of the HCS rats was significantly greater than that of the 3 other groups of rats (+17.2%; p < 0.01; +27.1%; p < 0.001 and +34.6%; P < 0.001 vs the control, HC and HF rats respectively). NT did not vary in the midbrain and particularly in the ventral tegmental area. Its concentrations were significantly higher in the 2 HC groups than in the HF rats both in the paraventricular (PVN; p < 0.02) and dorsomedial nuclei (DMN; p < 0.03). In the DMN, they were positively correlated with energy intake (r = 0.39; p = 0.027). These results indicate that hypothalamic neurotensin is indeed involved in the long-term modulation of feeding behavior by diet composition and that fat is the more potent macronutrient for its regulation.

Animals↗
PubMed1996

[Evaluation of smoking in chronic severe respiratory insufficiency patients treated with long-term oxygen at home].

Two hundred and fifty patients with chronic respiratory insufficiency (202 men and 48 women), being treated by oxygen therapy at home were included in a study, which aim was to estimate the proportion of patients who were either smokers or exposed to passive smoking, by the use of a questionnaire and measurement of cotininuria. Urinary sample and autoquestionnaire collection was carried out by the nurses of the Lorraine's association of home respiratory assistance. Urinary continine was measured by radio immuno assay. Twenty one smokers, 186 ex-smokers and 43 non-smokers were identified through the questionnaire. Of the 21 self confessed smokers 20 had a urinary cotinine level over 250 ng/ml, 1 smoker lower than 250 ng/ml; among the professed non-smokers, 42 had a level lower than 100 ng/ml and 1 over 250 ng/ml but the contininuria creatinuria ratio classified this latter in the non-smokers non exposed to passive smoking group. Among the 186 declared ex-smokers, 20 over 250 ng/ml were probably smokers, 160 lower than 100 ng/ml could be considered as non-smokers, and finally 100 in between could be assessed as non-smokers exposed to passive smoking. The results enabled 43 smokers (17%) and 5 (2%) exposed to passive smoking to be identified. They confirm the unreliability of smoking habits questionnaires and the importance of cotininuria in the detection of nicotine poisoning.

Adult↗
PubMed1995

The immunological impairment of vasopressin (AVP) neurons into paraventricular nuclei modifies AVP expression in suprachiasmatic nuclei.

A monoclonal antibody (MAb) to vasopressin (AVP) inhibits the synthesis and the release of AVP when injected near the AVP-producing neurons. In the present experiments, the AVP-MAb was microinjected near the paraventricular (PVN) or the supraoptic (SON) neurons of the rat hypothalamus and the AVP expression was measured in the suprachiasmatic nuclei (SCN). When microinjected near PVN, the AVP-MAb modified the AVP mRNA studied by in situ hybridization, and the AVP immunoreactive content of SCN, whereas it failed to show some effect when injected near SON. This confirms the privileged relationships between AVP-producing neurons in SCN and PVN.

Animals↗
PubMed1995

Neurotensin decreases with fasting in the ventromedian nucleus of obese Zucker rats.

Neurotensin (NT) inhibits food intake when injected either in brain ventricles or in hypothalamic nuclei such as the ventromedian nucleus (VMN). NT concentrations are lower in obese than in lean Zucker rats in several hypothalamic nuclei, including the VMN. In this experiment, we studied the influence of the feeding state on NT concentrations in different brain areas of 10-week-old lean (n = 27) and obese (n = 27) Zucker rats that were fasted for 48 hours and then refed for 6 hours. NT level was measured in the microdissected areas by radioimmunoassay. Obese rats ingested approximately 50% more food than lean rats in the ad libitum (ad lib) condition (P < .001) and 12% more during the refeeding time (NS). NT concentrations in the median eminence (ME) were 50% lower in obese than in lean rats (P < .001). This decrease could be related to a 20% decrease in the arcuate nucleus (ARC) of the obese rats (P < .04). NT concentrations in the ME and ARC, which are important for the control of pituitary hormone secretion by NT, were not changed by the feeding state in both genotypes. NT varied with the feeding state in the VMN only (P < .04). Concentrations were 45% lower in fasted (FD) obese rats than in ad lib or refed (RF) obese rats (1.09 +/- 0.25 ng/mg protein v 1.98 +/- 0.36 ad lib and 1.62 +/- 0.11 RF, P < .05). They remained unchanged in lean rats. NT variations in the VMN of obese rats could contribute synergistically with other neuropeptides to the abnormal feeding behavior of these rats.

3-Hydroxybutyric Acid↗
PubMed1995

The immunological impairment of arcuate neuropeptide Y neurons by ricin A chain produces persistent decrease of food intake and body weight.

Neuropeptide Y is demonstrated as a potent orexigenic peptide when injected into the rat hypothalamic paraventricular nuclei. The neuropeptide Y innervation of paraventricular nuclei originates from both hypothalamic arcuate nuclei and brainstem neurons, whose specific role in the control of food intake is still under discussion. To assess the role of the arcuate neuropeptide Y in the regulation of food intake, we propose a new method for immunologically impairing the neuronal secretion of neuropeptide Y from a unique brain site. The monoclonal antibody to the neuropeptide Y precursor epitope, the C-flanking peptide, was microinjected with two cellular toxins (the ricin A chain and the monensin) into the hypothalamic arcuate nuclei or paraventricular nuclei. One microinjection into the arcuate nuclei reduced the food intake and body weight gain for 10 days. It prevented the food intake stimulation usually induced by a 12 h food deprivation. This decrease of food intake was not due to the aversive properties of monoclonal antibody or cellular toxins, or the immunoneutralization of the biologically active neuropeptide Y, because (i) the acute effect of the microinjection into the arcuate nuclei promoted a transient increase of the food intake likely induced by a strong release of neuropeptide Y from the arcuate neurons which were immunologically damaged, and (ii) the C-flanking peptide monoclonal antibody binds neither neuropeptide Y nor its receptors. The microinjection was inefficient when C-flanking peptide monoclonal antibody was replaced by non-specific rat immunoglobulins or when the C-flanking peptide monoclonal antibody/toxins mixture was injected into the paraventricular nuclei. The data bring further arguments in two domains.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1994

Putative neuropeptide Y antagonist failed to decrease overeating in obese Zucker rats.

A central dysregulation of several neuropeptides could be at the origin of the marked hyperphagia of the obese Zucker rat, a well-known animal model used for the study of obesity. Neuropeptide Y (NPY), which stimulates food intake and increases early in life in obese rats, plays a major role in the development of this hyperphagia. The aim of our experiment was to test a proposed NPY antagonist namely PYX-2 in obese hyperphagic Zucker rats in order to know if it could be an interesting drug for limiting their food intakes. Four doses of PYX-2 (50-1000 pmol) were injected in a counterbalanced order in the lateral brain ventricles of 10 adult male Zucker rats. Food intake was recorded 0.5, 1, 2, 3, 6, and 23 h after PYX-2 injection and compared either to the rat's spontaneous food intake or to the food intake following injection of artificial CSF (vehicle) only. It was not modified by any dose of PYX-2 whatever the time considered (1 h after injection: 4.3 +/- 0.5 (1000 pmol) vs 4.6 +/- 0.8 (CSF) g; 23 h period: 27.0 +/- 1.9 (1000 pmol) vs 26.6 +/- 2.9 (CSF) g; N.S.). Thus, PYX-2, the putative NPY antagonist, totally failed to inhibit food intake in the obese rats. The absence of effect of PYX-2 on food intake can be explained by the structure of PYX-2, a modified 27-36 amino acid sequence that may not be recognized by the Y1-type NPY receptors which are involved in the regulation of feeding behavior.

Amino Acid Sequence↗
PubMed1994

Increased threshold concentrations of neuropeptide Y for a stimulatory effect on food intake in obese Zucker rats--changes in the microstructure of the feeding behavior.

A central dysregulation of several neuropeptides could be at the origin of the marked hyperphagia of the obese Zucker rat, a well-known animal model used for the study of obesity. Neuropeptide Y (NPY), which strongly stimulates food intake and increases early in life in obese rats, plays a major role in the development of this hyperphagia. The aim of our experiment was to measure the feeding responses of lean (n = 8) and obese (n = 17) male Zucker rats to several doses of exogenous NPY injected in the lateral brain ventricle. We analyzed the microstructure of the rats' feeding behavior with an automatic device for 8 h post-injection. NPY stimulated food intake both in the lean and obese rats in a dose-dependent manner (P < 0.001). However, the minimal effective dose was always 3-4 times greater in the obese rats than in the lean ones (range: 0.43-0.53 vs. 0.12-0.18 microgram/brain; P < 0.001). Meal size, meal duration and time spent eating significantly increased in the lean rats (P < 0.05 or less). The last two parameters also increased in the obese rats but with the highest dose (5 micrograms) only. The obese Zucker rats were therefore less sensitive to NPY than the lean ones, probably because of their already high endogenous NPY levels. The modifications in the eating behavior indicate that NPY could overcome the satiety signals.

Animals↗
PubMed1994

Hypothalamic neuropeptides could mediate the anorectic effects of fenfluramine.

Oxytocin, vasopressin and corticotrophin releasing factor have anorectic properties when injected centrally. We studied the kinetics of these neuropeptides by injecting fenfluramine, a drug which reduces food intake, in Long Evans rats. The drug was injected daily through a double chronic cannula implanted above the paraventricular nucleus of the hypothalamus; the rats had free access to pure macronutrients. The rats lost weight during the treatment. Their total caloric intake decreased mostly because the carbohydrate intake decreased, while the protein intake increased slightly. The synthesis and release of brain oxytocin and vasopressin were increased and the release of corticotrophin releasing factor was stimulated. The neuropeptides could be involved in fenfluramine-triggered mechanisms.

Animals↗