Oxytocin and electrical stimulation of the paraventricular hypothalamic nucleus produce antinociceptive effects that are reversed by an oxytocin antagonist

Responses of hepatic afferent nerves to intraportal bolus injection of hypertonic solutions were examined in anesthetized rats. Hepatic afferent nerve activity increased in response to an intraportal injection of 0.75 M NaCl or NaHCO3 but did not respond to a similar injection of 1.5 M mannitol, 0.75 M LiCl, or 0.15 M NaCl, implying that nerves in the hepatoportal area are sensitive to increases in Na concentrations and that this leads to stimulation of hepatic afferent nerve activity. To study central activation in response to stimulation of the hepatic Na-sensitive mechanism, c-fos induction was monitored. After electrical stimulation of hepatic afferent nerves, neurons containing Fos-like immunoreactivity (Fos-li) were found in the area postrema, nucleus of the solitary tract, paraventricular hypothalamic nucleus, and supraoptic nucleus at 90 min after stimulation. Induction of Fos-li was also studied after simultaneous infusion of 0.45 M NaCl into the portal vein and distilled water into the inferior vena cava in conscious rats so as to keep the total amount of solution introduced into the systemic circulation isotonic, thus avoiding changes in mean arterial pressure, plasma osmolality, and plasma NaCl concentrations. Fos-li-containing neurons were found in the same regions in which they were found after electrical stimulation. However, few, if any, Fos-li-containing cells were found if the rats were hepatically denervated or if they received an intraportal infusion of hypertonic LiCl or mannitol. These data provide evidence for involvement of the brain stem and forebrain structures in NaCl regulatory functions induced by stimulation of the hepatoportal Na-sensitive mechanism. However, stimulation of the hepatoportal osmosensitive mechanism does not activate these central structures.

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The Dorsomedial Hypothalamic Nucleus In Autonomic And Neuroendocrine Homeostasis

Canadian Journal of Neurological Sciences / Journal Canadien des Sciences Neurologiques ◽

10.1017/s0317167100019971 ◽

1975 ◽

Vol 2 (1) ◽

pp. 45-60 ◽

Cited By ~ 44

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.

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

Canadian Journal of Physiology and Pharmacology ◽

10.1139/y94-014 ◽

1994 ◽

Vol 72 (1) ◽

pp. 89-96 ◽

Cited By ~ 29

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.

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