Quantitative analysis of corticotropin-releasing factor and arginine vasopressin mRNA in the hypothalamus during chronic morphine treatment in rats: an in situ hybridization study.

The content of corticotropin-releasing factor (CRF) and arginine vasopressin (AVP) in the hypothalamic paraventricular nucleus (PVN) increases during chronic morphine treatment. Because these experiments cannot distinguish between increased synthesis or reduced release, the present study measured changes in CRF and AVP mRNAs in the PVN by in situ hybridization. Concomitantly, changes in noradrenaline turnover in the PVN and changes in plasma corticosterone release were determined. Male rats were implanted with placebo (naive) or morphine pellets for 7 days. On day 7, groups of rats received an acute injection of either saline i.p. or morphine (30 mg/kg, i.p.). Acute morphine injection did not change the total size of the labelled area for CRF mRNA in the PVN of naive or morphine-pelleted rats, indicating that the number of CRF-containing neurones was unchanged. On the other hand, in rats chronically treated with morphine, the intensity of labelling for CRF mRNA was significantly reduced, suggesting a decrease in the synthesis of CRF. In placebo rats, injection of saline or morphine did not affect the surface hybridized for AVP mRNA. By contrast, in the morphine-group injected with saline, there was a significant reduction in the number of labelled neurones, measured by the size of labelled area. Similarly, there was a decrease in intensity of AVP mRNA expression in the parvocellular and magnocellular neurones of the PVN in the morphine-group injected with saline, suggesting a decreased synthesis of AVP in these neurones. In parallel with the decrease in the expression of CRF and AVP mRNAs in the PVN, there was a pronounced decrease in noradrenaline turnover and in the release of corticosterone in the morphine-pelleted rats. In conclusion, present results show that, in addition to modifications in corticosterone secretion and in noradrenaline turnover, chronic morphine administration produces a reduction in the synthesis of CRF and AVP.

Galanin receptor antagonists decrease fat preference in Brattleboro rat.

The Brattleboro rat eats spontaneously 46% of its diet per day in fat when given a choice of carbohydrate, protein and fat. An overexpression of galanin (GAL) has been also observed in the hypothalamic paraventricular nuclei (PVN). This associative correlation has led to a hypothesis of a functional relation between central galanin expression and the preference for a lipid diet. In the present experiments, the effects of two GAL receptor antagonists, C7 and galantide, on fat consumption and central overexpression of GAL were investigated. Both antagonists were injected into either the cerebral ventricles or directly above the PVN, and the diet consumption followed for the subsequent 24h. C7 decreased significantly fat consumption when injected into the ventricles or directly above the PVN. In contrast, galantide must be injected above the PVN to show the same effect. However, the two antagonists did not modify GAL mRNA expression in the PVN when they were injected 2h before sacrifice. These experiments confirm a functional link between the preferential consumption of fat and hypothalamic Galanin; different subtypes of the GAL receptor are probably involved, since both Galanin antagonists were differently efficient in decreasing spontaneous fat selection of the Brattleboro rat.

Hypothalamic and limbic expression of CRF and vasopressin during lactation: implications for the control of ACTH secretion and stress hyporesponsiveness.

Lactation is associated with physiological and behavioral changes that optimize conditions for development of the offspring. Although neuroendocrine and emotional stress responses are blunted, the central mechanisms involved are unclear. In addition to a reduction in stimulatory noradrenergic inputs to paraventricular nucleus (PVN) neurons, we demonstrate that lactation induces: (1) unique phenotypic changes in neuropeptide expression by hypothalamic PVN neurons (reduced expression of corticotropin-releasing factor (CRF) mRNA and increased expression of vasopressin mRNA in parvocellular PVN neurons); and (2) changes in pituitary sensitivity to CRF (reduced) and vasopressin (increased) as a consequence of differential CRF/vasopressin secretion into the hypophysial portal blood. Neurons in the bed nucleus of the stria terminalis (BNST) and the central amygdala (CeA) that are implicated in the control of the hypothalamopituitary-adrenal axis also display changes in lactation: expression of CRF mRNA in the CeA is reduced, consistent with the diminished responsiveness to acoustic startle observed in nursing mothers. In contrast, expression of CRF mRNA is increased in the dorsolateral portion of the BNST, probably because of the tonic increases in endogenous glucocorticoid production during this period. Using immuno-targeted lesions of CRF or vasopressin in the PVN of virgin females, we have shown that CRF neurons of the PVN send inhibitory projections to the dorsolateral portion of the BNST and stimulatory inputs to CRF neurons in the CeA. Thus, it is possible that lactation-induced changes in the activity of parvocellular PVN neurons might also modulate the expression of neuropeptides and neurotransmitters in the BNST and the amygdala.

Plasma leptin and hypothalamic neuropeptide Y and galanin levels in Long-Evans rats with marked dietary preferences.

Neuropeptides present in the hypothalamus and new messengers in the periphery such as leptin modulate food intake in mammals. Neuropeptide Y (NPY) and galanin in microdissected brain areas and plasma leptin levels were measured by specific radioimmunoassays during the resting period in rats selected for their strong preference either for carbohydrate or fat, but with identical energy intake. NPY concentrations were 23% lower (p <.02) in carbohydrate-preferring (CP) than in fat-preferring (FP) rats in the parvocellular part of the paraventricular nucleus (PVN), which is one of the main areas involved in the regulation of feeding behavior. On the other hand, galanin was significantly (+25%, p = .03) higher in CP rats than in FP rats in the magnocellular part of the PVN. Plasma leptin was more than 50% higher in FP rats than in CP rats (p < .01) and highly correlated with the fat preference (r = 0.57; p = .003) and body weight gain. We conclude that the rats with a spontaneous and marked dietary preference have a characteristic peptidergic profile. Due to their anatomical relationships, neuropeptide Y could act in conjunction with galanin in a peptidergic balance located in the paraventricular nucleus. This model integrates information provided by the energy stores and translated by peripheral messengers such as leptin which could act in a counterregulatory manner in order to limit the overweight induced by the ingestion of unbalanced diets.

Galanin-R1 receptor mRNA expression in the hypothalamus of the Brattelboro rat.

Using in situ hybridization the regulation of mRNA encoding the galanin receptor R1 was investigated in the mutant Brattelboro (diabetes insipidus) rat. We here report an increase of the galanin receptor R1 mRNA levels in the hypothalamic supraoptic and paraventricular nuclei of the mutant strains. The increase seemed to be confined to magnocellular neurons, since no changes were detected in galanin receptor R1 mRNA levels in the extra-hypothalamic nucleus of the olfactory tract. The results confirm that osmotic stimulation induces up-regulation of galanin receptor R1 mRNA levels. This may increase the sensitivity to galanin peptide, the endogenous ligand for this receptor.

Dietary preferences of Brattleboro rats correlated with an overexpression of galanin in the hypothalamus.

Galanin (GAL) is a neuropeptide cosynthesized with vasopressin (AVP) in neurons of the hypothalamo-neurohypophysial system. It increases food intake when injected into the brain and elicits an overconsumption of fat. The Brattleboro rat (DI) is genetically unable to produce AVP; the AVP-deficient-producing neurons of the hypothalamo-neurohypophysial system of DI rats are chronically stimulated and DI rats suffer from diabetes insipidus. We studied the central expression of GAL and the dietary preferences in the DI rat. GAL was overexpressed in the hypothalamus of the DI rat. GAL mRNA was higher by 1.8-fold in the supraoptic (P < 0.05) and by four-fold in the paraventricular nuclei (P < 0.001) of male and female DI rats compared with those of control Long Evans (LE) rats. However, GAL mRNA was lower in the arcuate nuclei of DI rats and equal to that of LE rats in the dorsomedian nuclei. We also measured a high preference for a lipid diet (45% of the daily consumption) when DI rats ate from a choice of the three macronutrients. Chronic infusion with deamino-8D-AVP (agonist of AVP V2 receptors) prevented the diabetes insipidus and the chronic stimulation of the hypothalamo-neurohypophysial system of the DI rats. However, the treatment did not suppress the overexpression of GAL, nor did it affect the rats' preference for a lipid diet. We conclude that the DI rat provides a novel animal model in which a spontaneous dietary preference correlates with the overexpression of one of the hypothalamic peptides, GAL.

Hypothalamic neuropeptide Y content and mRNA expression in weanling rats subjected to dietary manipulations during fetal and neonatal life.

Hypothalamic neuropeptide Y (NPY) is present very early during the fetal life and is rapidly functional in the regulation of feeding behavior after birth. In the present experiment, we tried to determine the influence that the diet type ingested by dams during gestation and lactation would have on the growth and hypothalamic and pancreatic peptides of their progeny immediately after weaning. The dams were fed on either a high-carbohydrate (HC), a high-fat (HF) or a control diet ad libitum. At 3 days of age, the HC pups weighed significantly more than the two other groups (P < 0.02 vs. C and P < 0.002 vs. HF). At weaning, the HF rats were significantly lighter than the two other groups (P < 0.001). Food intake was significantly lower in the HF rats than in the two other groups 3 days (P < 0.002) and 5 days after weaning (P < 0.02). Plasma glucose of the HF rats was significantly lower than that of the control rats (P < 0.05) and of the HC rats (P < 0.01). Immunoreactive insulin in the HF rats was also significantly lower than that in the control rats (-53%; P < 0.001) and in the HC rats (-47%; P < 0.001). NPY content and mRNA expression in the arcuate nucleus were not significantly different between the three groups. NPY concentration only varied in the ventromedian nucleus. In the control rats, it was significantly lower than that of the HC rats (-35%; P < 0.01) and that of the HF rats (-32%; P < 0.002). These data demonstrated that the regulatory mechanisms of feeding behavior in offspring are completely and differentially modified by the macronutrient content of the diets ingested by their mother. Both peripheral and central mediators were strongly implicated. These modifications could have long-term repercussions on body weight and composition.

Leptin (ob) mRNA and hypothalamic NPY in food-deprived/refed Syrian hamsters.

Food deprivation in the laboratory rat decreases plasma leptin and insulin, elevates glucocorticoid concentration, and increases the activity of the neuropeptide Y (NPY) system and feeding drive. In contrast, Syrian hamsters fail to modify feeding behaviour in response to various food scarcity paradigms. Two components of the neuroendocrine-hormonal response to food deprivation, adipose tissue-derived leptin and hypothalamic NPY, are investigated in the Syrian hamster. ob (leptin) mRNA was less abundant in subcutaneous than abdominal adipose tissue, but not to the extent observed in other rodents. Food deprivation for 48 h reduced ob mRNA in inguinal and retroperitoneal white adipose tissue; gene expression was partially restored by refeeding. In contrast, in epididymal fat there was no effect on ob mRNA. NPY concentrations in hypothalamic nuclei were also unaffected by feeding state. The predicted amino acid sequence of leptin from the Syrian hamster was over 90% homologous with Djungarian hamster and mouse sequences, and the leptin receptor gene (OB-R), and specifically the long intracellular splice variant, OB-Rb, was expressed in the same forebrain and hypothalamic regions that have been described in laboratory mice and rats, including hypothalamic arcuate, dorsomedial, and ventromedial nuclei. The failure of food deprivation to affect NPY and feeding behaviour in Syrian hamsters is unlikely to be due to defects in the leptin system, although there may be region-specific differences in the regulation of leptin signaling in laboratory rats and Syrian hamsters.

Alterations in corticotropin-releasing factor and vasopressin content in rat brain during morphine withdrawal: correlation with hypothalamic noradrenergic activity and pituitary-adrenal response.

The modification in the activity of noradrenergic neurons projecting to the hypothalamus and the pituitary-adrenal response during morphine withdrawal as well its correlation with alterations in corticotropin-releasing factor (CRF) and vasopressin (AVP) content in different brain areas was analyzed. Male rats were implanted with placebo (naïve) or morphine (tolerant/dependent) pellets for 7 days. On day 8, groups of rats received an acute injection of saline s.c. (control) or naloxone (1 mg/kg s.c.) and were decapitated 30 min later. After administration of naloxone to tolerant rats (withdrawal) we found a striking parallelism between an enhanced activity of hypothalamic noradrenergic neurons and an increased corticosterone secretion; concomitantly, the CRF but not the AVP content in the paraventricular nucleus was decreased, which might reflect an increased release of the peptide. During withdrawal, CRF content also was decreased in the arcuate nucleus, whereas no changes were found in the median eminence, dorsomedial, ventromedial nuclei or in the bed nucleus of the stria terminalis. AVP content levels were not modified in arcuate nucleus, supraoptic or in the suprachiasmatic nuclei. Present data suggest that a hypothalamic noradrenergic hypersecretion may be involved in a selectively increased activity of CRF neurons in the paraventricular nucleus and arcuate nucleus and then in the enhanced release of corticosterone induced by morphine withdrawal. However, we did not find any correlation between opioid withdrawal-induced alterations in the pituitary-adrenal axis and AVP modifications.

Differential regulation of corticotropin-releasing factor and vasopressin in discrete brain regions after morphine administration: correlations with hypothalamic noradrenergic activity and pituitary-adrenal response.

The changes in the content of corticotropin-releasing factor (CRF) and arginine vasopressin (AVP) in discrete brain nuclei during chronic opioids administration have not been well established. We evaluated the effects of acute and chronic morphine administration on the content of CRF and AVP in different hypothalamic and extrahypothalamic (bed nucleus of the stria terminalis, BNST) nuclei in rats. Concomitantly, changes in hypothalamic noradrenaline (NA) turnover [estimated by the 3-methoxy-4-hydroxyphenylethyleneglycol MHPG/NA ratio] and in plasma corticosterone release (as a marker of the activity of the hypothalamus-pituitary-adrenal axis) were determined. Male rats were implanted with placebo (naïve) or morphine (tolerant) pellets for 7 days. On day 8, groups of rats received an acute injection of either saline i.p. or morphine (30 mg/kg i.p.) and were sacrificed 30 min later. Acute morphine injection to naïve rats increased both the release of corticosterone and the hypothalamic NA turnover. CRF and AVP showed no modifications in the paraventricular nucleus (PVN) or in the median eminence (ME). CRF content decreased in the ventromedian nucleus (VMN) and increased in the BNST, but did not change in the arcuate nucleus (AN). AVP was elevated in the supraoptic nucleus (SON) but not changed in the suprachiasmatic nucleus (SCN). In chronic morphine-treated rats, there was a pronounced decrease in the NA turnover and in the release of corticosterone, which indicates that tolerance develops to the acute effects of morphine. Correspondingly, CRF and AVP were enhanced in the PVN and decreased in the ME, when compared with naïve rats injected with morphine. CRF content was decreased in the AN and in the BNST, but increased in the VMN. The AVP content was decreased in the SON, and no modifications were seen in the SCN. The present study shows that, in addition to the modifications in corticosterone secretion and in hypothalamic NA turnover, chronic morphine administration produces a complex response in the CRF and AVP systems. These modifications might contribute to the behavioral, emotional and neuroendocrine alterations produced during opioid tolerance.

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.

Changes in hypothalamic oxytocin levels during morphine tolerance.

The role of hypothalamic oxytocin neurons in the hypothalamus-pituitary-adrenal (HPA) axis adaptation during opioid tolerance has not been explored. In this study the modification of oxytocin levels in different hypothalamic nuclei was determined after acute or chronic morphine exposure. Male rats were implanted with placebo (naïve) or morphine (tolerant) pellets for 7 days. On day 8, groups of rats received an acute injection of either saline i.p. or morphine (30 mg/kg i.p.) and were sacrificed 30 min later. In morphine-tolerant rats, there was a decrease in the oxytocin content in the median eminence (ME) and in the supraoptic nucleus (SO) after acute injection of saline or morphine. No modifications were seen in the paraventricular nucleus (PVN). The present study demonstrates that chronic morphine administration alters the brain oxytocin system, which suggests that this peptide might contribute to the behavioural, emotional and neuroendocrine responses to opioids.

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.

Hypothalamic NPY and prepro-NPY mRNA in Djungarian hamsters: effects of food deprivation and photoperiod.

Two catabolic states leading to loss of body weight were compared in the Djungarian hamster (Phodopus sungorus campbelli). Hypothalamic neuropeptide Y (NPY) and gene expression for NPY and corticotropin-releasing factor (CRF) were examined after withdrawal of food for 48 h or exposure to short photoperiod for 10 or 20 wk. Food deprivation was accompanied by increases in both NPY and prepro-NPY mRNA in the hypothalamic arcuate nucleus (ARC). Increases in gene expression were limited compared with published data from the rat and were inversely related to predeprivation body weight. Exposure to short photoperiod for 20 wk reduced body weight by 39%, but the activity of the NPY-ergic system was not affected; peptide concentration and gene expression were similar in short photoperiod hamsters and long photoperiod controls. The hypothalamic NPY-ergic system of the Djungarian hamster is sensitive to weight loss due to imposed manipulations of energy balance, but the catabolism observed in short photoperiod gives rise to a body weight that is appropriate to the season encoded by the photoperiod. CRF gene expression was not affected by food deprivation or short photoperiod.

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.

Macronutrient type independently of energy intake modulates hypothalamic neuropeptide Y in Long-Evans rats.

Neuropeptide Y (NPY) induces a robust feeding response when it is injected in the hypothalamus. It stimulates both carbohydrate and fat intakes. Diets rich in either macronutrient are known to induce obesity and to modify feeding behavior. The aim of the present study was to determine the effects of long-term ingestion of these diets on hypothalamic NPY in relation with food intake and body weight gain and composition. For this purpose, three groups of weanling Long-Evans rats were fed either a well-balanced diet, a high-carbohydrate (HC) diet (high starch plus 25% sucrose solution), or a high-fat (HF) diet during 14 weeks. Body weight and food intake were recorded during this period. At the end of the experiment, NPY was measured in several microdissected brain areas, and some adipose tissues (AT) depots were sampled. HF rats weighed significantly more than the two other groups (p < 0.02). They were also fattier (+ 30-50% in AT weights; p < 0.01). Energy intake (EI) of the HC rats was significantly greater than that of the control (+ 15%; p < 0.02) and HF rats (+ 34%; p < 0.01) during the week preceding killing. EI of HF rats over the whole experiment was lower than that of the two groups (p < 0.01).(ABSTRACT TRUNCATED AT 250 WORDS)

Galanin in the hypothalamus of fed and fasted lean and obese Zucker rats.

Galanin (GAL), a 29 aminoacid peptide, is widely distributed in the central nervous system and especially in the hypothalamus. It strongly stimulates food intake when it is injected in the paraventricular nucleus (PVN) of normal rats. The obese Zucker rat with a well-established hyperphagia is characterized by a general dysregulation of some important neuropeptides involved in the regulation of feeding behavior e.g. neurotensin, NPY or CCK and the aim of this study was to measure GAL in different microdissected brain areas in lean (Fa/Fa) and obese (fa/fa) male Zucker rats. As feeding status may modulate the central peptide concentrations, it was measured in ad libitum fed rats and in 48-h fasted rats of both genotypes. GAL was measured by a specific radioimmunoassay in the arcuate nuclei (ARC) and parvocellular (PVNp) and magnocellular (PVNm) parts of the PVN as well as in the median eminence (ME), median preoptic area (MPOA), supraoptic (SON) and dorsomedian (DMN) nuclei. Two-way analysis of variance revealed a very significant effect of genotype in the PVNp (P < 0.001), SON (P < 0.001) and in the ME (P < 0.02). No significant variations at all were noted in the ARC, PVNm, MPOA and DMN. GAL concentrations were more than doubled in the PVNp and SON of ad lib obese rats when compared to the ad lib lean rats (P < 0.005). On the other hand, in the ME where GAL concentration was about 4-fold greater than in the other areas, there was a 20 to 30% decrease in GAL concentrations in the obese rat (P < 0.05).(ABSTRACT TRUNCATED AT 250 WORDS)

Passive immunization and hypothalamic peptide secretion.

Passive immunization is a common approach used to eliminate the biological activity of an endogenous substance by its binding to a specific antibody (Ab). Surprisingly little information has been gathered on the mechanisms involved. Moreover, the possibility that immunoneutralization could affect also the secretion of the antigen itself has been mostly ignored. To study hypothalamic neuropeptide secretion under the condition of passive immunization, labeled and unlabeled monoclonal antibody (MoAb) against arginine vasopressin (AVP) was injected intravenously. After 2 h a similar amount of 125I-MoAb was found in hypophyseal portal and peripheral (femoral artery) plasma, showing a distribution volume of 73.2 ml/kg. Assessment of the MoAb dilution in the same plasma samples from the binding studies revealed substantially higher dilutions (800-5,700 ml/kg). Such a MoAb dilution (saturation) would be attained by the binding of 130-290 pmol AVP/ml plasma. The calculated amount of plasma AVP decreased by one half within the interval from 2 to 24 h after Ab injection, similarly as did the 125I-MoAb content. Intravenous injection of polyclonal corticotropin-releasing hormone (CRH) Ab resulted in a decrease of plasma adrenocorticotropin and corticosterone levels. After 24 h the dilution of the Ab in portal plasma exceeded two times that in peripheral plasma. CRH concentrations of 0.6-2.5 pmol/ml were found by specific radioimmunoassay after its dissociation from the Ab in plasma. The CRH concentration was higher in portal than in peripheral plasma and was related to the amount of the Ab injected. CRH mRNA levels in the paraventricular nucleus were significantly increased in CRH Ab as compared with normal rabbit serum injected rats.(ABSTRACT TRUNCATED AT 250 WORDS)

Effect of food deprivation and refeeding on the concentration of vasopressin and oxytocin in discrete hypothalamic sites.

Recent evidence has implicated hypothalamic peptides, such as arginine vasopressin (AVP) and oxytocin (OT) in the control of feeding behavior. In this study, we investigated the impact of food deprivation (48 h) and subsequent refeeding (6 h) on the concentration of AVP and OT in discrete hypothalamic areas, as well as in the neurohypophysis. We also estimated in these rats certain peripheral measures, including hydroelectrolytic parameters, plasma and urine AVP, and plasma corticosterone. The results of this study revealed that food deprivation for 48 h produced little change in OT concentration in the various hypothalamic nuclei studied, including the paraventricular and supraoptic nuclei, with the exception of the median eminence (ME), where a significant decline (-36%; p < 0.05) was detected. This effect was not significantly reversed by 6 h of refeeding. With respect to AVP concentration, food deprivation caused a reliable decline exclusively in the parvocellular subdivision of the paraventricular nucleus (pPVN; -45%; p < 0.01) and in the supraoptic nucleus (SON; -45%; p < 0.01). No change in AVP was detected in the ME or in most other hypothalamic nuclei examined. Refeeding for 6 h actually potentiated the effect of food deprivation, decreasing further from baseline the content of AVP in the pPVN and SON. The only other hypothalamic area to exhibit a change in AVP content was the ventromedial nucleus, where AVP level increased (p < 0.001) after deprivation and declined to normal after 6 h of refeeding. The content of AVP and OT in the neurohypophysis was unaffected by food deprivation and subsequent refeeding.(ABSTRACT TRUNCATED AT 250 WORDS)

Specific hypothalamic neuropeptide Y variation with diet parameters in rats with food choice.

Neuropeptide Y (NPY) preferentially stimulates carbohydrate intake rather than fat intake but there is no information on the effects of food choice on the concentration of NPY in the brain. We measured brain NPY concentrations in male adult rats that had to choose between a high fat and a high carbohydrate diet or were fed a control diet for 2 weeks. In rats with food choice, energy intake increased (+17%). NPY levels increased in the parvocellular part (PVNp) of the PVN and decreased in the lateral hypothalamus and were significantly correlated with the carbohydrate-to-fat energy ratio but not with total energy intake. This suggests that hypothalamic NPY might be involved in food choice and that PVNp is important in the regulation of feeding behaviour by NPY.