Mesencephalic lesions in female rats resulting in normophagia and reduced body weight.

The effects of bilateral mescencephalic lesions in the area of the ventral noradrenergic bundle (VNA) were studied in immature and mature female rats. The food intake consumption of the immature lesioned rats did not differ from sham operated controls whether fed a chow or high fat diet. However, after the surgery the body weights of the two groups began to diverge with the immature lesioned rats obtaining a significantly lower body weight. By the end of the study the immature lesioned rats were also significantly shorter than the controls. Both groups showed normal body composition throughout the measurement period. Upon refeeding after a one day fast the immature female rats defended their lower than normal pre-fast body weight. These data are in good agreement with our earlier findings using immature male rats. The mature lesioned animals also showed normal food consumption when fed a chow type diet. However the lesioned animals did show a brief hyperphagia when placed on a high fat diet. Unlike the immature lesioned rats the body weight of these lesioned animals did not differ from their sham operated controls. It is suggested that lesions in the area of the VNA may result in hyperphagia or, in no effects on food intake or body weight as reported by others or normophagia with reduced body weight. Exact lesion placement may be responsible for these divergent findings.     

Mesencephalic lesions resulting in normophagia,reduced weight and altered metabolism

The effects of bilateral lesions of the ventral noradrenergic bundle (VNA) were studied in male rats. In contrast to data reported by others, hyperphagia and obesity were not observed following VNA lesions. Indeed, except for a depression during the first three postoperative days, food intake (FI) of the VNA lesioned animals (VNAL) was normal. Interestingly, the body weight (BW) of the VNAL was significantly reduced compared to the controls, and a pair feeding study indicated that this depression of BW was not due to their FI. Computation of FI per metabolic size showed that the VNAL actually had a significantly increased FI compared to the controls. After a two day fast the VNAL lost more metabolic size than controls and upon refeeding they defended their pre-fast BW. The VNAL rats showed normal body composition and circulating glucose, insulin and prolactin. They had reduced free fatty acids, triglycerides, growth hormone and body length. The data suggest that the mesencephalon influences BW set point, some metabolites and possibly overall metabolism.     

Intracranial estradiol in ovariectomized guinea pigs: Effects on ingestive behaviors and body weight

The present study was undertaken to evaluate the effects of intracranial estradiol stimulation on food intake (FI), water intake (WI), and body weight (BWt) of ovariectomized guinea pigs (GPs). Thirty-five GPs were implanted with bilateral guide cannulae aimed at either the ventromedial hypothalamus, paraventricular nucleus (PVN), or preoptic area and then were stimulated unilaterally with cholesterol and estradiol 17-β, yielding a total of 70 stimulation sites.Across all GPs, estradiol implants significantly reduced FI, WI and BWt relative to implants of cholesterol. The possibility that the behavioral changes observed were due to the peripheral rather than central effects of the implants was evaluated by comparing the results of stimulations which produced vaginal membrane rupture (VMR) to the results of cases without VMR. There were no significant differences between these groups on any of the dependent variables studied, indicating that peripheral estradiol sufficient to induce VMR was neither necessary nor sufficient to account for the behavioral changes.Histological analysis revealed that implants in the ventromedial-arcuate region (VM/ARC) and PVN significantly lowered FI and BWt, with the effects being greatest in the PVN. Placements in other areas, on the average, did not significantly suppress FI or BWt. The effect of central estradiol on WI was more diffuse. No significant effect of implant location was found for the estrogenic suppression of drinking.These findings are the first demonstration that estradiol applied to particular brain areas can lower FI, WI, and BWt of ovariectomized GPs. The results also indicate that the VM/ARC region of the hypothalamus is not the sole locus of estrogen's effects on FI and BWt in this species, since these parameters were also reduced by estrogenic stimulation of the PVN.     

Chronic central administration of apelin-13 over 10 days increases food intake, body weight, locomotor activity and body temperature in C57BL/6 mice

The peptide apelin has been located in a wide range of tissues, including the gastrointestinal tract, stomach and adipose tissue. Apelin and its receptor has also been detected in the arcuate and paraventricular nuclei of the hypothalamus, which are involved in the control of feeding behaviour and energy expenditure. This distribution suggests apelin may play a role in energy homeostasis, but previous attempts to discern the effects of apelin by acute injection into the brain have yielded conflicting results. We examined the effect of a chronic 10-day intracerebroventricular (i.c.v.) infusion of apelin-13 into the third ventricle on food intake, body temperature and locomotor activity in C57BL/6 mice. Apelin-13 (1 microg/day) increased food intake significantly on days 3-7 of infusion; thereafter, food intake of treated and control individuals converged. This convergence was potentially because of progressive conversion of apelin-13 to [Pyr(1)]apelin-13 which has a four-fold lower receptor binding affinity at the orphan G protein-coupled receptor, APJ. Locomotor activity was also higher in the apelin-treated mice, especially during the nocturnal peak, when most feeding occurs, and the first hours of the light phase. Body temperature was also elevated during this increased period of activity, but was otherwise unaffected. Apelin-13-infused animals gained more weight than the saline-infused controls, suggesting the elevated locomotor activity did not offset the increased food intake. Elevated locomotion and the consequent increases in body temperature were probably secondary effects to the increased food intake. These results suggest that apelin-13 may play a central role in the control of feeding behaviour and is one of only two peripheral ligands known to stimulate rather than inhibit intake. As apelin production is elevated during obesity, this may provide an important feed-forward mechanism exacerbating the problem. Antagonists of the apelin receptor may therefore be useful pharmaceuticals in the treatment of obesity.     

The role of oxytocin in regulation of appetitive behaviour,body weight and glucose homeostasis

Obesity and its associated complications have reached epidemic proportions in the USA and also worldwide, highlighting the need for new and more effective treatments. Although the neuropeptide oxytocin (OXT) is well recognised for its peripheral effects on reproductive behaviour, the release of OXT from somatodendrites and axonal terminals within the central nervous system (CNS) is also implicated in the control of energy balance. In this review, we summarise historical data highlighting the effects of exogenous OXT as a short‐term regulator of food intake in a context‐specific manner and the receptor populations that may mediate these effects. We also describe what is known about the physiological role of endogenous OXT in the control of energy balance and whether serum and brain levels of OXT relate to obesity on a consistent basis across animal models and humans with obesity. We describe recent data on the effectiveness of chronic CNS administration of OXT to decrease food intake and weight gain or to elicit weight loss in diet‐induced obese (DIO) and genetically obese mice and rats. Of clinical importance is the finding that chronic central and peripheral OXT treatments both evoke weight loss in obese animal models with impaired leptin signalling at doses that are not associated with visceral illness, tachyphylaxis or adverse cardiovascular effects. Moreover, these results have been largely recapitulated following chronic s.c. or intranasal treatment in DIO non‐human primates (rhesus monkeys) and obese humans, respectively. We also identify plausible mechanisms that contribute to the effects of OXT on body weight and glucose homeostasis in rodents, non‐human primates and humans. We conclude by describing the ongoing challenges that remain before OXT‐based therapeutics can be used as a long‐term strategy to treat obesity in humans.     

Relative normophagia and organ growth in growth-retarded weanling rats with dorsomedial hypothalamic lesions.

Weanling rats with ventromedial (VMNL) and dorsomedial (DMNL) hypothalamic lesions and sham-operated controls were maintained up to 198 days after operation. Food intake was measured throughout the experiment and organ weights were recorded at various periods of sacrifice. Comparisons were made between controls and VMNL and DMNL rats, respectively. Food intake and organ weights were expressed in absolute terms and relative to body mass and Kleiber's "metabolic size." VMNL rats were always normophagic and showed lower organ weights, regardless of manner of computation. Rats with DMNL, on the other hand, were absolutely hypophagic but relatively normophagic for considerable periods of time when food intake was referred to body mass. A similar relationship obtained for organ weights. The data fit well with previous results and with a hypothesis that holds that DMNL bring about a "resetting" of some central nervous control system that not only allows the rat so operated to subsist on lower substrate levels but also regulates normal growth in relation to body mass.     

The role of the ventral noradrenergic bundle in relation to endorphins in the control of core temperature, open-field and ingestive behaviour in the rat

Discrete, bilateral, radiofrequency destruction of the ventral noradrenergic bundle (VB) resulted in a pronounced fall in levels of noradrenaline in the hypothalamus but not in the cortex.On days 4 and 12, but not 28, post-surgery, VB-lesioned rats were hyperactive (rearing and ambulation) upon exposure to a novel open-field space. This hyperactivity was greatly attenuated by naloxone, which did not significantly modify sham activity. These data suggest that the VB may be involved in the control of locomotor-exploratory activity via an interaction with an endorphinergic system.On day 4, but not 12 or 25, VB-lesioed rats displayed a significant elevation in core temperature (Tc). No difference in the hyperthermia elicited by introduction into the open-field was, however, seen between VB-lesioned and sham rats on day 4. In both groups, this rise in Tc was strongly attenuated by naloxone. These data indicate that the VB may be involved in the control of Tc but that it does not mediate novelty-stress evoked hyperthermia, for which endorphins are primarily responsible.Within 7 days post-surgery, VB-lesioned rats developed an enhancement of daily food intake which led to a slight obesity. From day 15 onward, a hyperdipsia was also seen in VB-lesioned rats. Naltrexone reduced the food and water intake of both sham and VB-lesioned animals but failed to totally block this hyperphagia. It is suggested that the VB is involved in the regulation of daily ingestive behaviour and that endorphins do not exclusively mediate the VB-lesion induced hyperphagia.     

Seasonal regulation of food intake and body weight in the male Siberian hamster: studies of hypothalamic orexin (hypocretin), neuropeptide Y (NPY) andpro-opiomelanocortin (POMC)

The aim of these experiments was to investigate the relationship between hypothalamic expression of orexin (also called hypocretin), neuropeptide Y (NPY) and pro-opiomelanocortin (POMC) mRNA and seasonal cycles of body weight and food intake in the Siberian hamster. Adult males were transferred from long days of 16 h light and 8 h dark to short days of 8 h light and 16 h dark, a procedure known to induce major reductions in food intake and body weight in this species. After 8 weeks of exposure to short days, while body weight was declining, hypothalamic NPY mRNA levels as assessed by in situ hybridization were slightly lower (P < 0.05) than in age-matched controls exposed to long days. After 12 weeks with short days, when body weight would be expected to have reached its seasonal nadir, POMC mRNA levels were lower (P < 0.05) than in hamsters under long days. At no stage did orexin mRNA levels in hamsters under short days differ significantly from levels in those under long days. To investigate further the role of these peptide systems in seasonal changes in body weight and food intake, two provocative tests were carried out. Firstly, a 48-h fast induced a significant increase (P < 0.025) in hypothalamic NPY mRNA levels in both long- and short-day conditions, but did not change hypothalamic POMC or orexin mRNA levels. Secondly, systemic (intraperitoneal) treatment with recombinant murine leptin (5 mg/kg body weight) significantly decreased (P < 0.01) food intake over a 6-h post-treatment period in both long- and short-day conditions. However, this acute leptin treatment did not induce significant changes in hypothalamic orexin, NPY or POMC mRNA abundance. The increase in NPY expression in both long- and short-day conditions following food restriction and the suppression of food intake by leptin in both conditions suggests that acute homeostatic mechanisms operate in both long-day (obese) and short-day (nonobese) conditions. The lack of major changes in orexin, NPY and POMC in such different metabolic states suggest that other central systems must play a greater role in generating these states. Such findings are consistent with the 'sliding set-point' hypothesis, that is, seasonal cycles in food intake and fat metabolism are brought about by as yet unknown central mechanisms that chronically alter the level ('set point') around which homeostasis occurs, rather than resulting from changes in the potency of the acute feedback mechanisms themselves.     

Dopaminergic treatment is associated with decreased body weight in patients with Parkinson's disease and dyskinesias

Background and purpose:  Several studies suggested that patients with advanced Parkinson's disease (PD) showed a too low body weight when compared with age-matched, healthy subjects. We aimed to investigate whether PD patients with dyskinesias display body weight alterations and to observe any correlations between medication and other putative determinants.
Methods:  Charts of 166 PD patients with fluctuations and dyskinesias, admitted within 6 months to a German movement disorders clinic, were investigated for body mass index (BMI), age at onset, disease duration, Unified Parkinson's Disease Rating Scale motor score, eating coordination and medication.
Results:  Analysis showed that 4.2% of PD patients were underweight (BMI < 18.5 kg/m²), 46.4% were normal (BMI > 18.5–25 kg/m²), 33.7% were overweight (BMI > 25–30 kg/m²), 15.7% were obese (BMI > 30 kg/m²). Daily levodopa dosage per kg and total dopaminergic dosage per kg body weight were negatively correlated with BMI. Overall, patients' BMI had not significantly changed within 2 years of follow-up.
Conclusions:  In sum, advanced PD patients showed a reduced BMI when compared with a control population obtained from an age-matched group taken from a survey of the German Federal Office for Statistics. Our findings indicate that patients with a lower BMI received a higher cumulative levodopa dosage and that levodopa may be responsible for weight loss in PD.     

Reduction of food intake and body weight by chronic intraventricular insulin infusion

This study examined the effect of chronic infusions of insulin in one of three doses (5, 7.5 or 10 mU/day) into the third ventricle, on food and water intake and body weight in the rat. Solutions were infused via osmotic minipumps at a rate of 1 microliter/hour for seven days. The two highest doses of insulin produced a dose-related suppression of food intake and weight loss, which was greater than the effect produced by 5 mU/day or a control infusion of Ringers solution. The effect of 5 mU/day on food and water intake and body weight was similar to the effect of the control infusion. All groups treated with insulin decreased food intake during the day and night, although only differences in nighttime food intake were statistically significant. Ten mU/day also produced a significantly greater reduction in water intake than each of the other solutions. Weight loss in the animals infused with insulin could not be explained by a decrease in caloric intake alone. Food intake returned to normal in all groups by the end of a seven day post-infusion period, with recovery being slowest among the animals receiving the highest doses of insulin. All animals recovered body weight at approximately the same rate. These results provide further evidence for the view that brain insulin plays a role in the regulation of food intake and body weight.     

氟西汀治疗抗精神病药所致体质量增加

目的：探讨氟西汀治疗抗精神病药所致体质量(体重)增加的疗效及不良反应。方法：对20例抗精神病药所致体质量增加的患者进行18个月的氟西汀治疗．观察其Quetelet指数的变化。结果：治疗4个月末Quetelet指数明显下降,6个月末疗效极为显著,且疗效持续。未见明显药物不良反应。结论：应用氟西汀治疗抗精神病药所致体质量增加安全有效。     

Links between the appetite regulating systems and the neuroendocrine hypothalamus: lessons from the sheep

The hypothalamus is integral to the regulation of energy homeostasis and the secretion of hormones from the pituitary gland. Consequently, hypothalamic systems may have a dual purpose in regulating both neuroendocrine function and appetite. To date, most studies investigating the interface between appetite and hormone secretion have been performed in rats or mice that have been acutely fasted or baring a genetic abnormality causing either obesity or aphagia. By contrast, various physiological models, including chronic food-restriction or photoperiodically driven changes in voluntary food intake, add further perspective to the issue. In this regard, sheep provide an innovative model whereby long-term changes in body weight or extended feeding rhythms can be investigated. This review compares and contrasts data obtained in different species with regard to the neuroendocrinology of appetite, and discusses the benefits and knowledge gained from using various nonrodent models with a particular emphasis on a ruminant species.     

Excessive disgust caused by brain lesions or temporary inactivations: mapping hotspots of the nucleus accumbens and ventral pallidum

Disgust is a prototypical type of negative affect. In animal models of excessive disgust, only a few brain sites are known in which localized dysfunction (lesions or neural inactivations) can induce intense ‘disgust reactions’ (e.g. gapes) to a normally pleasant sensation such as sweetness. Here, we aimed to map forebrain candidates more precisely, to identify where either local neuronal damage (excitotoxin lesions) or local pharmacological inactivation (muscimol/baclofen microinjections) caused rats to show excessive sensory disgust reactions to sucrose. Our study compared subregions of the nucleus accumbens shell, ventral pallidum, lateral hypothalamus, and adjacent extended amygdala. The results indicated that the posterior half of the ventral pallidum was the only forebrain site where intense sensory disgust gapes in response to sucrose were induced by both lesions and temporary inactivations (this site was previously identified as a hedonic hotspot for enhancements of sweetness ‘liking’). By comparison, for the nucleus accumbens, temporary GABA inactivations in the caudal half of the medial shell also generated sensory disgust, but lesions never did at any site. Furthermore, even inactivations failed to induce disgust in the rostral half of the accumbens shell (which also contains a hedonic hotspot). In other structures, neither lesions nor inactivations induced disgust as long as the posterior ventral pallidum remained spared. We conclude that the posterior ventral pallidum is an especially crucial hotspot for producing excessive sensory disgust by local pharmacological/lesion dysfunction. By comparison, the nucleus accumbens appears to segregate sites for pharmacological disgust induction and hedonic enhancement into separate posterior and rostral halves of the medial shell.     

The effects of galanin-like peptide on energy balance, body temperature and brain activity in the mouse and rat are independent of the GALR2/3 receptor

Galanin-like peptide (GALP) is a neuropeptide that is thought to act on the galanin receptors GALR1, GALR2 and GALR3. In rats, i.c.v. injection of GALP has dichotomous actions on energy balance, stimulating feeding over the first hour, but reducing food intake and body weight at 24 h, as well as causing an increase in core body temperature. In mice, GALP only induces an anorexic action, and its effects on core body temperature are unknown. One aim of the present study was to determine the effects of GALP on core body temperature in mice. Intracerebroventricular injection of GALP into conscious mice had no effect on feeding over 1 h, but caused a significant reduction in food intake and body weight at 24 h. It also caused an immediate drop in core body temperature, which was followed by an increase in body temperature. To understand these different effects of GALP on energy balance in mice compared to rats, and to determine the involvement of GALR2 and GALR3, immunohistochemistry was performed to localise c-Fos, a marker of cell activation. Intracerebroventricular injection of GALP induced c-Fos expression in the parenchyma surrounding the ventricles, the ventricular ependymal cells and the meninges in mice and rats. GALP also induced c-Fos expression in the supraoptic nucleus, dorsomedial hypothalamic nucleus, lateral hypothalamus and nucleus tractus solitarius in rats but not in mice. Central administration of a GALR2/3 agonist in rats did not induce c-Fos in any of the brain regions that expressed this protein after GALP injection, and had no effect on food intake, body weight and body temperature in rats or mice. These data suggest that GALP induces differential effects on energy balance and brain activity in mice compared to rats, which are unlikely to be due to activation of the GALR2 or GALR3 receptor.     

Effect of ventral noradrenergic bundle transection and locus coeruleus lesions on urinary 3-methoxy-4-hydroxyphenylethyleneglycol (MHPG) excretion in the rat

Urinary 3-methoxy-4-hydroxyphenylethyleneglycol (MHPG) excretion was determined in rats after central noradrenergic pathway interruption by ventral bundle transection or by locus coeruleus (LC) lesions. The transection prevented an increase in urinary MHPG that occurred in sham-operated animals, an effect that was presumed to be due to loss of cerebrospinal fluid (CSF). Electrolytic lesioning of the LC, which was not attended by loss of CSF, had no effect on baseline MHPG excretion but diminished the response to subsequent administration of the alpha-adrenergic blocking agent, phenoxybenzamine (PBZ). Since the contribution of brain MHPG to total urinary MHPG is small, the observed effects of these procedures are most likely due to disrupted central regulation of peripheral sympathetic nerve activity.     

Paraventricular nucleus lesions exaggerate dietary obesity but block photoperiod-induced weight gains and suspension of estrous cyclicity in Syrian hamsters

Lesions of the paraventricular nucleus (PVN) of the hypothalamus block short photoperiod-induced testicular regression in Syrian hamsters. We examined the effects of PVN or sham lesions on the short photoperiod-induced increases in body weight and adiposity in female Syrian hamsters. PVN lesions did not affect body weight when hamsters were housed in a long photoperiod (LD, 16:8) and fed Purina laboratory rodent chow (No. 5001). However, when fed a high-fat diet both groups gained weight, and the hamsters with PVN lesions gained approximately twice as much as the sham-operated controls. When the hamsters were exposed to a short photoperiod (LD, 8:16), only the hamsters with sham lesions displayed the typical increase in body weight. No further increase in body weight or parametrial fat pad weight was seen when the hamsters with PVN lesions were exposed to the short photoperiod. The lack of a short photoperiod-induced increase in body weight gain in hamsters with PVN lesions seems unlikely to be due to a "ceiling effect" on body weight gain because we have routinely observed neurally intact, melatonin-treated female Syrian hamsters with body weight in excess of 250 g. Finally, the short photoperiod interrupted estrous cyclicity in sham-lesioned hamsters but not in those with PVN lesions. Thus, PVN lesions exaggerate dietary obesity but prevent short photoperiod-induced weight gains and vaginal acyclicity in female Syrian hamsters.     

Relationship between weight, levodopa and dyskinesia: the significance of levodopa dose per kilogram body weight

Purpose:  Levodopa dose per kilogram body weight is reported to be a significant factor for dyskinesia in Parkinson's disease. We have investigated this hypothesis in data from the studies comparing ropinirole versus levodopa as the initial therapy.
Methods:  Data from the ropinirole versus levodopa studies 056 and REAL-PET in early Parkinson's disease were pooled and manipulated to calculate levodopa dose per kilogram body weight. Logistic regression analysis was performed to investigate significant variables for the development of dyskinesia. Only the patients on levodopa monotherapy or with ropinirole were analyzed.
Results:  Analysis of levodopa therapy patients revealed that dyskinetic patients had received significantly higher absolute levodopa dose and levodopa dose per kilogram body weight. Logistic regression revealed that the most significant factor was the higher levodopa dose per kilogram body weight, P  = 0.005, odds ratio 1.078, 95% CI 1.023–1.135; younger age was the second factor – P  = 0.026. Variables of gender, absolute levodopa dose, weight, disease duration and initial motor Unified Parkinson's disease rating score were not significant.
Conclusion:  Higher levodopa dose per kilogram body weight is an independently significant factor for developing dyskinesia. This relationship should be considered in treatment of Parkinson's disease patients aiming to prevent and manage dyskinesia.     

Lithium in pigmented eye rats: Effects of dose and time of day on drinking, body weight, retinal and blood distribution

Lithium has been implicated in chronobiology (Seggie, et al., 1982, 1983). Previous work was done in Wistar rats, an Albino species, which lack the enzyme for synthesis of eye pigment. This pigment is important in regulation of light cued rhythms. The present project extends observations to Long Evans rats, a strain which has a pigmented eye. Groups of adult male rats were fed one of three diets: (1) normal laboratory chow; (2) a low lithium diet: lab chow supplemented with 30 mM/kg lithium chloride; and (3) a high lithium diet: lab chow supplemented with 50 mM/kg lithium chloride. Adult male rats were housed individually with free access to diet and water under a 12 hour light/12 hour dark schedule. After six weeks on the diets, body weight, water intake, plasma, red blood cell and retinal lithium and retinal weight were measured every 4 hours throughout the 24 hour cycle following sacrifice by rapid decapitation. Plasma lithium levels on the high diet were 0.57 ± 0.02 mEq/1 and did not evidence a diurnal rhythm. Plasma lithium levels on the low diet were 0.35 ± 0.01 mEq/1 and evidenced a small, but significant diurnal rhythm with levels lowest just before darkness and normal food intake. Red blood cell lithium levels were significantly higher than plasma levels at 0.83 ± 0.02 and 0.52 ± 0.02 mEq/1 for the high and low diets. Low diet, but not high diet red blood cells lithium levels evidenced a significant rhythm with a pattern similar to that seen in plasma lithium levels. Retinal lithium levels evidenced no diurnal change on either diet and were 0.82 ± 0.05 mEq/kg and 0.55 ± 0.02 mEq/kg for the high and low diet. Retinal weight was 15.5 ± 2.0 mg for controls and was not affected by lithium in the diet. Body weight did not Evidence diurnal change on any of the diets: however, both the high and the low lithium diet groups weighed significantly less than controls (354 ± 4.8 g and 411 ± 7.4 g vs. 437 ± 7.8 g respectively). Water intake evidenced a significant diurnal rhythm with maximum intake during dark hours and was significantly elevated on the high, but no on the low diet at all time points. in pigmented eye compared to Albino rats, the 50 mM/kg dose lithium diet resulted in lower, but less variable plasma and red blood cell lithium levels, but equivalent effects on body weight and drinking (Seggie et al, 1982). The low dose lithium diet gave mixed results. Pigmented eye retinal weight was unaffected by lithium: however, lithium content of retina suggested that this tissue handles lithium in a manner similar to brain (Bond, 1975). These data suggest strain and possible species differences in the metabolism of lithium as it relates to chronobiology.     

Body weight changes after neurochemical manipulations of lateral amygdala: Noradrenergic and dopaminergic mechanisms

The feeding behavior of rats was studied after neurochemical lesions of lateral amygdalar terminal fields of mesolimbic dopaminergic (DA) and coerular noradrenergic (NA) systems. 6-Hydroxydopamine (6-OHDA) with or without desmethylimipramine (DMI) premedication was bilaterally injected into the lateral amygdala or periamygdaloid-piriform area. Lateral amygdalar injections of 6-OHDA resulted in hyperdipsia, hyperphagia and body weight increase with a relative decrease in amygdalar NA concentration, while 6-OHDA plus DMI treatments were followed by weight decrease and a mild decrease in DA level. When the cannulas were placed into the periamygdaloid-piriform cortex nothing but body weight increase developed. The importance of the actual balance of the two amygdalar catecholaminergic (CA) systems in feeding is discussed.