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PubMed2000

Not all peripheral immune stimuli that activate the HPA axis induce proinflammatory cytokine gene expression in the hypothalamus.

Administration of low doses of lipopolysaccharide (LPS) that do not disrupt the blood-brain barrier (BBB) results in the expression of interleukin-1 beta (IL-1 beta), IL-6, and tumor necrosis factor-alpha (TNF alpha) in the hypothalamus in parallel to stimulation of the hypothalamus-pituitary-adrenal (HPA) axis. This endocrine response is triggered by peripheral cytokines, and we recently obtained evidence that brain-borne IL-1 contributes to its maintenance. LPS preferentially stimulates cells of the macrophage lineage and B lymphocytes. The possibility that primarily stimulation of other types of peripheral immune cells also results in the expression of proinflammatory cytokines in the brain and in the activation of the HPA axis was investigated. Our results showed that, in contrast to LPS, administration of the superantigen staphylococcal enterotoxin B (SEB), which stimulates T cells by binding to appropriate V beta domains of the T-cell receptor, did not result in induction of IL-1 beta, IL-6, and TNF alpha expression in the hypothalamus. Furthermore, although IL-2 transcripts in the spleen were highly increased, expression of this gene was not detected in the brain. However, as with LPS, SEB administration also results in elevated levels of glucocorticoids in blood. Therefore, our data suggest that increased expression of proinflammatory cytokines in the brain is not a necessary step in the stimulation of the HPA axis by SEB.

Animals↗
PubMed1969

Acetylcholine and related enzymes in the neural lobe and anterior hypothalamus of the rabbit.

1. Acetylcholine (ACh), cholinesterases and choline acetyltransferase (choline acetylase) were estimated in the neural lobe and hypothalamus of the adult male rabbit. Acetylcholine was also estimated in the neural lobes and hypothalami of some other mammals.2. Acetylcholine-like activity was measured by bio-assay using the leech dorsal muscle preparation.3. Characterization experiments indicated that about 90% of the activity measured was due to acetylcholine.4. Mean acetylcholine content in the neural lobe of the rabbit, after extraction with perchloric acid, was 4.38 +/- 0.98 mug/g fresh tissue, and 4.87 +/- 1.53 mug/g in the hypothalamus.5. Acetylcholine was also found to be present, in comparable concentrations, in the neural lobe of man and in the neural lobes and hypothalami of ox, rat and hedgehog.6. Acetylcholinesterase, present in the neural lobe and hypothalamus of the rabbit, hydrolysed 1.74 +/- 0.11 mu-moles of substrate/min/g and 3.78 +/- 0.60 mu-moles substrate/min/g fresh tissue respectively.7. The concentration of butyrylcholinesterase was about one tenth that of acetylcholinesterase in both tissues.8. Choline acetyltransferase present in the neural lobe and in the hypothalamus synthesized 87 +/- 22 mug ACh/hr/g fresh tissue and 378 +/- 149 mug respectively.

Acetylcholine↗
PubMed1970

Osmosensitive single neurones in the hypothalamus of unanaesthetized monkeys.

1. We recorded with tungsten micro-electrodes the activity of single neurones in the supraoptic nucleus (NSO) and adjacent regions of the hypothalamus while repeatedly injecting solutions of varying tonicity into the common carotid artery of trained, unanaesthetized monkeys who accepted the experimental restraints without anxiety.2. Intracarotid injections of mildly hypertonic solutions of sodium chloride produced a characteristic behavioural response during and immediately after injection: e.e.g. ;arousal,' lip and tongue smacking, chewing, irregular sniffing respiration and associated mildly increased movement of face, eyes and body.3. Of the 130 cells analysed during hypertonic intracarotid injections, 105 (81%) were osmosensitive. Twenty-five (19%) of the cells studied during similar injections were non-osmosensitive. On the basis of the anatomical location of the cells, the pattern of discharge to intracarotid osmotic stimuli and the response to arousing sensory stimuli, we divided the osmosensitive cells into two major groups, ;specific' and ;non-specific' osmosensitive cells.4. Fifty-two (50%) of the osmosensitive cells we labelled ;specific' because they responded to an intracarotid injection of hypertonic sodium chloride, generally did not respond to non-noxious arousing sensory stimuli and were located in or near the supraoptic nucleus. We found two subtypes of these ;specific' osmosensitive cells: (a) twenty-one (20%) NSO cells with ;biphasic' responses, that is, acceleration followed by inhibition; (b) thirty-one (30%) cells in the immediate perinuclear zone of the NSO with ;monophasic' responses, subdivided into twenty-one (20%) cells that accelerated and ten (10%) that were inhibited.5. Fifty-three osmosensitive cells (50%), located diffusely in the anterolateral hypothalamus, were ;non-specific', responding both to intracarotid injections of hypertonic sodium chloride and also to sensory stimuli that were mildly arousing. Two groups of ;non-specific' osmosensitive cells showed monophasic responses; thirty-five (34%) cells accelerated and seventeen (16%) of them were inhibited.6. The ;monophasic' specific osmosensitive neurones lying in the immediate perinuclear zone of the supraoptic nucleus in the primate could conceivably be the ;osmoreceptors' of Verney. The ;biphasic' specific osmosensitive neurones in the NSO may well represent the secretory cells of this system. From our data, the ;non-specific' osmosensitive neurones, scattered diffusely in the anterolateral hypothalamus, have little to do with osmoregulation. Some of these cells located in the perinuclear zone of the NSO could act as interneurones, however, conveying afferent input to the osmoreceptor-secretory complex of the supraoptic nucleus.

Animals↗
PubMed1971

The role of sodium and calcium ions in the hypothalamus in the control of body temperature of the unanaesthetized cat.

1. Isolated regions of the anterior, posterior and other areas of the hypothalamus of the unanaesthetized cat were perfused by means of push-pull cannulae lowered through permanently implanted guide tubes. Each site was perfused for a 30 min interval at a rate of 50 mul./min. Concentrations of sodium, calcium, potassium and magnesium ions in the perfusate were altered selectively.2. Sodium ions in a concentration which varied from 13.6 to 68.0 mM in excess of the level in extracellular fluid caused a steep rise in the temperature of the cat when the solution was perfused at sites located within the posterior hypothalamic area. Shivering, vasoconstriction, and piloerection accompanied the increase in temperature. When the chloride was replaced in the perfusate by the toluene-p-sulphonate salt of sodium, the hyperthermia was equally intense. Solutions containing excess sodium ions perfused within the anterior and other hypothalamic areas produced either a slight fall or rise in temperature as well as other physiological changes.3. Calcium ions in a concentration which varied from 2.6 to 10.4 mM in excess of the physiological level perfused at the same sites within the posterior region of the hypothalamus produced a sharp fall in body temperature, which was accompanied by vasodilatation and a decrease in the activity of the cat. When solutions containing excess calcium were perfused in the anterior and other hypothalamic areas, no consistent change in temperature occurred.4. Potassium or magnesium ions in concentrations which varied from two to ten times the level in extracellular fluid had virtually no effect on the temperature of the cat when they were perfused in the anterior, posterior or other areas of the hypothalamus.5. We conclude that the constancy in the ratio between sodium and calcium ions in the posterior hypothalamus may be the inherent mechanism by which the set-point for body temperature is determined.

Animals↗
PubMed1971

Participation of the anterior hypothalamus in the baroreceptor reflex.

1. On the basis of discrete electrical stimulation in the pre-optic region and anterior hypothalamus of anaesthetized cats, a depressor area has been defined, stimulation of which elicits a fall of arterial blood pressure of 30-50 mm Hg and a bradycardia of some 25%, caused by inhibition of sympathetic vasomotor tone and by vagal activation respectively. These are accompanied by a reduction in rate and depth of respiration.2. The depressor area, from which this pattern of response is elicited, lies ventral and caudal to the anterior commissure, and extends caudally in the dorsal hypothalamus, dorsal to the fornix.3. The pattern of response elicited from identified points in the depressor area was shown to be indistinguishable from that to baroreceptor afferent stimulation.4. A lesion destroying the hypothalamic depressor area bilaterally reduced the response to baroreceptor afferent stimulation. Lesions in the medullary depressor area which spared a large part of the nucleus of the tractus solitarius also reduced, but did not abolish, the baroreceptor reflex response. The two lesions combined abolished the reflex.5. It is concluded that the whole brain-stem depressor area, from the hypothalamus through the mid-brain to the medulla, constitutes a functional unit which integrates the response to baroreceptor afferent stimulation.

Animals↗
PubMed1976

Stimulation of the rabbit hypothalamus: caudal projections to respiratory and cardiovascular centres.

1. Electrical stimulation of a small area of the hypothalamus, lying about 2 mm dorsal to the lateral margin of the mammillary bodies, evoked a characteristic complex of effects in the anaesthetized rabbit. 2. The observed effects included apneusis followed by tachypnoea, increased arterial blood pressure, and vagally mediated bradycardia. Exophthalmost and pupillodilatation was commonly seen. The ears were erected and the vibrissae drawn forward. Somatic effects were weaker, but often included increased extensor tone, especially in the forelimbs. 3. The intensity of these effects was dependent upon the frequency of stimuli within the trains. Effects were weak or absent below 20 shocks/sec, and were near-maximal above 60 shocks/sec, when employing constant-current rectangular wave stimuli of 100-300 muA, 1 msec pulse duration and 5-9 sec train duration. 4. The effects were not dependent upon connexions with the cerebral cortex, but were mediated by pathways that projected ipsilaterally from each side of the hypothalamus through the mesencephalon. 5. The evidence suggests that this region of the rabbit hypothalamus is partly homologous with that hypothalamic area associated with the defence reaction in cat. However, the over-all responses to stimulation in the anaesthetized rabbit differed considerably from those described in the anaesthetized carnivore, suggesting that their integrated physiological responses to emotional threat are dissimilar.

Animals↗
PubMed1981

Responses of supraoptic neurones in the intact and deafferented rat hypothalamus to injections of hypertonic sodium chloride.

1. Recordings were made from a total of fifty-three neurones in the supraoptic nuclei of four groups of rats: intact rats, animals in which the hypothalamus had been partly denervated by anteriorly or posteriorly placed semicircular cuts, and rats with a totally deafferented hypothalamus. 2. When first encountered, cells from intact animals fired at a mean rate of 5.08 +/- 0.78 spikes/sec, those from posteriorly isolated hypothalami at 3.93 +/- 0.63 spikes/sec, those from the anteriorly isolated hypothalami at 2.05 +/- 0.83 spikes/sec, and those from totally isolated hypothalami at 0.99 +/- 0.46 spikes/sec. 3. When stimulated osmotically by an intraperitoneal injection of ml. 1.5 M-NaCl, eight out of eight cells in intact rats showed a significant increase in firing rate between 20 and 30 min after the injection. Six out of nine cells in posteriorly isolated hypothalami showed significant but smaller responses. No increase in firing rate could be detected in seven cells from totally isolated hypothalami or from eight cells in hypothalami partly isolated by anterior cuts. 4. The results imply that under the conditions of these experiments by the spontaneous activity of the supraoptic nucleus in intact animals was maintained by an extrahypothalamic excitatory input, that partial hypothalamic isolation reduced its intensity, possibly by unmasking an inhibitory input, and that total isolation reduced it to an even greater extent. Osmotic activation of supraoptic cells was only possible when the anterior connexions of the hypothalamus were intact. Thus the cerebral osmo-receptors for vasopressin release may be situated outside the supraoptic nuclei.

Action Potentials↗
PubMed1983

Effect of stimulation or lesioning of the hypothalamus upon gonadotrophin secretion in the guinea-pig.

The effect of electrical stimulation of the anterior hypothalamus of the guinea-pig upon follicle-stimulating hormone (FSH) and luteinizing hormone (LH) secretion during two phases of the oestrous cycle was examined and compared with the response to electrolytic or radio-frequency lesions placed in the same area. The secretion of LH was briefly increased by electrical stimulation of the hypothalamus, with a greater response occurring over days 7-8 (luteal phase) of the oestrous cycle than on days 13-14 (follicular phase). An equivalent rise in LH output was produced by placement of direct current (d.c.) lesions in the hypothalamus, whereas lesions made with radio-frequency current produced a small increase only on days 13-14. The secretion of FSH was not changed by any procedure.

Animals↗
PubMed1977

Prolactin-like immunoreactivity: localization in nerve terminals of rat hypothalamus.

Antibodies to rat prolactin were used in immunohistochemical studies of the hypothalamus and preoptic area of the rat. Evidence was obtained that a protein immunochemically related to prolactin was stored in networks of nerve terminals of many hypothalamic areas such as the arcuate nucleus, the dorsomedial hypothalamic nucleus, and periventricular regions of the hypothalamus and preoptic area. The neuronal storage of a prolactin-like protein in the hypothalamus was unaffected by hypophysectomy.

Animals↗
PubMed1982

(+)-Amphetamine binding to rat hypothalamus: relation to anorexic potency for phenylethylamines.

Saturable and stereospecific binding sites for (+)-[3H]amphetamine were demonstrated in membrane preparations from rat brain. The density of these binding sites varies among brain regions and is highest in the hypothalamus and brainstem. Specific (+)-[3H]amphetamine binding in hypothalamus is largely confined to synaptosomal membranes, rapidly reversible, and sensitive to both heat and proteolytic enzymes. Scatchard analysis of the equilibrium binding data revealed two distinct sites with apparent affinity constants of 93 and 300 nanomoles per liter, respectively. The effects of various psychotropic drugs as well as a number of putative neurotransmitters and related agonists and antagonists in displacing specific (+)-[3H]amphetamine binding demonstrate that these binding sites are not associated with any previously described neurotransmitter or drug receptors, but are specific for amphetamine and related phenylethylamine derivatives. Furthermore, the relative affinities of a series of phenylethylamine derivatives for (+)-[3H]amphetamine binding sites in hypothalamic membranes is highly correlated to their potencies as anorexic agents. These results suggest the presence of specific receptor sites in hypothalamus that mediate the anorexic activity of amphetamine and related drugs.

Animals↗
PubMed2000

Specific binding of [3H]ketanserin to hypothalamus membranes of juvenile rainbow trout, Oncorhynchus mykiss.

This study examines the existence and pharmacological specificity of [3H]ketanserin binding in hypothalamus of juvenile rainbow trout. Hypothalamic membranes were incubated with [3H]ketanserin (selective 5HT2 antagonist) under several experimental conditions; reactions were terminated by filtration and bound radioactivity was counted by liquid scintillation spectroscopy. Tissue dilution experiments revealed that specific [3H]ketanserin binding (B(sp)) was tissue dependent; 1 hypothalamus equivalent per tube (1100 +/- 115 cpm/mg protein) was subsequently used throughout the rest of this study. In association experiments, B(sp) increased progressively with time, achieved equilibrium binding levels (1192 +/- 120 cpm/mg protein) within 80 min, and remained stable for at least 60 min thereafter; k(obs), and k(+1) were 0.032 and 0.048 min(-1) x nM(-1), respectively. In dissociation experiments, B(sp) completely dissociated within 20 min following addition of excess ketanserin; k(-1) and t1/2 were 0.0803 min(-1) and 8.7 min, respectively. B(sp) was saturable (2500 +/- 256 cpm/mg protein); Scatchard-calculated values for the equilibrium dissociation constant (K(D)) and capacity (Bmax) were 0.48 nM, and 125 fmol/mg protein, respectively. B(sp) was differentially displaced by structurally related competitors, with a rank order of potency of ketanserin = mianserin > ritanserin > serotonin (5HT) = spiperone >> methiothepin mesylate > metergoline = DOI ((+/-)-2-5-dimethoxy-4-iodoamphetamine hyrobromide) > 2-methyl-5HT > alpha-methyl-5HT >>>> 5HIAA (5-hydroxyindole acetic acid) = reserpine. These findings provide pharmacological evidence for the presence of a 5HT2-like receptor subtype in the trout hypothalamus.

Animals↗
PubMed2004

Aqueous extract of ma huang suppresses neuropeptide Y expression in food-deprived rat hypothalamus.

Ma huang, the dried plant stem of ephedra intermedia Schrenk et C.A., contains an ephedrine-type alkaloid and has been used for weight loss. Neuropeptide Y (NPY), a 36-amino acid peptide, is concentrated in the hypothalamus and stimulates feeding desire. In this study, the effect of ma huang on the expressions of NPY in the hypothalamus of rats was investigated using immunohistochemistry. Food-deprivation enhanced the NPY expression in the hypothalamus. ma huang suppressed the food-deprivation-induced enhancement of NPY expression. Present results suggest that ma huang curbs the food desire by suppressing the NPY expression under food-deprivation conditions.

Animals↗
PubMed2005

Food deprivation differentially modulates orexin receptor expression and signaling in rat hypothalamus and adrenal cortex.

Although starvation-induced biochemical and metabolic changes are perceived by the hypothalamus, the adrenal gland plays a key role in the integration of metabolic activity and energy balance, implicating feeding as a major synchronizer of rhythms in the hypothalamic-pituitary-adrenal (HPA) axis. Given that orexins are involved in regulating food intake and activating the HPA axis, we hypothesized that food deprivation, an acute challenge to the systems that regulate energy balance, should elicit changes in orexin receptor signaling at the hypothalamic and adrenal levels. Food deprivation induced orexin type 1 (OX1R) and 2 (OX2R) receptors at mRNA and protein levels in the hypothalamus, in addition to a fivefold increase in prepro-orexin mRNA. Cleaved peptides OR-A and OR-B are also elevated at the protein level. Interestingly, adrenal OX1R and OX2R levels were significantly reduced in food-deprived animals, whereas there was no expression of prepro-orexin in the adrenal gland in either state. Food deprivation exerted a differential effect on OXR-G protein coupling. In the hypothalamus of food deprived rats compared with controls, a significant increase in coupling of orexin receptors to Gq, Gs, and Go was demonstrated, whereas coupling to Gi was relatively less. However, in the adrenal cortex of the food-deprived animal, there was decreased coupling of orexin receptors to Gs, Go, and Gq and increased coupling to Gi. Subsequent second-messenger studies (cAMP/IP3) have supported these findings. Our data indicate that food deprivation has differential effects on orexin receptor expression and their signaling characteristics at the hypothalamic and adrenocortical levels. These findings suggest orexins as potential metabolic regulators within the HPA axis both centrally and peripherally.

Adrenal Cortex↗
PubMed1983

Evidence for a longitudinal pathway in rat hypothalamus that controls FFA mobilization.

In initial exploratory experiments, bilateral, symmetrical, relatively large electrolytic lesions were produced, injuring anterior, middle, and posterior hypothalamus but respecting the midlateral region. Only lesions in the preoptic-anterior hypothalamic region and in the posterior hypothalamus were effective in blocking free fatty acid (FFA) mobilization induced by intravenous 2-deoxyglucose. Lesions in the ventromedial hypothalamus were ineffective. In subsequent experiments, suppression of plasma FFA response to the drug was observed in rats with small, globular (0.5-1.0 mm diam), bilateral lesions either in the preoptic (PO) or in the lateral hypothalamic (LH) areas. Groups of animals were then prepared in which a unilateral lesion in the PO area was combined with a contralateral lesion in the LH area. Plasma FFA response to 2-deoxyglucose in these rats was also blocked but not in rats having only unilateral lesions. The hyperglycemic response to 2-deoxyglucose was not affected in any of the experimental groups. These data suggest that a longitudinal pathway connecting PO, LH, and posterior hypothalamic areas is involved in FFA mobilization from adipose tissue in rats.

Animals↗
PubMed1993

Gastric vagal-evoked and greater splanchnic-evoked unitary responses in the hypothalamus.

Gastric vagal and greater splanchnic nerve fibers were electrically stimulated to localize and characterize neuronal interactions in the hypothalamus of anesthetized cats. Extracellular recordings from 635 hypothalamic units were identified that responded to electrical stimulation of the left greater splanchnic nerve or gastric vagal fibers serving the proximal stomach. A total of 504 hypothalamic units in this group received input from both gastric vagal and greater splanchnic nerves. The gastric vagal-evoked hypothalamic (GVeH) and greater splanchnic-evoked hypothalamic (SeH) responses were widely distributed in the medial, paraventricular, and dorsomedial nuclei and lateral hypothalamus. The conduction velocity of the SeH response was significantly greater than the GVeH response. The latency of the SeH response showed two peaks [58 +/- 15.7 (SD) ms and 136 +/- 18.3 (SD) ms] indicating that the splanchnic input terminated on two different groups or populations of hypothalamic neurons. It also suggested that different pathways or fiber diameters in the pathway may be involved in the transmission of splanchnic input to the hypothalamus. The majority of the GVeH and SeH unitary responses were multiple spikes or short trains of action potentials. Excitatory and inhibitory responses were observed in tonically active hypothalamic units that responded to gastric vagal or greater splanchnic input. The duration of decreased excitability to gastric vagal or greater splanchnic input was significantly greater than the period of increased excitability. The condition-test paradigm was used to determine the time course of convergent gastric vagal-greater splanchnic input on single hypothalamic neurons.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1987

Electrical stimulation in perifornical lateral hypothalamus decreases coronary blood flow in cats.

Based on evidence implicating the central nervous system in the regulation of coronary vascular resistance and the knowledge that the hypothalamus is a central site for integration of cardiovascular control, studies were undertaken to determine if electrical stimulation in the hypothalamus produced coronary vasoconstriction. In anesthetized cats, following beta-adrenergic receptor blockade, stimulation in perifornical lateral hypothalamus produced a transient decrease in coronary blood flow velocity (30 +/- 5%), a small pressor effect (7 +/- 2 mmHg), and an initial decrease in hindquarter blood flow velocity (51 +/- 5%). The decrease in coronary flow velocity, which had an onset latency of 1-3 s and a duration of 5-15 s, was abolished by ipsilateral stellate ganglionectomy and by intravenous and intracoronary prazosin. The coronary vasoconstriction produced by hypothalamic stimulation was not different from that produced by cardioaccelerator nerve stimulation. These results suggest that electrical stimulation of a hypothalamic site produces an alpha-adrenergic receptor-mediated decrease in coronary blood flow that is unmasked by beta-adrenergic receptor blockade, requires the integrity of ipsilateral cardiac sympathetic innervation, and mimics the coronary response to cardioaccelerator nerve stimulation.

Adrenergic beta-Antagonists↗
PubMed1975

Evoked release of [14C]norepinephrine from the rat hypothalamus during feeding.

The pattern of catecholamine release was studied at sites adjacent to the lateral ventricle or in the anterior, dorsomedial or ventromedial hypothalamus of the rat as it was feeding. Endogenous stores of norepinephrine (NE) were first labeled by the microinjection of [14C]NE into these circumscribed sites. Subsequently, [14C]NE release was examined by repeated perfusions of an artificial cerebrospinal fluid through a push-pull cannula at the rate of 23 mul/min for 5-10 min every 30 min. After successive control perfusates were collected, food or water was given to the animal. During an interval of feeding, a significant efflux of [14C]NE and its metabolites occurred reliably from midline structures of the hypothalamus at the level of the ventromedial nucleus. Although the feeding-related output of [14C]NE detected within the anterior hypothalamus was lower, [14C]NE was also released from this region when the rat pressed a lever to obtain food pellets. These results support the view that endogenous catecholamines underlie, at least partially, diencephalic mechanisms controlling food intake, including sensory, motor, or motivational components.

Animals↗
PubMed2002

Expression of dopaminergic receptors in the hypothalamus of lean and obese Zucker rats and food intake.

As revealed by previous microdialysis studies, basal and food intake-accompanied dopamine release significantly differs in the hypothalamus of obese vs. lean Zucker rats. In the present study, we determined whether dopaminergic receptors are also compromised in obesity. Dopaminergic D(1) and D(2) receptor mRNA expression was studied in the ventromedial hypothalamus (VMH), lateral hypothalamic area (LHA), and the adenohypophysis (AH) of obese and lean Zucker rats using RT-PCR technique. In obese Zucker rats, we found an upregulation of D(1) receptor mRNA in the VMH and AH and a downregulation in the LHA, whereas D(2) receptor mRNA was downregulated in both the VMH and LHA, but not changed in the AH, compared with lean rats. Also, an increase of D(1) receptor staining was seen in the paraventricular nucleus of obese rats by immunohistochemistry. We selected the VMH to test if the observed changes in the dopamine receptor expression of obese rats induce behavioral sensitization to dopamine as expressed by hyperphagia. The overnight food-deprived rats received a single VMH injection (10 nmol) of sulpiride (D(2) receptor antagonist) or saline as control, then food was provided and 1-h food intake was measured. Food intake after sulpiride vs. saline injection was greater in obese rats but was not different in lean rats. Our data suggest that downregulation of D(2) receptor in the hypothalamus at least in the VMH induces behavior sensitization for having large meals. Low D(2) receptor expression may be causal for an exaggerated dopamine release observed in obese rats during food ingestion and for reduced satiety feedback effect of dopamine. High level of D(1) receptor expression in the VMH and low in the LHA may also contribute to the specific feeding pattern in obese rats represented by large meal size and low meal number.

Animals↗