Current Topics in Neuroendocrinology - Böcker
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There is no doubt that a major problem of present day research workers, especially in the life sciences, is the plethora of publications of all kinds, abstracts, short communications, full papers in journals of varying quality, reviews and proceedings of symposia with, in addition, an unprecedented duplication of publications. Even for experts working in the field, it is almost impossible to keep an up-to-date view of all current research articles. The Western grant and career system encourages scientists to publish as much as possible. The editors and publishers of our new series are convinced that the format of Current Topics in Neuroendocrinology leads a way out of this confusion. Each volume is conceived as a concise up-to-date textbook on one well-defined and currently exciting subject. Different from classic textbooks, however, the speed of publication compares favorably with that of many journals; this ensures an immediacy which is im possible in textbooks. On the other hand, topics to be included in this series are also sufficiently reliable, with enough work being done to treat them from several aspects. Each volume will supply four to six chapfers treating such a broad topic as neuroendocrinology from several points of view, for example, anatomic, electrophysiologic, endocrine and behavioral views. Wh~re clinical data are immediately available, they will be included. No other 36Iles treating the nervous or endocrine systems provides such a coordinated set of chapters on an interesting topic in each volume.
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The most prominent function of the central nervous system is the control of motor functions by rapidly transmitted impulses through efferent cranial and spinal peripheral nerves. Besides electrically transmitted neural impulses, humoral mechanisms with more sustained actions are exercised by the brain and spinal cord to regulate body homeostasis. Thus, the brain may be regarded as an "endocrine gland" discharging neurohormones (peptides) either into the general circulation (neurohypophyseal hormones) or into the hypothalamo-adenohypophyseal portal circulation (releasing and inhibiting hormones). The brain, therefore, which is protected by the blood-brain barrier from disturbing and potentially noxious exogenous and endogenous agents circulating in the blood, has to have certain neurohemal regions beyond this barrier, such as the neural lobe and the median eminence (infundibulum), where neurohor mones have free access to the blood stream. To regulate somatic and autonomic functions in the best possible way, the central nervous system is highly dependent on feedback signals conveyed through somatic and visceral afferent nerves as well as on peripheral humoral signals such as peripheral hormones and other circulating substances that are under homeostatic regulation, e. g. , peptides, arnines, electrolytes, and other biologically active agents. In this chapter, the role of the blood-brain barrier in the regulation of these sub stances will be discussed with special emphasis on the access through the blood-brain barrier to cardiovascular centers. 2 The Blood-Brain Barrier 2.
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With contributions by Clarke, G.; Lang, R.E.; McKinley, M.J.; Merrick, L.P.; Rascher, W.; Richter, D.; Sofroniew, M.; Unger, T.; Weindl, A.
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It is well established that progesterone plays a role in the brain and hypophysis as a facilitator and inhibitor of sexual behavior and gonadotropin release in the female rat (Everett 1961; Caligaris et al. 1971; Brown-Grant and Naftolin 1972; Dorner 1972; Meyerson 1972; Barraclough 1973; Goldman and Zarrow 1973; Mann and Barraclough 1973; Freeman et al. 1976; Feder and Marrone 1977; Goodman 1978; Attardi 1981), guinea pig (Morin and Feder 1974), and primates (Odell and Swerdloff 1968; Spies and Niswender 1972; Yamaji et al. 1972; Karsch et al. 1973; Dierschke et al. 1973; Knobi11974; Clifton et al. 1975). In an attempt to learn whether a specific progesterone uptake mechanism exists in the brain and the hypophysis, the distribution and retention pattern of radioactivity after in vivo injection of labeled progesterone was studied. Early work of Kato (1963) did not show a selective uptake of radioactivity in the hypo- thalamus of immature and estrogen-primed immature rats after injection oflow- specific-activity [14C]progesterone, but some tendency of the reticular formation to take up radiation was observed.Laumas and Farooq (1966) reported that after intravenous administration of labeled progesterone to ovariectomized estrogen- treated rats, radioactivity in the brain and pituitary appeared to show a very slight, insignificant increase 1-2 min after injection, but the uptake pattern was not definite, as had been seen with estradiol. Seiki et al.
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0 Behavioral Reaction Effect of Effect of Species Route of Dose of Reference - 0 oxytocin vasopressin treatment oxytocin (mol/animal) p r-' 11 Extinction of active avoidance Facilitation Opposite Rat i. p. 2x 10- SCHULZ et al. (1974, 1976); ~ (bench-jumping) reaction TELEGDY and KovAcs (1979a) 0 12 10- < Extinction of active avoidance Facilitation Opposite Rat i. c. v. BOHUS et aI. (1978b) "', 0 (pole-jumping) reaction '" 10 2 x 10- Extinction of active avoidance Delay Similar Rat s. c. WALTER et aI. (1978); (pole-jumping) behavior BoHUS et al. (1978b) 12 10- Acquisition of active avoidance Delay No effect Rat i. c. v. BoHUS et al. (1978b) (pole-jumping) behavior 11 2x 10- Acquisition of active avoidance No effect No effect Rat i. p. SCHULZ et al. (1974) (bench-jumping) behavior 10 Passive avoidance (step-down) Attenuation Opposite Rat i. p. 2x 10- KovAcs et al. (1978) behavior 13 10- Passive avoidance (step-through) Attenuation Opposite Rat i. c. v. BoHUS et al. (1978a, b); behavior KovAcs and DE WmD (1983) 14 2. 5 x 10- Passive avoidance (step-through) Attenuation Opposite Rat Hippocampus, KovAcs et al.(1979) behavior dorsal raphe 14 Passive avoidance (step-through) Facilitation Similar Rat Septum 2. 5 x 10- KovAcs et al. (1979) behavior 8 10- Passive avoidance (choice No effect No effect Rat ? SAGHAL and WRIGHT (1984) measure) 7 Attenuation of puromycin- 10- No effect Effective Mouse s. c WALTER et al.
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With contributions by numerous experts
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The tridecapeptide neurotensin (NT) was first identified in bovine hypothalamic extracts and characterized by Carraway and Leeman (1973,1975,1976) and has subsequently been found in all classes of vertebrates (Carraway and Leeman 1976; Kitabgi et al. 1976; Kataoka et al. 1979; Langer et al. 1979; Reinecke et al. 1980a; Cooper et al. 1981; Grant et al. 1982; Carraway et al. 1982; Eldred and Karten 1983), many invertebrates (Reinecke et al. 1980 b; Grimmelikhuijzen et al. 1981; Price et al. 1982), and certain bacteria (Bhatnagar and Carraway 1981). It is distributed throughout the mammalian central nervous system (CNS) (Uhl and Snyder 1977 a, b), gastrointestinal tract (Sundler et al. 1977; Schultzberg et al. 1980), cerebrospinal fluid (CSF), adrenals, pancreas, and plasma (Fernstrom et al. 1980). When administered systemically, the peptide has a variety of effects such as hypotension, hyperglycemia, decreased gastric acid secretion, decreased gut motility, and altered secretion of anterior pituitary hormones (Leeman and Carraway 1982).NT apparently does not cross the blood-brain barrier in appre- ciable quantities; however, when administered directly into the CNS, it produces a number of physiological and behavioral effects. A burgeoning body of evidence supports the role of NT as a neurotransmitter or neuromodulator. Thus far, het- erogeneous CNS distribution, release of NT upon neuronal depolarization, satu- rable and specific binding of NT to receptors, and degradation by peptidases have all been demonstrated.
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The role of electrical signalling in the control of endocrine secretions by the brain has been clear for many years. Recently, the influences of hormones on synthetic events in neuroendocrine cells have raised new questions concerning the peptides released from such neurons. This volume concentrates on the relation between these two fields and asks how electrical action potentials facilitate secretion of substances from nerve cells which control endocrine events. While stimulus-secretion coupling has been studied extensively in other physiological contexts, this is the first treatment of the phenomenon in an exclusively neuroendocrine setting.
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Latest issue in the CURRENT TOPICS IN NEUROENDOCRINOLOGY se-ries which has been gaining a great deal of reputation as aprimary source for reviews in neuroendocrinology and relatedareas in the past few years.
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1.1 Mechanism of Action of Glucocorticoid Hormones The current model of glucocorticoid hormone action is summarized in Fig. 1. After synthesis, glucocorticoids are secreted into the blood stream and trans- ported to target cells where they bind with high affinity (K-1O-9M) and d specificity to the intracellular glucocorticoid receptor (GR) protein. The sub- cellular localization of hormone-free GR is still a controversial issue. However, most data support the idea that unliganded GR is in the cytoplasmic compartment or loosely associated with the nucleus (Picard and Yamamoto 1987; Gustafsson et al. 1987 and references therein; LaFond et al. 1988; Gasc et al. 1989). Upon ligand binding, GR is activated into a form capable of interacting with DNA. The mechanism of GR activation probably involves a conformational change and dis- sociation from nonreceptor components, e.g., the 90-kDA heat shock protein (hsp90: Pratt et al. 1988; Bresnick et al. 1989; Denis and Gustafsson 1989). The subcellular location of activated GR has been firmly established to be inside the nucleus. In vivo, the hormone-receptor complex interacts with specific DNA Activation r:::.. ~ qc [!3-GC ...&.GC~ j ~ ?, BIOLOGICAL EFFECTS " t , Active Protein , , ~Vl\lent.