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PubMed1996

Changes in brain neurotransmitters in hypothalamus related to feeding behavior in LEC rat.

In the present study, neurotransmitters related to the regulation of food intake were investigated in hypothalamus of LEC rats. The experiment was conducted using LEC and LEA (control) rats aged 4, 10 and 20 weeks. Cu concentration in hypothalamus of LEC rats aged 4 weeks was lower than that in the control, and similar to the control in 10 weeks of age. In contrast, Cu concentration of LEC rats aged 20 weeks was significantly higher (p < 0.01) than that in the control. The acetylcholine release from lateral hypothalamus of LEC rats aged 4 weeks was significantly higher (p < 0.05) than that in the control, but no significant difference of acetylcholine release was found between LEC and control rats aged 10 and 20 weeks. The metabolism of serotonin (5-HT) in hypothalamus of LEC rats was facilitated in 20 weeks of age. Furthermore, the 5-hydroxytryptophan, precursor of 5-HT in LEC rats aged 10 weeks was significantly higher (p < 0.05) than that in the control. No significant difference was found in norepinephrine (NE), dopamine (DA), 3, 4-dihydroxyphenyl acetic acid and homovanilic acid concentrations in each age of hypothalamus, except a significant decrease in NE concentration in LEC rats aged 10 weeks (p < 0.05). The daily and total food intake were suppressed in LEC rats from a young age. Furthermore, blood glucose, albumin and total cholesterol concentrations in LEC rats were lower than those in the control rats. The present study demonstrated that age dependent changes in Cu concentration and the metabolism of neurotransmitters related to the regulation of food intake occurred in hypothalamus of LEC rats. These results suggest that suppression of the food intake observed in LEC rats is not only due to hepatitis but also due to suppressive effects of feeding regulation center in central nervous system.

Acetylcholine↗
PubMed1998

Effect of ionizing radiation on the release of cholecystokinin in the hypothalamus of the rat.

This study was designed to identify the mechanisms underlying the reduction in food intake in rats. Measurements were made of the release of cholecystokinin (CCK) stimulated by potassium chloride in the hypothalamus after (a) gamma irradiation (60Co), (b) treatment with the CCK-A and CCK-B antagonists L-364,718 and L-365,260 with and without radiation, (c) bilateral abdominal vagotomy, and (d) vagotomy with and without radiation and with and without L-364,718. The concentrations of CCK in hypothalamus perfusate were measured by a radioimmunoassay. Exposure of rats to 1, 3, 5 and 10 Gy (1 Gy/min) increased release of CCK in the hypothalamus in a manner that was dependent on dose. A dose of 5 Gy was chosen for further studies. Intraperitoneal (i.p.) administration of 10, 20 and 50 microg/kg of L-364,718 did not induce significant changes in release of CCK in sham-irradiated animals. However, the drug decreased the release of CCK induced by radiation in a dose-dependent manner. In contrast to L-364,718, 20-50 microg/kg of L-365,260 decreased the release of CCK in the hypothalamus in sham-irradiated animals but did not decrease release of CCK induced by exposure to radiation. Vagotomy produced an insignificant reduction in release of CCK compared to that in sham-irradiated controls. However, vagotomy decreased release of CCK in irradiated rats compared to the irradiated rats without vagotomy. Vagotomy and i.p. administration of 10, 20 and 50 microg/kg of L-364,718 decreased release of CCK in irradiated rats compared to that in irradiated rats without vagotomy. However, i.p. administration of 10, 20 and 50 microg/kg of L-364,718 did not induce significant decreases in release of CCK in the hypothalamus of vagotomized and irradiated animals compared to those in rats that were vagotomized and irradiated but not treated with L-364,718. These results demonstrate that radiation increases the release of CCK in the hypothalamus, and that this effect is inhibited by vagotomy and the administration of a CCK-A receptor antagonist. A CCK-A receptor antagonist may be used to mitigate a radiation-induced deficit in food intake.

Animals↗
PubMed1976

Single unit recording in hypothalamus and preoptic area of estrogen-treated and untreated ovariectomized female rats.

Single unit activity was recorded with micropipettes in the medial hypothalamus and preoptic area of urethane-anesthetized ovariectomized female rats. Some females had received long-term estradiol treatment, while others had been left untreated. In the medial preoptic region and bed nucleus of the stria terminalis, estrogen-treated rats had fewer cells (compared to untreated rats) with recordable spontaneous activity, due primarily to a loss of cells with very slow firing rates. In the basomedial hypothalamus, estrogen-treated rats had more cells (than untreated rats) with recordable spontaneous activity, due primarily to an increase in the number of cells with slow firing rates. Responsiveness of neurons to somatosensory stimulation was generally low. If present it was depressed by estrogen treatment in medial preoptic area and bed nucleus of stria terminalis, while it tended to be elevated by estrogen treatment in medial anterior hypothalamus and basomedial hypothalamus. Differences in the effects of long-term systemic estrogen treatment on medial preoptic neurons compared to basomedial hypothalamus are paralledled by differences in the control of lordosis by these neurons in female rats.

Animals↗
PubMed1983

Dopamine-stimulated adenylate cyclase in hypothalamus: influence of estrous cycle in female and castration in male rats.

The activity of dopamine- and norepinephrine-stimulated adenylate cyclase in hypothalamus and amygdala was studied during the estrous cycle of the female and following castration of the male rat. In the medial hypothalamus but not in the anterior hypothalamus or amygdala, stimulation of adenylate cyclase by dopamine was enhanced during proestrus and following castration. There were no changes in norepinephrine-stimulated adenylate cyclase in medial hypothalamus. Thus, an interaction may exist between gonadal hormones and dopamine receptors linked to adenylate cyclase in medial hypothalamus. The rapidity of the changes in receptor sensitivity suggests that this interaction plays an important role in physiological regulation.

Adenylyl Cyclases↗
PubMed1986

Diminished alpha 2-adrenoceptor-mediated modulation of noradrenergic neurotransmission in the posterior hypothalamus of spontaneously hypertensive rats.

An azepine derivative, 6-allyl-2-amino-5,6,7,8-tetrahydro-4H-thiazolo-[4,5-d]-azepine (B-HT 920; 100 nM), inhibited the evoked noradrenaline release from slices of rat posterior hypothalamus, and yohimbine (100 nM) potentiated the release from slices of rat anterior and posterior hypothalamus. In the posterior hypothalamus of 4- and 15-16-week-old spontaneously hypertensive rats (SHRs), as compared with age-matched Wistar-Kyoto rats (WKYs), the inhibitory effect of B-HT 920 and the facilitatory effect of yohimbine were decreased. In the anterior hypothalamus there was no significant difference in the yohimbine effect between WKYs and SHRs, at either age. It is concluded that alpha 2-adrenoceptor-mediated autoinhibition of noradrenergic neurotransmission is diminished in the posterior hypothalamus of SHRs.

Animals↗
PubMed1983

In vivo studies of somatostatin-14 and somatostatin-28 biosynthesis in rat hypothalamus.

The biosynthesis of somatostatin-14 (SRIF-14) and somatostatin-28 (SRIF-28) was studied in rat hypothalamus after injection of 35S-labeled cysteine into the third ventricle. Cysteine specific activity was quantitated, and found to decline rapidly after injection of the labeled amino acid: less than 0.1% of the injected label remained as free cysteine in the hypothalamus 30 min post injection. Incorporation of label into SRIF-14 and SRIF-28 reached maximum values 8 h post injection, compared with a labeling maximum at 1-2 h for acid-precipitable protein. Within 2 h after [35S]cysteine injection, nearly half of the total labeled hypothalamic SRIF appeared in the medial basal hypothalamus; 24-h post injection this percentage reached approximately 75%. Colchicine administration dramatically reduced the appearance of labeled SRIF in medial basal hypothalamus, but had no apparent effect on the total incorporation of [35S]cysteine into SRIF-14, SRIF-28, or acid-precipitable protein, or on radioimmunoassayable SRIF levels. These results suggest that 1) the technique employed for administering [35S] cysteine delivers the label as a pulse; 2) the timing of the appearance of labeled amino acid in SRIF-14, SRIF-28, and acid-precipitable protein is consistent with initial synthesis of a larger prohormone, followed by conversion to peptide products; and 3) the newly synthesized peptides are rapidly transported to the medial basal hypothalamus by a colchicine sensitive mechanism.

Animals↗
PubMedDate not supplied

[The mechanisms of the influence of the anterior and posterior hypothalamus on the electrical activity of the large hemispheres of the forebrain and on autonomic reactions in hens].

Studies have been made of the effect of stimulation of the anterior and posterior hypothalamus on the electrical activity of the hemispheres, arterial blood pressure, heart and respiration rates. Mainly desynchronizing mechanisms were revealed in the ascending influences from both the anterior and posterior hypothalamus. Concerning the descending influences, it was found that stimulation of the anterior hypothalamus evokes depressor reactions, whereas stimulation of the posterior hypothalamus results in pressor reactions. Peculiarities of evolutionary development of the ascending and descending mechanisms of the posterior and anterior hypothalamus are discussed.

Animals↗
PubMed1987

[Dynamics of oxygen tension in different areas of the hypothalamus during the sleep-wakefulness cycle].

In wakefulness and paradoxical sleep, fast waves prevailed in the PO2 oscillations in the posterior hypothalamus whereas in slow wave sleep fast oscillations of PO2 prevailed in the anterior hypothalamus and preoptic area. These shifts of the PO2 during wakefulness and PS seem to reflect an enhancement of the functional activity of the posterior hypothalamus. During slow wave sleep, the functional activity must be enhanced in the anterior hypothalamus and preoptic area, while in the posterior hypothalamus it is suppressed.

Animals↗
PubMed1976

[Reactions of the neurons of the anterior and posterior regions of the hypothalamus to light stimulation and stimulation of the splanchnic and sciatic nerves].

Responses of single hypothalamic neurons to splanchnic, sciatic nerves and photic stimulation were studied in anesthetized, curarized cats. It is found that units of the posterior and anterior hypothalamus are "convergence neurons" with multisensory inputs. Convergence of somatosensory and visceral (splanchnic) impulses to such neurons was complete. No neurons responding only to the splanchnic nerve stimulation were found. In the posterior hypothalamus some units responded only to stimulation of splanchnic and sciatic nerves and were unresponsive to a flash. On the contrary, in the anterior hypothalamus a part of units responded only to photic stimulation. The polysensory neurons of the posterior and anterior hypothalamus were of a nonspecific modality: they responded with a similar pattern of phasic or tonic discharge with a predominance of phasic responses. Units were more often excited than inhibited. A high responsibility (68%) of spontaneously active neurons to somato-visceral and photic stimulation was observed in the posterior, as well as in the anterior hypothalamus. The principles of functional organization of hypothalamic afferent system are discussed.

Animals↗
PubMed1990

Excitotoxic lesions of the lateral hypothalamus made by N-methyl-d-aspartate in the rat: behavioural, histological and biochemical analyses.

The purpose of this study was to determine whether the excitotoxin N-methyl-d-aspartate (NMDA) could be used to make lesions within the lateral hypothalamus and what effect they had on regulatory behaviour. Larger doses of NMDA were effective in the lateral hypothalamus but tended to spread into adjacent structures; smaller doses made lesions which were contained within the lateral hypothalamus and zona incerta. Lesions which damaged the lateral hypothalamus and surrounding tissue had no effect on the concentration of dopamine (or its metabolites) in the dorsal or ventral striatum. The large lesions, including extrahypothalamic damage, were associated with long-term deficits in lab chow and water intake, but rats with lesions restricted to the lateral hypothalamus made good recoveries, eating and drinking normally from around the tenth day post-operation. Body weight gain was normal in these rats, though there was a long-term loss of body weight compared to controls. Unoperated rats with food intake yoked to lesioned rats showed identical long-term changes in body weight, suggesting that the changes in body weight of lesioned rats may be a reflection of changes in eating and drinking rather than a disruption of a body weight set-point mechanism. Motor deficits were not found; all rats were able to consume without difficulty saccharin solutions. All lateral hypothalamic lesioned rats failed to respond to dehydrating, dipsogenic or glucoprivic challenges. It is concluded that NMDA is an effective toxin in the rat lateral hypothalamus, sparing ascending dopamine fibres, and that the main effect of such lesions is an impairment in responding to physiological challenges.

3,4-Dihydroxyphenylacetic Acid↗
PubMed2000

Synchronized release of dopamine and serotonin in the medial and lateral hypothalamus of rats.

A positive linear correlation between dopamine and serotonin release was found in the ventromedial hypothalamus and in the lateral hypothalamic area in fasting rats and in fed rats during intermeal intervals. Dopamine release in the ventromedial hypothalamus positively correlated with dopamine and serotonin release in the lateral hypothalamic area, which occurred only during intermeal intervals and was non-significant during the meal consumption periods or during fasting. Meal size correlated significantly only with a decrease in serotonin release in the lateral hypothalamic area. The study was designed to evaluate the relationship between dopamine and serotonin release in these hypothalamic areas and their dependence on feeding status. Microdialysis was performed simultaneously via two probes, one in the ventromedial hypothalamus and the other in the contralateral lateral hypothalamic area, of freely moving male lean Zucker rats over 24h with preserved light and dark phase, either with ad libitum access to food and water, or when no food was available. Dopamine and serotonin concentrations were measured by high-performance liquid chromatography with electrochemical detection in 20-min dialysis samples. Time-series analysis was applied to determine linear correlations between monoamines and in relation to food intake. Data showed that release of dopamine and serotonin is synchronized within the ventromedial hypothalamus and lateral hypothalamic area, particularly in the dark phase and when no food was ingested. However, synchronized release of monoamines between these nuclei occurred only during intermeal intervals: the periods of satiety. These findings suggest a tight relationship between dopaminergic and serotonergic systems of the lateral hypothalamic area and ventromedial hypothalamus, which is influenced by the feeding state and which may be involved in maintaining the balance within and between the centers of the parasympathetic and sympathetic nervous systems. The data also illustate that food intake is coupled unequivocally to the release of dopamine and serotonin in the hypothalamus, suggesting it as a mechanism of activation of postsynaptic neurons associated with new metabolic status.

Animals↗
PubMed2003

Precursor-protein convertase 1 gene expression in the mouse hypothalamus: differential regulation by ob gene mutation, energy deficit and administration of leptin, and coexpression with prepro-orexin.

The expression of precursor-protein convertase (PC)1, PC2 and paired basic amino acid cleaving enzyme four mRNA was studied by in situ hybridisation in regions of the hypothalamus involved in energy regulation in relation to obese (ob) gene mutation and energy deficit. PC1 gene was differentially expressed in hypothalamic nuclei of mice from different genetic backgrounds or energetic status, whereas no differences in expression were observed for either the PC2 or paired basic amino acid cleaving enzyme four genes. In obese ob/ob mice, PC1 mRNA levels were increased in the paraventricular nucleus, decreased in the lateral hypothalamus and unchanged in the ventromedial nucleus and arcuate nucleus relative to lean controls. In response to intraperitoneal injection of murine leptin, PC1 mRNA levels in obese ob/ob mice decreased in the arcuate nucleus, increased in the lateral hypothalamus and were unchanged in both the paraventricular nucleus and ventromedial nucleus. In mice deprived of food for 24 h, PC1 mRNA levels were reduced in the ventromedial nucleus, increased in the lateral hypothalamus and unchanged in the paraventricular nucleus and arcuate nucleus relative to ad libitum-fed controls. Overall, whilst the data show effects related to leptin and energetic status, they do not support a strong and consistent link between PC1 gene expression and energy balance. This suggests that if PC1 is important to the control of energy balance then protein expression and activity, rather than gene expression may be the more critical parameters of regulation. The relationship between PC1 and candidate energy balance-related genes in the lateral hypothalamus was investigated by dual in situ hybridisation. PC1 mRNA was localised in prepro-orexin mRNA expressing neurons in the lateral hypothalamus, which suggests a functional relationship.

Animals↗
PubMed2002

Spatial and temporal variation of passer Per2 gene expression in two distinct cell groups of the suprachiasmatic hypothalamus in the house sparrow (Passer domesticus).

In mammals, the major pacemaker controlling circadian rhythmicity is located in the hypothalamic suprachiasmatic nuclei. Although there is evidence for the presence of a hypothalamic circadian oscillator in birds from lesioning studies, neuroanatomical, neurochemical and functional investigations have failed to identify its exact location. Two cell groups in the avian hypothalamus have been shown to bear characteristics of the mammalian suprachiasmatic nucleus: the suprachiasmatic nucleus and the lateral hypothalamic retinorecipient nucleus. We cloned an avian period homologue (pPer2) and investigated the temporal and spatial expression pattern of this gene in the house sparrow hypothalamus using in situ hybridization. Applying quantitative morphometry, we found rhythmic expression of pPer2 during light-dark as well as in constant conditions in the suprachiasmatic nucleus and in the lateral hypothalamus. The temporal and spatial distribution of pPer2 expression in the suprachiasmatic nucleus suggest a longitudinal compartmentalization of the nucleus with period gene expression being initiated in the most rostral portion of the suprachiasmatic nucleus before lights on. In the lateral hypothalamus, phasing of pPer2-rhythmicity appeared different from the suprachiasmatic nucleus. The major difference between light-dark and constant conditions was a decrease in the amplitude of pPer2 rhythmicity in the suprachiasmatic nucleus. Our data demonstrate that, unlike in mammals, Per gene expression in the suprachiasmatic hypothalamus of the house sparrow is not confined to a single cell group, indicating a more complex organization of the circadian oscillator in the hypothalamus of birds.

Animals↗
PubMed1980

Surgical syndromes of the hypothalamus.

The clinical syndromes described with lesions of the hypothalamus are summarized in Table 9.5-9.7. The anterior hypothalamic syndrome consists of insomnia and loss of thirst regulatory mechanisms. In occasional larger lesions which interrupt the output from the supraoptic and paraventricular nuclei, diabetes insipidus has been noticed. In the tuberal region of the hypothalamus the most prominent findings are those that are caused by the disruption of the final common pathway to the pituitary. This results in endocrinopathy, most often the syndrome originally reported by Frohlich, with failure of sexual maturation and obesity. In the tuberal region, differences between lesions of the medial and lateral portions are quite marked. Medial lesions result in obesity while bilateral lesions result in anorexia and emaciation. The diencephalic syndrome of infancy with it's severe emaciation in young years and obesity in later years clearly indicates a different organizational pattern in the neonatal hypothalamus. Emotional disorders may be seen with lesions either in the medial or lateral hypothalamus at the tuberal level. Finally, in the posterior hypothalamic region, which includes the greatest effector apparatus, hypersomnia, apathy, and poikilothermia have been reported. Emotional disturbances and the Wernicke-Korsakoff syndrome also seemed to be associated with lesions in this area. The hypothalamus remains the single most important integrator of vegetative and endocrinologic regulation of the body. Cushing said of the hypothalamus, "here in this hidden spot, almost to be covered with a thumb nail, lies the very main spring of primitive existence: vegetative, emotional and reproductive".

Adenoma↗
PubMed1993

Neurons in the paraventricular nucleus of the hypothalamus that project to the sexually dimorphic lower lumbar spinal cord concentrate 3H-estradiol in the male rat.

The location and distribution of estradiol-concentrating neurons in the hypothalamus afferent to segments of lumbar spinal cord that contain the sexually dimorphic spinal nucleus of the bulbocavernosus (SNB) were determined by combining retrograde fluorescent tract tracing with steroid hormone autoradiography. Injections of Fluorogold were made into segments of L5-L6 of the spinal cord of adult male rats and 12 days later animals were castrated. One week following castration, males received injections of [3H]estradiol and were perfused. Their brains were then processed for steroid hormone autoradiography. Following exposure times of 11 to 12 months, autoradiograms were developed and the hypothalamus was analyzed for neurons that concentrate estradiol and project to the spinal cord. Numerous neurons in the hypothalamus projected to the spinal cord, specifically neurons in the paraventricular nucleus (PVN), the lateral hypothalamus and the dorsal area of the hypothalamus. Although many subnuclei of PVN, as well as lateral hypothalamus, contained Fluorogold labelled neurons and estradiol concentrating neurons, the majority of double labeled cells were found in the lateral parvocellular (LP) subnucleus of PVN. Approximately 30% of the neurons in the lp subnucleus that projected to spinal cord also concentrated estradiol. Up to one half of the estradiol-concentrating neurons in lp sent axons to the lower lumbar spinal cord. These results suggest that some of the effects of gonadal steroid hormones on SNB development, plasticity and function may in fact, be indirect, via steroid-sensitive afferents.

Afferent Pathways↗
PubMed1995

Interferon-alpha acts at the preoptic hypothalamus to reduce natural killer cytotoxicity in rats.

We previously demonstrated that an intracerebroventricular injection of recombinant human interferon-alpha (rhIFN-alpha) reduced the cytotoxicity of splenic natural killer (NK) cells in rats and mice. In the present study, we investigated the brain sites at which rhIFN-alpha acts to suppress splenic NK activity in unanesthetized rats implanted unilaterally with a chronic hypothalamic cannula. A microinjection of 200 U of rhIFN-alpha into the medial part of the preoptic hypothalamus reduced NK activity to approximately 60% of control 30 min after the injection. Administration of 50 U of rhIFN-alpha also decreased NK activity to approximately 80%. The injection of 200 U of rhIFN-alpha into other hypothalamic areas (lateral preoptic hypothalamus, ventromedial hypothalamus, lateral hypothalamus, and paraventricular nucleus) had no effect. The medial preoptic hypothalamus-rhIFN-alpha-induced immunosuppression was completely blocked by splenic denervation, but not by adrenalectomy. These results suggest that IFN-alpha suppresses splenic NK activity predominantly through the medial preoptic hypothalamus-sympathetic pathway.

Animals↗
PubMed1976

Involvement of the avian hypothalamus in defensively conditioned heart rate change.

Hypothalamic involvement in visually conditioned heart rate change (established by pairing light and foot-shock) was studied in 128 pigeons by evaluating conditioning performance following lesions of various hypothalamic areas. Extensive destruction of the posterior hypothalamus severely impaired development of conditioned heart rate change. Anterior hypothalamic lesions also produced serious deficits, though not as severe as following posterior hypothalamic damage. Partial posterior hypothalamic, unilateral and tuberal lesions produced only minor to moderate deficits. The critical locus for profound impairment of conditioned response development appeared to be the medial hypothalamus, and it is suggested that more specifically it is the terminal field of the archistriatal projection upon the medial hypothalamus. It is concluded that the medial hypothalamus is essential for the development of defensively conditioned heart rate change, and based on previous findings it is suggested that the critical descending pathway for expression of this conditioned response involves the archistriatal projection upon the medial hypothalamus and subsequently a polysynaptic pathway through the ventral brainstem.

Animals↗
PubMed1976

The efferent connections of the ventromedial nucleus of the hypothalamus of the rat.

The efferent connections of the ventromedial nucleus of the hypothalamus (VMH) of the rat have been examined using the autoradiographic method. Following injections of small amounts (0.4-2.0 muCi) of tritium labeled amino acids, fibers from the VMH can be traced forward through the periventricular region, the medial hypothalamus and the medial forebrain bundle to the preoptic and thalamic periventricular nuclei, to the medial and lateral preoptic areas, to the bed nucleus of the stria terminalis and to the ventral part of the lateral septum. Some labeled axons continue through the bed nucleus of the stria terminalis into the stria itself, and hence to the amygdala, where they join other fibers which follow a ventral amygdalopetal route from the lateral hypothalamic area and ventral supraoptic commissure. These fibers terminate in the dorsal part of the medial amygdaloid nucleus and in the capsule of the central nucleus. A lesser number of rostrally directed fibers from the VMH crosses the midline in the ventral supraoptic commissure and contributes a sparse projection to the contralateral amygdala. Descending fibers from the VMH take three routes: (i) through the medial hypothalamus and medial forebrain bundle; (ii) through the periventricular region; and (iii) bilaterally through the ventral supraoptic commissure. These three pathways are interconnected by labeled fibers so that it is not possible to precisely identify their respective terminations. However, the periventricular fibers seem to project primarily to the posterior hypothalamic area and central gray, as far caudally as the anterior pole of the locus coeruleus, while the medial hypothalamic and medial forebrain bundle fibers apparently terminate mainly in the capsule of the mammillary complex, in the supramammillary nucleus and in the ventral tegmental area. The ventral supraoptic commissure fibers leave the hypothalamus closely applied to the medial edges of the two optic tracts. After giving off their contributions to the amygdala, they continue caudally until they cross the dorsal edge of the cerebral peduncle to enter the zona incerta. Some fibers probably terminate here, but others continue caudally to end in the dentral tegmental fields, and particularly in the peripeduncular nucleus. Within the hypothalamus, the VMH appears to project extensively to the surrounding nuclei. However, we have not been able to find evidence for a projection from the VMH to the median eminence. Isotope injections which differentially label the dorsomedial or the ventrolateral parts of the VMH have shown that most of the long connections (to the septum, amygdala, central tegmental fields and locus coeruleus) originate in the ventrolateral VMH, and there is also some evidence for a topographic organization within the projections of this subdivision of the nucleus.

Animals↗