Participation of the dorsomedial hypothalamic nucleus in the “feeding center” and water intake circuitry of the weanling rat

Bernardis, Lee L.

doi:10.1007/bf02312740

Cited by 67 publications

(21 citation statements)

References 23 publications

(10 reference statements)

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“…Animals with DMNL showed hypophagia. Several studies have suggested that this nucleus underlies the neural signaling of satiety factors (31,32). For instance, 24-h food deprivation increased NPY mRNA specifically in the DMN in Otsuka Long-Evans Tokushima fatty rats, a hyperphagic and obese model, due to lack of CCK-A receptor.…”

Section: Discussionmentioning

confidence: 99%

Galanin-Like Peptide Stimulates Food Intake via Activation of Neuropeptide Y Neurons in the Hypothalamic Dorsomedial Nucleus of the Rat

Kuramochi

Onaka²,

Kohno³

et al. 2006

Endocrinology

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Galanin-like peptide (GALP), a 29-amino-acid neuropeptide, is located in the hypothalamic arcuate nucleus (ARC), binds to galanin receptor subtype 2, and induces food intake upon intracerebroventricular (icv) injection in rats. However, neural mechanisms underlying its orexigenic action remain unclear. We aimed to identify the nuclei and neuron species that mediate the food intake in response to icv GALP injection. Intracerebroventricular injection of GALP, as powerfully as that of neuropeptide Y (NYP), increased food intake for the initial 2 h. GALP injected focally into the dorsomedial nucleus (DMN), but not the ARC, lateral hypothalamus, or paraventricular nucleus (PVN), stimulated food intake for 2 h after injection. In contrast, galanin injected into the DMN had no effect. DMN-lesion rats that received icv GALP injection showed attenuated feeding compared with control rats. In from the porcine intestine (1). It is widely distributed in the central and peripheral nervous systems and has various activities, including regulation of feeding behavior, cognition, nociception, and secretion of pituitary hormones (2-4). Three distinct galanin receptor subtypes, GalR1, GalR2, and GalR3, have been identified (5). These receptors show different tissue distributions: GalR1 is expressed mainly in the central nervous system, whereas GalR2 abundantly and GalR3 at low levels are expressed in both the central nervous system and peripheral tissue.Galanin-like peptide (GALP), a 60-amino-acid peptide whose residues 9 -21 are identical with galanin-(1-13), was isolated from the porcine hypothalamus (6). GALP has a higher affinity for GalR2 than GalR1. Therefore, GALP was initially suggested to be the endogenous ligand for GalR2 (6). Later, it was reported that the action of GALP in the hypothalamus was observed in GalR2-deficient mice (7). Thus, the receptor for GALP remains to be clarified. Several actions of GALP have been shown. Intracerebroventricular (icv) injection of GALP stimulates LH secretion, and it is blocked by treatment with antagonists of LHRH (8). In relation to the energy metabolism, GALP-containing neurons express leptin receptors, and deficiency of leptin function is associated with reductions in GALP protein and mRNA expression (9, 10). Gene expression of GALP is positively regulated by leptin, insulin, and thyroid hormone, the hormones implicated in energy metabolism (11,12).It has been reported that GALP mRNA is expressed in the arcuate nucleus (ARC) (9, 13), a feeding regulatory center, and that icv administration of GALP increases food intake in rodents (14), although the underlying mechanisms remain largely unknown. The present study aimed to identify the nucleus and neuron species that serve as effectors for the orexigenic action of GALP in rats. First, the target nucleus was studied using the following methods. The effects of focal injections of GALP into several hypothalamus nuclei on food intake were examined. Whether destruction of specific nucleus affects orexigenic effect of icv GALP injection wa...

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Section: Discussionmentioning

confidence: 99%

Galanin-Like Peptide Stimulates Food Intake via Activation of Neuropeptide Y Neurons in the Hypothalamic Dorsomedial Nucleus of the Rat

Kuramochi

Onaka²,

Kohno³

et al. 2006

Endocrinology

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“…Stainless steel wires, 0.25 mm in diameter, telescoped into 24-gauge hypodermic needles and spar varnish-coated except for about 0.2 mm at the tip, served as electrodes. The coordinates have been previously established [Bernardis and Skelton, 1965;Bernardis, 1970a]. The rats were divided into 3 groups: group 1 received lesions in the ventromedial hypothalamus (VMH), group 2 received lesions in the Belli nger/Bernardis/M endel dorsoniedial hypothalamus (DMH) and group 3 consisted of sham-operated controls with the electrode inserted into either the VMH or DMH, but without current flow.…”

Section: Methodsmentioning

confidence: 99%

Effect of Ventromedial and Dorsomedial Hypothalamic Lesions on Circadian Corticosterone Rhythms

Bellinger

Bernardis

Mendel³

1976

Neuroendocrinology

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Weanling rats received bilateral electrolytic lesions in the dorsomedial (DMH) or ventromedial (VMH) hypothalamic areas destroying primarily the dorsomedial (DMN) or ventromedial (VMN) hypothalamic nuclei. Sham-operated rats served as controls. Lesions in the VMN and DMN, both of which have previously been shown to disrupt normal diurnal feeding rhythms, were also observed to disrupt normal plasma corticosterone rhythms in the present study. The a.m. values of plasma corticosterone in the DMN-lesioned rats were higher than the sham-operated controls. In the p.m., the values of both VMN- and DMN-lesioned rats were lower than those of the controls but unchanged in comparison to their own a.m. concentrations. This disruption of the normal diurnal plasma corticosterone rhythm persisted for at least 9 post-operative weeks.

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“…Only food intake and body weight gains were depressed, and then only when DMN lesions were produced prior to the placement of the VMN lesions . These data indicate that the primary changes in the weanling rat VMN syndrome, once established, cannot be significantly altered by DMN lesions which by themselves decrease food intake and ponderal and linear growth (Bernardis, 1970a;Bernardis, 1970b;Bernardis and Frohman, 1971;Bernardis, 1973a). The failure of DMN lesions to attenuate the VMN syndrome is the more striking since extensive intermingling of fibers between the VMNand DMN has been reported to exist (Chi, 1970; Millhouse, 1969; Szentagothai et al, 1968).…”

mentioning

confidence: 72%

“…These data then do not support the hypothesis that pathways between the VMN and the lateral hypothalamic area are involved in the etiology of the weanling rat VMN syndrome (Schnatz et al, 1973). However, it is possible that sympathetic pathways might be involved, traveling in the dorsal longitudinal fasciculus of Schutz and connecting the VMN with the mesencephalon and autonomic centers in the neuraxis (Arees and Mayer, 1967;Ban, 1966;Krieg, 1932).Lesions primarily destroying the dorsomedial hypothalamic nuclei (DMN) of the weanling rat caused hypophagia and reduced ponderal and linear growth in the face of normal plasma glucose, insulin, growth hormone, and lipid levels (Bernardis, 1970a;Bernardis and Frohman, 1971;Bernardis, 1973a). For review see Bernardis (1975).…”

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confidence: 98%

Origin of endocrine‐metabolic changes in the weanling rat ventromedial syndrome

Bernardis

Goldman

1976

J of Neuroscience Research

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Destruction of the ventromedial hypothalamic nuclei (VMN) in the weanling rat without injury to the median eminence results in a series of somatic, endocrine, and metabolic changes that are characterized by normal food and water intake but decreased linear growth, normal body weight but increased carcass fat and reduced carcass protein, lean body mass, and water. The endocrine alterations comprise hyperinsulinemia in the face of normoglycemia, hypertriglyceridemia and hypercholesterolemia and reduced growth hormone levels. The metabolic changes include greater oxidation of glucose and incorporation into lipid and reduced palmitate oxidation but increased incorporation into lipid. Weanling rats with VMN lesions are normophagic in absolute terms, relative to body weight and per metabolic unit, but their nocturnal feeding and weight gain cycles are disrupted and their locomotor activity is reduced. The VMN are involved in the long-term control of feeding - as in the mature rat - as shown by intragastric preloading studies and dietary density manipulation, glucose preference tests and intraperitoneal injections with glucose. Hyperinsulinemia and hypertriglyceridemia are present four days after the VMN operation in the presence of subnormal food intake and plasma glucose levels. Manipulations of the fat content of the diet revealed that the hyperlipidemia is of both endogenous and exogenous origin and that lipoprotein lipase is increased; a 48-hour fast reduced the hyperlipidemia to control levels, however. This suggests that weanling VMN rat tissue may have an impaired ability to take up circulating lipid. An increased incorporation of glycerol into lipid may be due to induction of glycerokinase by hyperinsulinemia. Adipose tissue of weanling VMN rats showed glycerokinase by hyperinsulinemia. Adipose tissue of weanling VMN rats showed neither depressed lipolysis nor diminished lipolytic activity per milligram of tissue protein. Glucose oxidation and incorporation into adipose tissue is increased in several tissues in vitro and there is enhanced glucose disappearance from plasma and incorporation into tissue lipids in vivo. These changes develop within a short time after lesion production and persist at least partially up to six months: glucose utilization in liver increases already four hours after the operation whereas it takes 72 hours to commence in adipose tissue. Insulin resistance is not apparent either in vivo or in vitro. The decreased growth hormone levels are not critical to the metabolic changes, nor is the hyperinsulinemia totally necessary. The metabolic changes also appear on several different types of diet and persist with fasting. The latter does not reduce insulin sensitivity of VMN rat tissues, wheras it does so in normal rats. Mature rats developed the same metabolic changes even in the absence of hyperphagia. The metabolic alterations can be blocked by pharmacologic doses of glucocorticoids, but are enhanced by the administration of estrogen...

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Participation of the dorsomedial hypothalamic nucleus in the “feeding center” and water intake circuitry of the weanling rat

Cited by 67 publications

References 23 publications

Galanin-Like Peptide Stimulates Food Intake via Activation of Neuropeptide Y Neurons in the Hypothalamic Dorsomedial Nucleus of the Rat

Galanin-Like Peptide Stimulates Food Intake via Activation of Neuropeptide Y Neurons in the Hypothalamic Dorsomedial Nucleus of the Rat

Effect of Ventromedial and Dorsomedial Hypothalamic Lesions on Circadian Corticosterone Rhythms

Origin of endocrine‐metabolic changes in the weanling rat ventromedial syndrome

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