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PubMed2002

Distribution of melanin-concentrating hormone neurons projecting to the medial mammillary nucleus.

The melanin-concentrating hormone and neuropeptide glutamic acid-isoleucine are expressed in neurons located mainly in the hypothalamus that project widely throughout the CNS. One of the melanin-concentrating hormone main targets is the medial mammillary nucleus, but the exact origin of these fibers is unknown. We observed melanin-concentrating hormone and neuropeptide glutamic acid-isoleucine immunoreactive fibers coursing throughout the mammillary complex, showing higher density in the pars lateralis of the medial mammillary nucleus, while the lateral mammillary nucleus showed sparse melanin-concentrating hormone innervation. The origins of these afferents were determined by using implant of the retrograde tracer True Blue in the medial mammillary nucleus. Double-labeled neurons were observed in the lateral hypothalamic area, rostromedial zona incerta and dorsal tuberomammillary nucleus. A considerable population of retrogradely labeled melanin-concentrating hormone perikaryal profiles was also immunoreactive to neuropeptide glutamic acid-isoleucine (74+/-15% to 85+/-15%). The afferents from the lateral hypothalamic area, rostromedial zona incerta and dorsal tuberomammillary nucleus to the medial mammillary nucleus were confirmed using implant of the anterograde tracer Phaseolus vulgaris leucoagglutinin. In addition, using double-labeled immunohistochemistry, we found no co-localization between neurons expressing melanin-concentrating hormone and adenosine deaminase (histaminergic marker) in the dorsal tuberomammillary nucleus. We hypothesize that these melanin-concentrating hormone projections participate in spatial memory process mediated by the medial mammillary nucleus. These pathways would enable the animal to look for food during the initial moments of appetite stimulation.

Animals↗

PubMedDate not supplied

Effects of leptin and orexin-A on food intake and feeding related hypothalamic neurons.

The lateral hypothalamic area (LHA) and the ventromedial hypothalamic nucleus (VMH) have historically been implicated in ingestive behavior, energy balance and body mass regulation. The LHA is more closely associated with the initiation of eating; whereas the VMH mediates the cessation of eating. The parvocellular part of the paraventricular nucleus (pPVN) is also included in the suppressing mechanism. Recently, two hypothalamic peptides, orexin-A and orexin-B, localized in the posterior and lateral hypothalamic perifornical region were discovered in the rat brain and they increase food intake. Leptin, a protein encoded by an obesity gene, expressed in adipose tissue and released into the blood also affects food intake. Orexin and leptin receptors have been localized in the LHA, pPVN, and VMH. The purpose of this study was to measure food intake in the rat in response to leptin and orexin-A; and to determine their electrophysiological effects on feeding related hypothalamic neurons. Results clearly show that leptin suppresses food intake whereas orexin-A increases food intake. These differences are associated with leptin and orexin-A modulatory effects on LHA, pPVN, and VMH glucose responding neurons. In the LHA, leptin inhibits a larger proportion of both glucose-sensitive neurons (GSNs) and non-GSNs. In the pPVN, leptin increases more GSNs in comparison to non-GSNs. Whereas in the VMH, leptin increases the activity of glucoreceptor neurons (GRNs) in comparison to non-GRNs. Orexin-A had opposite effects: increases activity of GSNs more than the non-GSNs in the LHA and significantly suppresses GRNs in the VMH. In the pPVN, orexin-A had no observable effects on neurons that have a low density of orexin 2 receptors. Results are discussed in terms of hypothalamic neural circuits that are sensitive to endogenous food intake inducing and reducing substances.

Animals↗

PubMed1993

Alterations of serotonin receptor binding in the hypothalamus following acute denervation.

Quantitative autoradiography was used to determine the effect of acute serotonergic denervation with 5,7-dihydroxytryptamine (5,7-DHT) or serotonin 5HT1a and 5-HT1b receptors in male rats. Seven days after intrahypothalamic 5,7-DHT injection there was a significant increase in the density of 5HT1a receptors in the ventromedial and dorsomedial hypothalamic nuclei (VMN and DMN) of male rats. In adjacent sections. 5-HT1b receptors were significantly increased only in the VMN. No changes in receptor density were observed in the lateral hypothalamic area or hippocampus even though binding of [3H]paroxetine, which labels the presynaptic transporter site, was significantly decreased in all evaluated brain regions in 5,7-DHT-treated animals. In addition to demonstrating that 5-HT1a and 5-HT1b receptors are differentially regulated in different brain areas, these results show that in the brain regions examined both 5-HT1a and 5-HT1b receptors are primarily post-synaptic.

5,7-Dihydroxytryptamine↗

PubMed1993

Body fat and RNA content of VMH neurons in rats.

The epididymal and retroperitoneal fat content of 180-day-old male Wistar rats, coming from litters of eight pups was correlated with their RNA content in ventromedial hypothalamus (VMH) and lateral hypothalamic area (LHA) neurons. A significant negative correlation was found between the RNA content in VMH neurons and epididymal and retroperitoneal fat content. The results indicate a closed relationship between the body fat content and the functional activity of VMH.

Adipose Tissue↗

PubMed2000

Hypothalamic neuropeptide Y levels in weaning offspring of low-protein malnourished mother rats.

Maternal low-protein malnutrition during gestation and lactation (LP) is an animal model frequently used for the investigation of long-term deleterious consequences of perinatal growth retardation. Hypothalamic neuropeptides are decisively involved in the central nervous regulation of body weight and metabolism. We investigated neuropeptide Y (NPY) in distinct hypothalamic nuclei in the offspring of LP mother rats at the end of the critical hypothalamic differentiation period (20th day of life). Weanling LP offspring were underweight (P< 0.001) and hypoinsulinaemic (P< 0.05), while leptin levels were unchanged. NPY was significantly increased in the paraventricular hypothalamic nucleus (PVN) (P< 0.01) and lateral hypothalamic area (P< 0.05) in LP offspring. In contrast, NPY was unchanged in the ventromedial hypothalamic nucleus (VMN). These observations indicate a leptin-independent stimulation of the orexigenic ARC-PVN axis in undernourished LP rats at weaning. Furthermore a disturbed NPYergic regulation of the VMN is suggested, possibly contributing to alterations of the hypothalamic regulation of body weight and metabolism in LP offspring during life.

Animals↗

PubMed2003

Localization of the GABAergic and non-GABAergic neurons projecting to the sublaterodorsal nucleus and potentially gating paradoxical sleep onset.

We recently determined in rats that iontophoretic application of bicuculline or gabazine [two GABAa antagonists] and kainic acid (a glutamate agonist) in the sublaterodorsal nucleus (SLD) induces with a very short latency a paradoxical sleep-like state. From these results, we proposed that GABAergic and glutamatergic inputs to the SLD paradoxical sleep (PS)-executive neurons gate the onset of PS [R. Boissard et al. (2002) Eur. J. Neurosci., 16, 1959-1973]. We therefore decided to determine the origin of the GABAergic and non-GABAergic inputs to the SLD combining ejection of a retrograde tracer [cholera-toxin B subunit (CTb)] with glutamate decarboxylase (GAD) immunohistochemistry. The presence of GAD-immunoreactive neurons in the SLD was confirmed. Then, following CTb ejections centred on the SLD, combined with GAD and CTb immunohistochemistry, double-labelled cells were observed in the mesencephalic and pontine reticular nuclei and to a lesser extent the parvicellular reticular nucleus. A large number of GAD-negative retrogradely labelled cells was also seen in these structures as well as in the primary motor area of the frontal cortex, the central nucleus of the amygdala, the ventral and lateral bed nucleus of the stria terminalis, the lateral hypothalamic area, the lateral and ventrolateral periaqueductal grey and the lateral paragigantocellular reticular nucleus. From these results, we propose that the activation of PS-executive neurons from the SLD is due to the removal of a tonic inhibition from GABAergic neurons localized in the SLD, and the mesencephalic and pontine reticular nuclei. Strong non-GABAergic inputs to the SLD could be excitatory and responsible for the tonic glutamatergic input on the PS-on neurons we have previously described. They could also terminate on SLD GABAergic interneurons and be indirectly responsible for the inhibition of the PS-on neurons during waking and slow-wave sleep.

Animals↗

PubMedDate not supplied

Intense vasoconstriction and bradycardia evoked by stimulation of neurones within the midbrain ventral tegmentum of the rabbit.

Electrical stimulation of sites in the midbrain ventral tegmental area (VTA) and the lateral hypothalamic area of the anaesthetized rabbit elicited intense vasoconstriction and profound bradycardia. The same effects were elicited by microinjections of glutamate ions into the VTA but not the lateral hypothalamic area. Following baroreceptor denervation, the bradycardic component of the response was greatly reduced, but the vasoconstrictor component was unaffected. It is concluded that the cardiovascular response is generated by excitation of a cell group within the VTA, but within the hypothalamus the response arises from excitation of axons of passage.

Animals↗

PubMed1988

Direct effects of 3,4-dihydroxybutanoic acid gamma-lactone and 2,4,5-trihydroxypentanoic acid gamma-lactone on lateral and ventromedial hypothalamic neurons.

The mechanism of central actions of endogenous sugar acids, 3,4-dihydroxybutanoic acid gamma-lactone (3,4-DB) and 2,4,5-trihydroxypentanoic acid gamma-lactone (2,4,5-TP) which have been newly identified as satiety and hunger substances respectively, was investigated. Intracellular recordings were made from neurons in the lateral hypothalamic area (LHA) of rats and ventromedial hypothalamic nucleus (VMH) of guinea pigs, brain areas referred to as feeding and satiety centers, respectively. The LHA neurons hyperpolarized by 3,4-DB show no change in membrane input resistance while the depolarized VMH neurons are associated with an increase in membrane resistance. The mechanisms related to the action of 3,4-DB on these hypothalamic neurons are similar to those in case of glucose on the glucose-sensitive neuron in the LHA and the glucoreceptor neuron in the VMH. 2,4,5-TP depolarized LHA neurons but hyperpolarized VMH neurons with a decrease in the membrane resistance. Our findings indicate that 3,4-DB and 2,4,5-TP have reciprocal effects on each LHA and VMH neurons, with regard to neuronal excitability.

Action Potentials↗

PubMed1999

Disruption in neuropeptide Y and leptin signaling in obese ventromedial hypothalamic-lesioned rats.

Electrolytic lesions placed in the ventromedial hypothalamus (VMH) of rats induce instant hyperphagia and excessive weight gain. Since neuropeptide Y (NPY) is a potent hypothalamic orexigenic signal, and leptin secreted by adipocytes regulates NPY output, we tested the hypothesis that altered NPYergic-leptin signaling may underlie hyperphagia in VMH-lesioned rats. VMH-lesioned rats exhibiting hyperphagia and excessive weight gain in a time-related fashion were sacrificed on days 2, 7, and 21 post-surgery. Quite unexpectedly, NPY concentrations in the hypothalamic paraventricular nucleus (PVN), a major site of NPY release for stimulation of feeding, and in other sites, such as the dorsomedial nucleus, lateral hypothalamic area and median eminence-arcuate nucleus decreased, with the earliest diminution occurring on day 2 in the PVN only. In vitro basal and K+-evoked NPY release from the PVN of VMH-lesioned rats was significantly lower than that of controls. Analysis of hypothalamic NPY gene expression showed that although the daily decrease in NPY mRNA from 0800 to 2200 h occurred as in control rats, NPY mRNA concentrations were markedly reduced at these times in the hypothalami of VMH-lesioned rats. Leptin synthesis in adipocytes as indicated by leptin mRNA levels was also profoundly altered in VMH-lesioned rats. The daily pattern of increase in adipocyte leptin mRNA at 2200 h from 0800 h seen in controls was abolished, higher levels of leptin gene expression at 2200 h were maintained at 0800 h. The pattern of increase in serum leptin and insulin levels diverged in VMH-lesioned rats. Serum insulin concentration increased to maximal on day 2 and remained at that level on day 21-post-lesion; serum leptin levels on the other hand, increased slowly in a time-related fashion during this period. These results demonstrate that hyperphagia and excessive weight gain in VMH-lesioned rats are associated with an overall decrease in hypothalamic NPY and augmented leptin signaling to the hypothalamus. The divergent time course of increases in serum leptin and insulin levels suggest independent mechanisms responsible for their augmented secretion, and neither these hormones nor VMH lesions altered the daily rhythm in NPY gene expression. These observations underscore the existence of an independent mechanism controlling the daily rhythm in hypothalamic NPY gene expression and suggest that leptin feedback action requires an intact VMH.

Adipocytes↗

PubMed2004

In vitro increase in intracellular calcium concentrations induced by low or high extracellular glucose levels in ependymocytes and serotonergic neurons of the rat lower brainstem.

Pancreatic glucokinase (GK)-like immunoreactivities are located in ependymocytes and serotonergic neurons of the rat brain. The present study investigated in vitro changes in intracellular calcium concentrations ([Ca(2+)](i)) in response to low (2 mm) or high (20 mm) extracellular glucose concentrations in isolated cells from the wall of the central canal (CC), raphe obscurus nucleus (ROb), ventromedial hypothalamus (VMH), and lateral hypothalamic area (LHA) in male rats. An increase in [Ca(2+)](i) was found in cells from the CC (21.1% or 9.8% of ependymocytes), ROb (10.9% or 14.5% of serotonergic neurons), VMH (7.8% and 25.2% of neurons), and LHA (20% or 15.7% of neurons), when extracellular glucose levels were changed from 10 to either 2 or 20 mm, respectively. Most of the ependymocytes and serotonergic neurons responding to the glucose changes were immunoreactive to the anti-GK in the CC (96.8% for low glucose and 100% for high glucose) and ROb (100% for low and high glucose). The [Ca(2+)](i) increase was blocked with calcium-free medium or L-type calcium channel blocker. Cells with an increase in [Ca(2+)](i) in response to low glucose did not respond to high glucose and vice versa. Inhibition of GK activity with acute alloxan treatment blocked low or high glucose-induced [Ca(2+)](i) increases in most GK-immunoreactive cells from the CC or ROb. The glucose-sensitive [Ca(2+)](i) increase in neurons of the VMH and LHA was also alloxan-sensitive, but no cells taken from the VMH and LHA were immunoreactive to the antibody used. The present study further indicates that ependymocytes of the CC and serotonergic neurons in the ROb are also sensitive to the changes in extracellular glucose in a GK-dependent manner, but that the subtype of GK in these cells could be different from that in the VMH and LHA.

Alloxan↗

PubMed1986

Lateral hypothalamic innervation of the cerebral cortex: immunoreactive staining for a peptide resembling but immunochemically distinct from pituitary/arcuate alpha-melanocyte stimulating hormone.

The combination of retrograde transport of fluorescent dyes and indirect immunofluorescence has been used to study the putative neurotransmitter specificity of the tuberal lateral hypothalamic projection to the cerebral cortex. Injections of either fast blue or diamidino yellow dye into the cerebral cortex or hippocampus retrogradely labeled large, multipolar neurons scattered through the lateral hypothalamic area and zona incerta at the level of the ventromedial nucleus of the hypothalamus. Approximately 80% of these neurons stained immunohistochemically with an antiserum against alpha-melanocyte stimulating hormone (alpha-MSH). A second population of smaller, predominantly bipolar alpha-MSH-like immunoreactive neurons was seen in the arcuate nucleus and retrochiasmatic area, but none of these projected to the cerebral cortex. Immunohistochemical staining for ACTH (18-24), another proopiomelanocortin series peptide, or with an antiserum against alpha-MSH (4-10) demonstrated only the second of these cell groups. Our results indicate that the tuberal lateral hypothalamic projection to the cerebral cortex contains a substance similar but not identical to alpha-MSH, and that this material is probably not derived from the same proopiomelanocortin precursor as true alpha-MSH.

Adrenocorticotropic Hormone↗

PubMed1987

Participation of the central amygdaloid nucleus in the response of adrenocorticotropin secretion to immobilization stress: opposing roles of the noradrenergic and dopaminergic systems.

Bilateral lesions of the amygdaloid central nucleus (ACE) significantly diminished the secretion of ACTH in response to immobilization stress. Stress is associated with increased noradrenergic activity in the ACE and in the anterior and lateral hypothalamic areas. In comparison with intact stressed animals, lesion of the ACE reduced the noradrenergic activity in response to stress within the anterior and lateral hypothalamic areas, the arcuate and paraventricular nuclei of the hypothalamus and the bed nucleus of the stria terminalis. These results support the hypothesis of a stimulatory role for the noradrenergic system in the ACE on ACTH secretion. Stress decreased dopaminergic activity in the ACE, the cortical nucleus of the amygdala, the dorsomedial and ventromedial nuclei of the hypothalamus and the ventral tegmental area. In comparison with intact stressed rats, lesion of the ACE reduced dopaminergic activity in the anterior and lateral hypothalamic areas. Our results support the hypothesis of an inhibitory role of the dopaminergic system, particularly in the ACE, on ACTH secretion. This study also indicates that, in the control of ACTH secretion in response to immobilization stress, the noradrenergic and dopaminergic systems act in opposition to one another in certain brain structures such as the anterior and lateral hypothalamic areas and the ACE.

Adrenocorticotropic Hormone↗

PubMed1982

[Role of the lateral hypothalamus in the genesis of somato-autonomic responses].

Coagulation of medial and lateral parts of the lateral hypothalamic area increases latency of responses and decreases respiration, arterial blood pressure and heart rate responses to stimulation of the hypothalamic ventromedial nucleus. Coagulation of the perifornical region of the lateral hypothalamus completely eliminates the above autonomic responses. A new rigid integration which is characterized with the increased number of correlated relations between separate components of somato-autonomic responses, was postulated after correlation analysis of somato-autonomic parameters during stimulation of hypothalamic ventromedial nucleus in animals with lateral hypothalamic lesions. The data suggest that somato-autonomic responses to stimulation of negative emotion sites of the hypothalamus are mediated by those brain structures which are under ascending excitatory influences of the lateral hypothalamus.

Animals↗

PubMed1984

Hypothalamically-induced insulin release and its potentiation during oral and intravenous glucose loads.

Male Wistar rats were provided with bilateral cannulas in the lateral hypothalamic area (LHA) and cannulas in the left and right jugular vein. Freely moving rats provided in this way with cannulas were infused with transmitters in the LHA and with various substances in the blood circulation during simultaneous sampling of blood without disturbing the animals. Infusion of norepinephrine (NE) in the LHA resulted in increased insulin levels while plasma glucagon and blood glucose were nearly not affected. This LHA mediated insulin release was suppressed by atropine injection in the blood circulation suggesting a vagal contribution to the observed phenomenon. Administration of either an oral or i.v. glucose load during noradrenergic stimulation of the LHA elicited an exaggerated insulin response when compared to their controls. This LHA potentiated insulin response during an oral and i.v. glucose load could be suppressed by atropinization of the rats. It is concluded that meal-related stimuli are relayed to the NE-stimulated area of the LHA and that these stimuli modulate the output from this area of the LHA that is concerned with the release of insulin.

Animals↗

PubMed1988

Lateral and ventromedial hypothalamic influences on hepatic autonomic nerve activity in the rat.

Effects of hypothalamic stimulation and lesion on hepatic autonomic nerve activity were investigated in anesthetized rats. Stimulation of the lateral hypothalamic area increased activity of the hepatic vagal nerve and decreased activity of the splanchnic nerve. Lesion of this area produced a rapid and strong reduction of vagal nerve activity and induced either an increase or a decrease of splanchnic nerve activity. In contrast, stimulation of the ventromedial hypothalamic nucleus produced a strong inhibition of vagal nerve activity and facilitation of splanchnic nerve activity. However, lesion of this nucleus facilitated or inhibited activities in both nerve branches. The functional significance of the relationship between the hypothalamus and the hepatic autonomic nerve in regulation of glucose metabolism in the liver are discussed.

Animals↗

PubMed1984

A single-unit analysis of reciprocal relationships between the lateral and medial hypothalamus in rats.

The spontaneous activity of hypothalamic units was studied in chronic awake and ketamine-anesthetized rats. Ketamine appeared to decrease significantly the spontaneous firing of neurons in the ventromedial hypothalamic nucleus (VMH) but did not influence the activity in either the dorsomedial hypothalamic nucleus (DMH) or the lateral hypothalamic area (LHA). The responses obtained in the medial hypothalamus and the LHA after stimulation of the LHA and VMH, respectively, were not modified in either of the recording conditions. These responses corresponded to a pause in spontaneous activity, sometimes associated with a short-latency excitatory response, orthodromic or antidromic. The possibility of direct reciprocal connections between the LHA and the VMH has been discussed on the basis of electrophysiological and anatomical studies.

Anesthesia, General↗

PubMed1986

Control of sensorimotor function by dopaminergic nigrostriatal neurons: influence on eating and drinking.

The literature on the effects of lesions of the lateral hypothalamic area (LHA) on eating and drinking is reviewed in an effort to understand the function of the neural substrate destroyed. The data suggest that damage to the dopaminergic nigrostriatal neurons that course through the LHA results in a decrease in sensorimotor facilitation; that is, an increase in the threshold for responding to stimuli that elicit orientation, approach and consumption. This increase results in decreased consumption of food and water. Evidence is also reviewed suggesting the possibility that striatal dopaminergic activity may mediate a negative feedback signal related to blood glucose level that influences responsiveness to food, and therefore eating. There is no evidence that the nigrostriatal system mediates a similar signal related to water balance and drinking. A second deficit associated with LHA lesions, caused by damage to the pallidofugal neurons that descend through this area, is a dysfunction of motor control of the head and mouth. This results in an increase in the effort required to consume food and water, also leading to decreased consumption. These two behavioral factors: an increased threshold for responding to the sensory properties of food and water and an increase in the effort required to eat and drink are used to explain the symptoms making up the lateral hypothalamic syndrome without postulating changes in physiological regulatory (set point) mechanisms.

Animals↗

PubMed2001

Evidence that orexin-containing neurones provide direct input to gonadotropin-releasing hormone neurones in the ovine hypothalamus.

Orexins A and B (ORX) have been added recently to the growing list of neuropeptides implicated in feeding and drinking behaviour as well as neuroendocrine function. In the present study, we have used single and dual labelling immunohistochemistry and a rabbit polyclonal anti-orexin-A antibody, which recognizes both ORX A and B, to examine ORX pathways in the sheep hypothalamus. ORX immunoreactive cells were distributed in the dorsomedial hypothalamic nucleus, lateral hypothalamic area, zona incerta and perifornical area; a few cells were also observed in the anterior hypothalamic area. In contrast to distribution in the rat brain, most of the ORX immunoreactive cells are localized to the dorsomedial hypothalamic nucleus and perifornical area; scattered cells are found in lateral hypothalamic area. ORX immunoreactive fibres were widely distributed throughout the hypothalamus and preoptic area with dense innervation of the medial preoptic area and bed nucleus of stria terminalis. Dual labelling demonstrated widespread expression of the long form of the leptin receptor within all ORX cells that were examined. Thirty percent of the gonadotropin releasing hormone (GnRH) cells that were examined had ORX immunoreactive terminals in close contact with no regional or sex differences. FluoroGold injections into the preoptic area retrogradely labelled a subpopulation of ORX cells in the lateral hypothalamic/perifornical area, showing ORX cells of this region project to the preoptic and could potentially provide input to GnRH cells. These findings suggest an integral role for ORX in the regulation of GnRH cells in the sheep and thus provide evidence of a novel mechanism whereby leptin can influence reproductive neuroendocrine function.

Afferent Pathways↗