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Rapid Action (rapid + action)

Distribution by Scientific Domains

Medical Sciences	55%
Life Sciences	33%

Selected Abstracts

Rapid Action of Oestrogen in Luteinising Hormone-Releasing Hormone Neurones: The Role of GPR30

JOURNAL OF NEUROENDOCRINOLOGY, Issue 4 2009
E. Terasawa
Previously, we have shown that 17,-oestradiol (E2) induces an increase in firing activity and modifies the pattern of intracellular calcium ([Ca2+]i) oscillations with a latency < 1 min in primate luteinising hormone-releasing hormone (LHRH) neurones. A recent study also indicates that E2, the nuclear membrane impermeable oestrogen, oestrogen-dendrimer conjugate, and the plasma membrane impermeable oestrogen, E2 -BSA conjugate, all similarly stimulated LHRH release within 10 min of exposure in primate LHRH neurones, indicating that the rapid action of E2 is caused by membrane signalling. The results from a series of studies further suggest that the rapid action of E2 in primate LHRH neurones appears to be mediated by GPR30. Although the oestrogen receptor antagonist, ICI 182, 780, neither blocked the E2 -induced LHRH release nor the E2 -induced changes in [Ca2+]i oscillations, E2 application to cells treated with pertussis toxin failed to result in these changes in primate LHRH neurones. Moreover, knockdown of GPR30 in primate LHRH neurones by transfection with human small interference RNA for GPR30 completely abrogated the E2 -induced changes in [Ca2+]i oscillations, whereas transfection with control siRNA did not. Finally, the GPR30 agonist, G1, resulted in changes in [Ca2+]i oscillations similar to those observed with E2. In this review, we discuss the possible role of G-protein coupled receptors in the rapid action of oestrogen in neuronal cells. [source]

Rapid actions of oestrogen on gonadotropin-releasing hormone neurons; from fantasy to physiology?

THE JOURNAL OF PHYSIOLOGY, Issue 21 2009
Allan E. Herbison
Oestradiol (E2) exerts critical homeostatic feedback effects upon gonadotropin-releasing hormone (GnRH) neurons to maintain fertility. In the female, E2 has both negative and positive feedback actions to suppress and stimulate GnRH neuron activity at different times of the ovarian cycle. This review summarizes reported rapid E2 effects on native embryonic and adult GnRH neurons and attempts to put them into a physiological perspective. Oestrogen has been shown to rapidly modulate multiple processes in embryonic and adult GnRH neurons including intracellular calcium levels, electrical activity and specific second messenger pathways, as well as GnRH secretion itself. Evaluation of in vivo data suggests that there is no essential role for rapid E2 actions in the positive feedback mechanism but that they may comprise part of the negative feedback pathway. Adult GnRH neurons are only likely to be exposed to E2 from the gonads via the circulation with appropriate physiological E2 concentrations in the rodent being 10,50 pm for negative feedback ranging up to 400 pm for positive feedback. Although most studies to date have examined the effects of supraphysiological E2 levels on GnRH neurons, there is accumulating evidence that rapid E2 actions may have a physiological role in suppressing GnRH neuron activity. [source]

The role of peripheral Na+ channels in triggering the central excitatory effects of intravenous cocaine

EUROPEAN JOURNAL OF NEUROSCIENCE, Issue 4 2006
P. Leon Brown
Abstract While alterations in dopamine (DA) uptake appear to be a critical mechanism underlying locomotor and reinforcing effects of cocaine (COC), many centrally mediated physiological and affective effects of this drug are resistant to DA receptor blockade and are expressed more quickly following an intravenous (i.v.) injection than expected based on the dynamics of drug concentration in the brain. Because COC is also a potent local anesthetic, its rapid action on Na+ channels may be responsible for triggering these effects. We monitored temperatures in the nucleus accumbens, temporal muscle and skin together with conventional locomotion during a single i.v. injection of COC (1 mg/kg), procaine (PRO, 5 mg/kg; equipotential anesthetic dose), a short-acting local anesthetic drug that, like COC, interacts with Na+ channels, and cocaine methiodide (COC-MET, 1.31 mg/kg, equimolar dose), a quaternary COC derivative that is unable to cross the blood,brain barrier. In this way, we explored not only the importance of Na+ channels in general, but also the importance of central vs. peripheral Na+ channels specifically. COC induced locomotor activation, temperature increase in the brain and muscle, and a biphasic temperature fluctuation in skin. Though PRO did not induce locomotor activation, it mimicked, to a greater degree, the temperature effects of COC. Therefore, Na+ channels appear to be a key substrate for COC-induced temperature fluctuations in the brain and periphery. Similar to PRO, COC-MET had minimal effects on locomotion, but mimicked COC in its ability to increase brain and muscle temperature, and induce transient skin hypothermia. It appears therefore that COC's interaction with peripherally located Na+ channels triggers its central excitatory effects manifested by brain temperature increase, thereby playing a major role in drug sensing and possibly contributing to COC reinforcement. [source]

Tetrathiomolybdate anticopper therapy for Wilson's disease inhibits angiogenesis, fibrosis and inflammation

JOURNAL OF CELLULAR AND MOLECULAR MEDICINE, Issue 1 2003
G. J. Brewer
Abstract The need for agents to lower body copper in Wilson's disease, a disease which results from copper toxicity has been the driving force for the development of the effective anticopper drugs penicillamine, trientine, zinc, and now tetrathiomolybdate (TM). Because of its rapid action, potency, and safety, TM is proving to be a very effective drug for initial treatment of acutely ill Wilson's disease patients. Beyond this, TM has antiangiogenic effects, because many proangiogenic cytokines require normal levels of copper. This has led to use of TM in cancer, where it is generally effective in animal tumor models, and has shown efficacy in preliminary clinical studies. Most recently, it has been found that TM has antifibrotic and antiinflammatory effects through inhibition of profibrotic and proinflammatory cytokines. [source]

Rapid Action of Oestrogen in Luteinising Hormone-Releasing Hormone Neurones: The Role of GPR30

Paraquat and sustainable agriculture

PEST MANAGEMENT SCIENCE (FORMERLY: PESTICIDE SCIENCE), Issue 4 2004
Richard H Bromilow
Abstract Sustainable agriculture is essential for man's survival, especially given our rapidly increasing population. Expansion of agriculture into remaining areas of natural vegetation is undesirable, as this would reduce biodiversity on the planet. Maintaining or indeed improving crop yields on existing farmed land, whether on a smallholder scale or on larger farms, is thus necessary. One of the limiting factors is often weed control; biological control of weeds is generally of limited use and mechanical control is either often difficult with machinery or very laborious by hand. Thus the use of herbicides has become very important. Minimum cultivation can also be important, as it reduces the power required to work the soil, limits erosion and helps to maintain the organic matter content of the soil. This last aspect helps preserve both the structure of soil and its populations of organisms, and also sustains the Earth's soil as a massive sink for carbon, an important consideration in the light of global warming. The introduction of the bipyridinium herbicide paraquat in the early 1960s greatly facilitated weed control in many crops. Paraquat has the unusual property of being active only by direct spray onto plants and not by uptake from soil in which strong binding deactivates it. Together with its rapid action in light in killing green plant tissue, such properties allow paraquat to be used in many crops, including those grown by low-tillage methods. This paper reviews the ways in which agricultural systems have been and are being developed to make use of these properties, and provides a risk/benefit analysis of the world-wide use of paraquat over nearly 40 years. Copyright © 2004 Society of Chemical Industry [source]

Expanding view of aldosterone action, with an emphasis on rapid action

CLINICAL AND EXPERIMENTAL PHARMACOLOGY AND PHYSIOLOGY, Issue 4 2010
Gavin P. Vinson
Summary 1. The actions of aldosterone beyond the ,mineralocorticoid' designation continue to attract intense interest. In recent years, two aspects have received particular attention. These are, first, the potentially damaging direct actions of aldosterone on the heart and vascular system, and the clear benefit, as illustrated by the Randomized Aldactone Evaluation Study and Eplerenone Post-Acute Myocardial Infarction Heart Failure Efficacy and Survival trials, of including antialdosterone therapy in the treatment of cardiovascular disease. 2. Second, the importance of non-genomic actions of aldosterone has become clear, some of which might possibly be mediated by distinct membrane receptors. Over the past 5 years, evidence has arisen to bring these two aspects together, and now emphasizes the role of rapid, nongenomic actions of aldosterone on cardiovascular events. 3. However, despite many years of study, there is still no clear view of the nature of the receptors mediating non-genomic responses. We examine the evidence, and suggest that in many cases non-genomic actions are attributable to classical mineralocorticoid receptors. [source]

A Short History Of Nitroglycerine And Nitric Oxide In Pharmacology And Physiology

CLINICAL AND EXPERIMENTAL PHARMACOLOGY AND PHYSIOLOGY, Issue 4 2000
Neville Marsh
SUMMARY 1. Nitroglycerine (NG) was discovered in 1847 by Ascanio Sobrero in Turin, following work with Theophile-Jules Pelouze. Sobrero first noted the ,violent headache' produced by minute quantities of NG on the tongue. 2. Constantin Hering, in 1849, tested NG in healthy volunteers, observing that headache was caused with ,such precision'. Hering pursued NG (,glonoine') as a homeopathic remedy for headache, believing that its use fell within the doctrine of ,like cures like'. 3. Alfred Nobel joined Pelouze in 1851 and recognized the potential of NG. He began manufacturing NG in Sweden, overcoming handling problems with his patent detonator. Nobel suffered acutely from angina and was later to refuse NG as a treatment. 4. During the mid-19th century, scientists in Britain took an interest in the newly discovered amyl nitrite, recognized as a powerful vasodilator. Lauder Brunton, the father of modern pharmacology, used the compound to relieve angina in 1867, noting the pharmacological resistance to repeated doses. 5. William Murrell first used NG for angina in 1876, although NG entered the British Pharmacopoeia as a remedy for hypertension. William Martindale, the pharmaceutical chemist, prepared ,. . . a more stable and portable preparation': 1/100th of a grain in chocolate. 6. In the early 20th century, scientists worked on in vitro actions of nitrate-containing compounds although little progress was made towards understanding the cellular mode of action. 7. The NG industry flourished from 1900, exposing workers to high levels of organic nitrites; the phenomena of nitrate tolerance was recognized by the onset of ,Monday disease' and of nitrate-withdrawal/overcompensation by ,Sunday Heart Attacks'. 8. Ferid Murad discovered the release of nitric oxide (NO) from NG and its action on vascular smooth muscle (in 1977). Robert Furchgott and John Zawadski recognized the importance of the endothelium in acetylcholine-induced vasorelaxation (in 1980) and Louis Ignarro and Salvador Moncada identified endothelial-derived relaxing factor (EDRF) as NO (in 1987). 9. Glycerol trinitrate remains the treatment of choice for relieving angina; other organic esters and inorganic nitrates are also used, but the rapid action of NG and its established efficacy make it the mainstay of angina pectoris relief. [source]

Extra-nuclear signaling of estrogen receptors

IUBMB LIFE, Issue 8 2008
Xiao-Dong Fu
Abstract Estrogen controls multiple biological functions through binding to estrogen receptors (ERs). Traditionally, ERs have been regarded as transcription factors regulating the expression of target genes. However, growing evidence of rapid estrogen's actions in a number of tissues has been accumulating and alternative mechanisms of signal transduction have been proposed. These so called "extra-nuclear actions" do not require gene expression or protein synthesis and are independent of the nuclear localization of ERs. Indeed, some of these actions are elicited by ERs residing at or near the plasma membrane. Membrane-associated molecules such as ion channels, G proteins, the tyrosine kinase c-Src as well as growth factor receptors are modulated by liganded ERs within the membrane, leading to the activation of downstream cascades such as mitogen-activated protein kinase, phosphatidylinositol 3-OH kinase, protein kinase A, and protein kinase C. These cascades mediate some important rapid actions of estrogen, such as the activation of nitric oxide synthesis or the remodeling of actin cytoskeleton. In addition, these pathways are critical for the regulation of the expression of a number of target proteins implicated in cell proliferation, apoptosis, differentiation, movement, and homeostasis. In this manner, the extra-nuclear pathways are tightly integrated with the genomic pathways to orchestrate the full spectrum of estrogen's biological functions. The recent advancements in the characterization of the molecular basis of the extra-nuclear signaling of estrogen helps to understand the role of estrogen on human cells, and may in future turn out to be of relevance for clinical purposes. © 2008 IUBMB IUBMB Life, 60(8): 502,510, 2008 [source]