Modification by hypothalamic Lesions of the release of growth hormone (GH) following stimulation of the ventromedial hypothalamic nucleus in the rat

1983 ◽  
Vol 280 (1) ◽  
pp. 69-74 ◽  
Author(s):  
Masakatsu Kato ◽  
Mitsuo Suzuki ◽  
Tadao Kakegawa
Keyword(s):  
Growth Hormone ◽  
Hypothalamic Nucleus ◽  
Hypothalamic Lesions ◽  
Ventromedial Hypothalamic Nucleus ◽  
Stimulation Of

scholarly journals TUFTSIN ANALOG AND BEHAVIOUR OF RABBITS AFTER ELECTRIC STIMULATION OF VENTROMEDIAL HYPOTHALAMIC NUCLEUS (VMH)

1996 ◽  
Vol 7 (Supplement 1) ◽  
pp. 22 ◽  
Author(s):  
R CZABAK-GARBACZ ◽  
B CYGAN ◽  
A KRASOWSKI ◽  
I I KOZLOVSKII ◽  
M MAJ
Keyword(s):  
Electric Stimulation ◽  
Hypothalamic Nucleus ◽  
Ventromedial Hypothalamic Nucleus ◽  
Stimulation Of

scholarly journals Nesfatin-1 Influences the Excitability of Gastric Distension-Responsive Neurons in the Ventromedial Hypothalamic Nucleus of Rats

2017 ◽  
pp. 335-344 ◽  
Author(s):  
H. FENG ◽  
Q. WANG ◽  
F. GUO ◽  
X. HAN ◽  
M. PANG ◽  
...  
Keyword(s):  
Neuronal Activity ◽  
Nerve Fibers ◽  
Retrograde Tracing ◽  
Corticotropin Releasing Factor ◽  
Hypothalamic Nucleus ◽  
Gastric Distension ◽  
Mediated Effects ◽  
Ventromedial Hypothalamic Nucleus ◽  
Hippocampal Ca1 ◽  
Stimulation Of

The present study investigated the effects of nesfatin-1 on gastric distension (GD)-responsive neurons via an interaction with corticotropin-releasing factor (CRF) receptor signaling in the ventromedial hypothalamic nucleus (VMH), and the potential regulation of these effects by hippocampal projections to VMH. Extracellular single-unit discharges were recorded in VHM following administration of nesfatin-1. The projection of nerve fibers and expression of nesfatin-1 were assessed by retrograde tracing and fluoro-immunohistochemical staining, respectively. Results showed that there were GD-responsive neurons in VMH; Nesfatin-1 administration and electrical stimulation of hippocampal CA1 sub-region altered the firing rate of these neurons. These changes could be partially blocked by pretreatment with the non-selective CRF antagonist astressin-B or an antibody to NUCB2/nesfatin-1. Electrolytic lesion of CA1 hippocampus reduced the effects of nesfatin-1 on VMH GD-responsive neuronal activity. These studies suggest that nesfatin-1 plays an important role in GD-responsive neuronal activity through interactions with CRF signaling pathways in VMH. The hippocampus may participate in the modulation of nesfatin-1-mediated effects in VMH.

scholarly journals The Dorsomedial Hypothalamic Nucleus In Autonomic And Neuroendocrine Homeostasis

1975 ◽  
Vol 2 (1) ◽  
pp. 45-60 ◽  
Author(s):  
Lee L. Bernardis
Keyword(s):  
Growth Hormone ◽  
Electrical Stimulation ◽  
Food Intake ◽  
Present Report ◽  
Hypothalamic Nucleus ◽  
Control Mechanisms ◽  
Storage Site ◽  
Dorsomedial Hypothalamic Nucleus ◽  
Cervical Stimulation ◽  
Stimulation Of

SUMMARY:Median eminence and ventromedial hypothalamus have in the past been the principal foci of research in neuroendocrine and neurovisceral control mechanisms. The present report provides an overview of work involving the dorsomedial hypothalamic nucleus (DMN). This structure is located dorsal to the ventromedial hypothalamic nucleus (VMN) and extends anteroposteriorly from the plane of the largest cross section of the VMN to the plane of the dorsal premammillary nucleus. Fibers from the DMN pass with the periventricular system and the dorsal longitudinal fasciculus of Schütz and have been traced to the midbrain tegmentum and reticular formation. Intrahypothalamic connections involve intensive networks between DMN, lateral hypothalamic nucleus (LHN) and VMN. Regarding neurotransmitters, recent studies indicate that the DMN receives noradrenergic innervation along two pathways, a dorsal and a ventral one. Monoamine-containing systems approach the DMN from the lateral hypothalamus and the bulk of these fibers are carried in the medium forebrain bundle from their cells of origin in the brain stem. Studies of the vascular supply indicate that both VMN and DMN receive their blood supply from the internal carotid artery. It has been recently demonstrated that the DMN is involved in the control of food intake and possibly water intake as well. Discrete lesions in the DMN have caused hypophagia and hypodipsia, and implantation of epinephrine and norepinephrine in this area has initiated eating. Many years ago, electrical stimulation of this area was reported to cause eating. Although DMN lesions cause hypodipsia, they do not result in the reduced water/food intake ratios that are so characteristic of the VMN syndrome. DMN lesions are also followed by reduced spontaneous activity (running wheel), but this reduced activity is not accompanied by increased weight gain and accretion of adipose tissue, the latter being consistently observed in the VMN rat. Rather, carcass fat remains normal in the DMN rat and carcass protein is either normal or slightly increased. Many of the aforementioned changes in weanling rats with DMN lesions, however, are not matched by similar alterations in the intermediary metabolism of carbohydrate and lipid. Possibly this is due to a “resetting” of a central autonomic control system that makes it possible for the DMN rat to adapt more efficiently to a reduced influx of substrate, i.e. the consistent hypophagia. From a review of the literature it appears that the DMN and their circuitry are involved in only a few neuroendocrine, i.e. hypothalamohypophyseal control mechanisms. Both lesion and cervical stimulation experiments suggest an involvement of the DMN in the control of LTH. Circumstantial evidence points to the DMN as a possible formation and/or storage site of growth hormone inhibiting factor (GIF). Although DMN rats show reduced ponderal and linear growth, they have been found to have normal or elevated plasma growth hormone (GH) levels. Both lesion and stimulation studies have yielded the impression that the DMN is not involved in thyroid, i.e., thyrotropin stimulating hormone releasing factor (TSHRF) control. Electrical stimulation of the DMN has been reported to result in a positive correlation between adrenal blood flow and adrenal corticoid release in hypophysectomized dogs. This has been interpreted as a coordinated response at the level of a “dorsomedial sympathetic vasodilator relay” rather than a “true” neuroendocrine effect via corticotropin releasing factor (CRF). Experiments that failed to demonstrate a relationship between the DMN and the tonic and cyclic control of luteinizing hormone releasing factor (LHRF) are discussed. The data reviewed indicate the existence in the dorsomedial hypothalamus of an area that exerts a profound influence on many aspects of neurovisceral and some neuroendocrine control systems.

Electrical stimulation of the posterior and ventromedial hypothalamic nuclei causes specific activation of shivering and nonshivering thermogenesis

1994 ◽  
Vol 72 (1) ◽  
pp. 89-96 ◽  
Author(s):  
J. A. Thornhill ◽  
I. Halvorson
Keyword(s):  
Adipose Tissue ◽  
Electrical Stimulation ◽  
Brown Adipose Tissue ◽  
Posterior Hypothalamus ◽  
Hypothalamic Nucleus ◽  
Ventromedial Hypothalamic Nucleus ◽  
Hypothalamic Nuclei ◽  
Brown Adipose ◽  
Brown Adipose Tissue Thermogenesis ◽  
Stimulation Of

Experiments were designed to determine in the same animal whether electrical stimulation of the posterior hypothalamus and ventromedial hypothalamic nucleus could specifically evoke shivering and nonshivering (brown adipose tissue) thermogenesis, respectively, in anesthetized, normothermic rats. Urethane-anesthetized, male Long–Evans rats, kept at 37 °C, had colonic (Tc), gastrocnemius muscle (Tm), intrascapular brown adipose tissue (TIBAT), and tail (Tt) temperatures measured via thermistor probes, and electromyogram activity (differential multiunit activity from bipolar recording electrodes within gastrocnemius muscle) recorded, before and after unilateral electrical stimulation (monophasic 0.5-ms pulses of 200 μA at 50 Hz for 30 s) of the posterior hypothalamus and ventromedial hypothalamic nucleus (via stereotaxically implanted concentric stimulating electrodes). Each rat showed shivering (increased electromyogram activity) following posterior hypothalamic stimulation, which caused an immediate rise in Tm values with no change in TIBAT or Tt values. Electrical stimulation of the ventromedial hypothalamic nucleus of the same animals elicited no shivering activity, but significant increases in TIBAT values occurred with no change in Tm or Tt values. Results confirm that stimulation of the posterior and ventromedial hypothalamic nuclei in rodents specifically activates shivering and nonshivering (brown adipose tissue) effector mechanisms, respectively, to raise core temperature.Key words: posterior hypothalamus, shivering thermogenesis, ventromedial hypothalamus, intrascapular brown adipose tissue thermogenesis.

Effects of hypothalamic stimulation on gluconeogenesis and glycolysis in rat liver

1975 ◽  
Vol 228 (6) ◽  
pp. 1787-1793 ◽  
Author(s):  
T Shimazu ◽  
S Ogasawara
Keyword(s):  
Rat Liver ◽  
Phosphoenolpyruvate Carboxykinase ◽  
Glycolytic Enzyme ◽  
Hypothalamic Stimulation ◽  
Hypothalamic Nucleus ◽  
Hormonal Responses ◽  
Ventromedial Hypothalamic Nucleus ◽  
Gluconeogenic Enzyme ◽  
Marked Suppression ◽  
Stimulation Of

Hypothalamic effects on gluconeogenesis and glycosis in rat liver were studied byelectrical stimulations of the ventromedial hypothalamic nucleus (LH) without disturbing the animal's behavior. Stimulation of VMH caused a increase in the activity of phosphoenolpyruvate carboxykinase (PEPCK), a key gluconeogenic enzyme, and marked suppression of pyruvate kinase (PK), a key glycolytic enzyme, of the liver. Stimulationof LH, on the other hand, resulted in a decrease in PEPCK activity but did not alterPK activity. The maximal responses of these enzymes to hypothalamic stimulations were obtained after intermittent stimulations for 4 h. Differential estimations of thetwo isozymes of liver PK (types L and M) were made using antibody against typeM PK. The level of type M enzyme was not altered significantly on stimulation of either VMH or LH. The content of type L enzyme greatly decreased on stimulation of VMH but was not affected by stimulation of LH. The reciprical influences of VMH and LH on hepatic carbohydrate metabolism and their relation to neural-hormonal responses are discussed.

Effects of hypothalamic stimulation and lesion on adrenal nerve activity

1987 ◽  
Vol 253 (3) ◽  
pp. R418-R424 ◽  
Author(s):  
H. Yoshimatsu ◽  
Y. Oomura ◽  
T. Katafuchi ◽  
A. Niijima
Keyword(s):  
Anterior Part ◽  
Sympathetic Nerves ◽  
Middle Part ◽  
Hypothalamic Nucleus ◽  
Moderate Increase ◽  
Sympathoadrenal System ◽  
Nerve Activity ◽  
Hypothalamic Area ◽  
Ventromedial Hypothalamic Nucleus ◽  
Stimulation Of

Activity changes of efferent adrenal sympathetic nerves in response to bilateral manipulations of the hypothalamus, partly after intra-third cerebroventricular injection of 2-deoxy-D-glucose (2-DG) were investigated in anesthetized rats. Stimulation of the middle part of the lateral hypothalamic area (LHAm) increased adrenal nerve activity, whereas lesion caused rapid and remarkable decrease. Stimulation of the anterior part of the LHA (LHAa) tended to decrease the activity, and lesion produced either rapid decrease or late moderate increase. Stimulation of the ventromedial hypothalamic nucleus (VMH) did not affect the nerve activity, but lesion increased it gradually and then remarkably. Cerebroventricular infusion of 2-DG caused remarkable increase in activity that was suppressed by LHAm lesion. Subsequent infusion of 2-DG during the period of suppressed activity was no longer effective. The increased firing rate after 2-DG was suppressed by stimulation of the VMH, whereas lesion caused no change. These findings indicate that the central regulation of adrenal nerve activity is connected with individual hypothalamic regions and consequently depends on the degree and mode of activation of the sympathoadrenal system.

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