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The Dorsomedial Hypothalamic Nucleus In Autonomic And Neuroendocrine Homeostasis
- Lee L. Bernardis
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- Journal:
- Canadian Journal of Neurological Sciences / Volume 2 / Issue 1 / February 1975
- Published online by Cambridge University Press:
- 18 September 2015, pp. 45-60
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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.
Localization of Neuroendocrine Functions Within the Hypothalamus
- Lee L. Bernardis
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- Journal:
- Canadian Journal of Neurological Sciences / Volume 1 / Issue 1 / February 1974
- Published online by Cambridge University Press:
- 18 September 2015, pp. 29-39
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The results of lesion, stimulation, deafferentation, implantatión and transplantation studies employed in the identification of hypophysiotrophic control areas in the hypothalamus to date suggest the following probable locations: corticotropic releasing factor (CRF) is formed in a diffuse area along the base of the median eminence, if not the base of the entire hypothalamus. Follicle stimulating hormone releasing factor (FSHRF) is elaborated in the paraventricular-suprachiasmatic areas but its cyclic control may reside in the anterior hypothalamic area. Luteinizing hormone (LH) is controlled by luteinizing hormone releasing factor (LHRF) formed in the suprachiasmatic area: its cyclic control may be in the preoptic area. Prolactin is controlled by prolactin inhibiting factor (PIF) localized in a diffuse area comprising the ventromedial, dorsomedial, arcuate and paraventricular nuclei. The hypothalamic area involved in thyroid control is also rather large, since thyrotropin stimulating hormone releasing factor (TSHRF) has been found in an area including the supraoptic and chiasmatic nuclei. Growth hormone releasing factor (GHRF) is elaborated in a rather narrow zone, the ventromedial hypothalamic nuclei.
CMB Analysis of Boomerang & Maxima & the Cosmic Parameters {Ωtot,Ωbh2, Ωcdmh2, ΩΛ, ns}
- J. Richard Bond, P. A. R. Ade, A. Balbi, J. J. Bock, J. Borrill, A. Boscaleri, K. Coble, B. P. Crill, P. de Bernardis, P. Farese, P. G. Ferreira, K. Ganga, M. Giacometti, S. Hanany, E. Hivon, V. V. Hristov, A. Iacoangeli, A. H. Jaffe, A. E. Lange, A. T. Lee, L. Martinis, S. Masi, P. D. Mauskopf, A. Melchiorri, T. Montroy, C. B. Netterfield, S. Oh, E. Pascale, F. Piacentini, D. Pogosyan, S. Prunet, B. Rabii, S. Rao, P. L. Richards, G. Romeo, J. E. Ruhl, F. Scaramuzzi, D. Sforna, K. Sigurdson, G. F. Smoot, R. Stompor, C. D. Winant, J. H. P. Wu
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- Journal:
- Symposium - International Astronomical Union / Volume 201 / 2005
- Published online by Cambridge University Press:
- 26 May 2016, pp. 347-357
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- 2005
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We show how estimates of parameters characterizing inflation-based theories of structure formation localized over the past year when large scale structure (LSS) information from galaxy and cluster surveys was combined with the rapidly developing cosmic microwave background (CMB) data, especially from the recent Boomerang and Maxima balloon experiments. All current CMB data plus a relatively weak prior probability on the Hubble constant, age and LSS points to little mean curvature (Ωtot = 1.08±0.06) and nearly scale invariant initial fluctuations (ns = 1.03±0.08), both predictions of (non-baroque) inflation theory. We emphasize the role that degeneracy among parameters in the Lpk = 212 ± 7 position of the (first acoustic) peak plays in defining the Ωtot range upon marginalization over other variables. Though the CDM density is in the expected range (Ωcdmh2 = 0.17 ± 0.02), the baryon density Ωbh2 = 0.030 ± 0.005 is somewhat above the independent 0.019 ± 0.002 nucleosynthesis estimates. CMB+LSS gives independent evidence for dark energy (ΩΛ = 0.66 ± 0.06) at the same level as from supernova (SN1) observations, with a phenomenological quintessence equation of state limited by SN1+CMB+LSS to wQ < −0.7 cf. the wQ=−1 cosmological constant case.