scholarly journals A quantification of classic but unquantified positive feedback effects in the urban-building-energy-climate system

2022 ◽  
Vol 307 ◽  
pp. 118227
Author(s):  
Yukihiro Kikegawa ◽  
Kazusa Nakajima ◽  
Yuya Takane ◽  
Yukitaka Ohashi ◽  
Tomohiko Ihara
1971 ◽  
Vol 51 (1) ◽  
pp. 31-39 ◽  
Author(s):  
R. E. PETER

SUMMARY The effect on thyroid activity of a systemically ineffective dose of thyroxine (T4) implanted in the hypothalamus or pituitary of goldfish was tested. Thyroid activity was decreased by T4 implantation in either location, indicating that T4 has a negative feedback effect on the pituitary causing a decrease in thyrotrophin secretion, and a positive feedback effect on the hypothalamus stimulating the secretion of thyrotrophin inhibitory factor (TIF). Fish with a T4 or blank-control implant in the pituitary that had a damaged pituitary stalk, as a result of the operative procedures, were hyperthyroid, suggesting either that TIF is more effective in suppressing thyrotroph activity than T4 and that the effect of T4 was masked by the absence of TIF, or, less likely, that T4 negative feedback in the pituitary is not effective independent of TIF. The results were compared with the information about T4 feedback in mammals.


1984 ◽  
Author(s):  
◽  
Benjamin Adler

These studies tested the interrelated hypotheses that the ovarian hormones produce their positive feedback effects on luteinizing hormone (LH) secretion through activation of noradrenergic and adrenergic systems in specific hypothalamic regions. Furthermore, the ovarian hormones may alter the activity of opioid neuropeptide and Gamma-Aminobutyric Acid (GABA) systems to produce these alterations in catecholamine transmission and gonadotropin secretion. Radioimmunoassays were utilized to determine plasma LH and median eminence LHRH, and hypothalamic catecholamine concentrations were measured by radioenzymatic assay. The first two studies tested whether epinephrine (EPI) synthesis inhibition blocks the accumulation of median eminence LHRH that precedes the ovarian hormone-induced LH surge and also to test whether the stimulatory ovarian hormone regimen enhances the activity of hypothalamic EPI systems. Ovariectomized rats were primed with estradiol (EB), followed 2 days later by progesterone (Prog.). Animals were treated before Prog, administration with saline, one of the EPI synthesis inhibitors SKF 64139 or LY 78335, or the norepinephrine (NE) synthesis inhibitor, FLA-63. The catecholamine synthesis inhibitors blocked or delayed the LH surge. FLA-63 completely prevented the accumulation of LHRH in the median eminence that preceded the rise in LH release. However, selective reduction in EPI levels with SKF 64139 only partially prevented this increase in LHRH. A second EPI synthesis inhibitor, LY 78335, delayed both the LH surge and the rise in LHRH. In a second experiment, the administration of EB plus Prog, to ovariectomized rats increased the alpha-methyltyrosine (aMT) induced depletion of EPI in the medial basal hypothalamus (MBH). The depletion of NE after synthesis inhibition was enhanced in both the MBH and preoptic-anterior hypothalamus (POA). Experiments 3 and 4 examined a possible mechanism underlying these ovarian hormone effects on LH release and catecholamine activity. These studies tested whether the opiate antagonist, naloxone, which increases LH release, enhances the activity of NE and EPI neurons in the hypothalamus, and also tested whether morphine, an opiate agonist which decreases LH release, depresses the activity of hypothalamic NE and EPI activity. Administration of naloxone to EB-primed rats increased LH release and potentiated the depletion of NE in the POA and MBH, and enhanced the decline of EPI and dopamine (DA) in the MBH, suggesting increased catecholamine activity in these regions. Administration of the opiate agonist, morphine, to rats pretreated with EB and Prog., decreased LH and decreased the depletion of the catecholamines in the POA and MBH, suggesting reduced activity. In most cases, naloxone antagonized the inhibitory effect of morphine. Experiments 3, 6, and 7 examined the involvement of (GABA) systems in the positive feedback effects of EB and Prog, on LHRH and LH release. These studies tested 1) the effects of GABAergic drugs on the LH surge induced by EB and Prog., 2) whether GABA agonists reduce NE and EPI activity in the hypothalamus, and 3) whether a GABA agonist prevents the accumulation of median eminence LHRH induced by EB and Prog. Ovariectomized rats received the stimulatory EB plus Prog, treatment. Simultaneously with Prog., rats received either saline, the barbiturate, phenobarbital, the GABAg agonist, baclofen, the GABA^ agonist, muscimol, or either the GABA^ antagonist, bicuculline, or the putative GABAg antagonist, 5-aminovalerate. Additional experiments tested the effects of the GABA drugs on LH release in ovariectomized, hormonally untreated rats and in response to exogenous LHRH. The LH surge induced by EB+Prog. was blocked by treatment with either baclofen, muscimol, or phenobarbital. Bicuculline was ineffective in preventing the effect of baclofen and phonobarbital but partially prevented the effect of muscimol. Neither baclofen nor muscimol significantly affected LH release in hormonally untreated, ovariectomized rats or in rats receiving LHRH administration. In the results of Experiment 6, in EB plus Prog.-treated rats, baclofen and muscimol significantly reduced the concentrations of EPI and NE in the POA and MBH and prevented their decline after administration of otMT, suggesting decreased catecholamine transmission. In Experiment 7, rats were primed with the ovarian hormones and received, concurrently with Prog., either saline, or baclofen. The GABAg agonist, baclofen, blocked the LH surge and selectively increased LHRH concentrations. Experiment 8 tested 1) whether baclofen reverses the enhancement of LH release and catecholamine activity produced by naloxone, and 2) whether the opiate antagonist, nalmefene, prevents the blockade of the LH surge produced by baclofen. In the first study of Experiment 8, naloxone increased LH release and enhanced catecholamine activity in EB-primed rats. Baclofen was unable to reverse these effects. In the second study, baclofen administration to EB plus P treated rats blocked the LH surge and concomitant administration of nalmefene was unable to prevent this effect of baclofen. These results suggest that: 1) the ovarian hormones activate both NE and EPI systems to stimulate the early afternoon rise of LHRH in the median eminence and to induce the subsequent LH surge, 2) the ovarian hormones may produce their positive feedback effects on LH secretion by removing an inhibitory GABA or opioid neuropeptide influence on catecholamine transmission, allowing NE and EPI to stimulate LHRH, and subsequently, LH release, and 3) these modulatory actions of GABA and opiates may represent effects of two parallel, yet independent hypothalamic systems which regulate catecholamine neurotransmission and subsequently LH secretion.


2017 ◽  
Vol 114 (52) ◽  
pp. 13804-13809 ◽  
Author(s):  
Brian P. Kenealy ◽  
Kim L. Keen ◽  
James P. Garcia ◽  
Lucille K. Kohlenberg ◽  
Ei Terasawa

Negative and positive feedback effects of ovarian 17β-estradiol (E2) regulating release of gonadotropin releasing hormone (GnRH) and luteinizing hormone (LH) are pivotal events in female reproductive function. While ovarian feedback on hypothalamo–pituitary function is a well-established concept, the present study shows that neuroestradiol, locally synthesized in the hypothalamus, is a part of estrogen’s positive feedback loop. In experiment 1, E2 benzoate-induced LH surges in ovariectomized female monkeys were severely attenuated by systemic administration of the aromatase inhibitor, letrozole. Aromatase is the enzyme responsible for synthesis of E2 from androgens. In experiment 2, using microdialysis, GnRH and kisspeptin surges induced by E2 benzoate were similarly attenuated by infusion of letrozole into the median eminence of the hypothalamus. Therefore, neuroestradiol is an integral part of the hypothalamic engagement in response to elevated circulating E2. Collectively, we will need to modify the concept of estrogen’s positive feedback mechanism.


2009 ◽  
Vol 39 (9) ◽  
pp. 2052-2076 ◽  
Author(s):  
Yafang Zhong ◽  
Zhengyu Liu

Abstract Previous analyses of the Community Climate System Model, version 3 (CCSM3) standard integration have revealed pronounced multidecadal variability in the Pacific climate system. The purpose of the present work is to investigate physical mechanism underlying this Pacific multidecadal variability (PMV). To better isolate the mechanism that selects the long multidecadal time scale for the PMV, a few specifically designed sensitivity experiments are carried out. When the propagating Rossby waves are blocked in the subtropics from the midbasin, the PMV remains outstanding. In contrast, when the Rossby waves are blocked beyond the subtropics across the entire North Pacific, the PMV is virtually suppressed. It suggests that the PMV relies on propagating Rossby waves in the subpolar Pacific, whereas those in the subtropics are not critical. A novel mechanism of PMV is advanced based on a more comprehensive analysis, which is characterized by a crucial role of the subpolar North Pacific Ocean. The multidecadal ocean temperature and salinity anomalies may originate from the subsurface of the subpolar North Pacific because of the wave adjustment to the preceding basin-scale wind curl forcing. The anomalies then ascend to the surface and are amplified through local temperature–salinity convective feedback. Along the southward Oyashio, these anomalies travel to the Kuroshio Extension (KOE) region and are further intensified through a similar convective feedback. The oceanic temperature anomaly in the KOE is able to feed back to the large-scale atmospheric circulation, inducing a wind curl anomaly over the subpolar North Pacific, which in turn generates anomalous oceanic circulation and causes temperature and salinity variability in the subpolar subsurface. Thereby, a closed loop of PMV is established in the form of an extratropical delayed oscillator. The phase transition of PMV is driven by the delayed negative feedback that resides in the wave adjustment of the subpolar North Pacific via propagating Rossby waves, whereas the convective positive feedback provides the growth mechanism. A significant role of salinity variability is unveiled in both the delayed negative feedback and convective positive feedback.


1986 ◽  
Vol 116 ◽  
pp. 397-398
Author(s):  
G. Bodifee

As a consequence of positive feedback effects in interstellar chemical and star forming processes, a star formation region may undergo nonlinear oscillations.


1986 ◽  
Vol 111 (4) ◽  
pp. 467-473 ◽  
Author(s):  
P. A. Bowton ◽  
K. R. Bryant ◽  
S. A. Whitehead

Abstract. The effects of streptozotocin (STZ)-induced diabetes mellitus on the positive feedback action of steroids on luteinizing hormone (LH) secretion have been investigated in the oestrogen-primed ovariectomized rat. Rats treated with 40 mg/kg STZ 2 weeks before experimentation showed an attenuated LH surge in response to progesterone, an effect only partially restored by insulin replacement. When the same dose of the drug was injected just 24 h before the progesterone treatment it had no effect on the LH surge, while a high dose of 80 mg/kg STZ completely abolished the positive feedback action of the steroid. Insulin treatment did not reverse this effect. In parallel the effects of 2-week and 24-h diabetes on pituitary LH-releasing hormone (LRH) receptors were studied. Pituitary binding of a long acting LRH analogue was reduced in the 2-week diabetic animals, although a more dramatic reduction was observed in the rats treated with the high dose of STZ 24 h before testing. The results suggest that diabetes impairs the positive feedback effects of gonadal steroids resulting in a reduced release of LRH. However, the impairment is unlikely to be caused simply by hyperglycaemia but by non-specific toxic side effects of STZ and/or other metabolic changes associated with diabetes.


2011 ◽  
Vol 212 (3) ◽  
pp. 353-361 ◽  
Author(s):  
Christine Margaret Whitelaw ◽  
Jane Elizabeth Robinson ◽  
Peter Mark Hastie ◽  
Vasantha Padmanabhan ◽  
Neil Price Evans

The neurotransmitter galanin has been implicated in the steroidogenic regulation of reproduction based on work mainly conducted in rodents. This study investigated the temporal changes in the expression of galanin and its three receptor isoforms andGNRHandGNRHRmRNA in specific hypothalamic nuclei known to be involved in the regulation of reproductive cyclicity, namely the medial pre-optic area (mPOA), the rostral mPOA/organum vasculosum of the lamina terminalis, the paraventricular nucleus and the arcuate nucleus using an ovine model. Following synchronisation of their oestrous cycles, tissues were collected from ewes at five time points: the early follicular, mid follicular (MF) and late follicular phases and the early luteal and mid luteal phases. The results indicated significant differences in regional expression of most of the genes studied, with galanin mRNA expression being highest during the MF phase at the start of the GNRH/LH surge and the expression of the three galanin receptor (GalR) isoforms and GNRH and its receptor highest during the luteal phase. These findings are consistent with a role for galanin in the positive feedback effects of oestradiol (E2) on GNRH secretion and a role for progesterone induced changes in the pattern of expression of GalRs in the regulation of the timing of E2's positive feedback through increased sensitivity of galanin-sensitive systems to secreted galanin.


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