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NON-NEURONAL EXCITATORY NEUROTENSIN RECEPTORS ON THE TAENIA-COLI OF THE GUINEA-PIG - LACK OF INFLUENCE OF TETRODOTOXIN AND DYNORPHIN
No full textPicomoles of neurotensin caused contractions of the smooth muscles of the taenia coli and the myenteric plexus preparation of the guinea pig ileum. The musculotropic effect of neurotensin on the taenia coli was resistant to tetrodotoxin and to treatment with dynorphin. In contrast, the contractile activity of the neuropeptide in the ileum was substantially modified by pretreatment with tetrodotoxin or dynorphin. While neurotensin causes a direct muscular response on the taenia coli via activation of selective peptide receptor probably located on the muscle membrane, the neuropeptide causes a predominant indirect action on the ileum mediated apparently via the release of acetylcholine from the nerve terminals of the myenteric plexus. Neurotensin may play a role in the control of gut peristaltis either by modifying the release of neurotransmitters or by directly influencing of smooth muscles of the intestines
Going Beyond Counting First Authors in Author Co-citation Analysis
Get PDFThe present study examines one of the fundamental aspects of author co-citation analysis (ACA) - the way co-citation
counts are defined. Co-citation counting provides the data on which all subsequent statistical analyses and mappings
are based, and we compare ACA results based on two different types of co-citation counting - the traditional type that
only counts the first one among a cited work's authors on the one hand and a non-traditional type that takes into
account the first 5 authors of a cited work on the other hand. Results indicate that the picture produced through this non-traditional author co-citation counting contains more coherent author groups and is therefore considerably clearer. However, this picture represents fewer specialties in the research field being studied than that produced through the traditional first-author co-citation counting when the same number of top-ranked authors is selected and analyzed. Reasons for these effects are discussed
Variations on the Author
Get PDF“Variations on the Author” discusses two of Eduardo Coutinho’s recent films (Um Dia na Vida, from 2010, and Últimas Conversas, posthumously released in 2015) and their contribution to the general question of documentary authorship. The director’s filmography is characterized by a consistent yet self-effacing form of authorial self-inscription: Coutinho often features as an interviewer that rather than express opinions propels discourses; an interviewer that is good at listening. This mode of self-inscription characterizes him as an author who is not expressive but who is nonetheless markedly present on the screen. In Um Dia na Vida, however, Coutinho is completely absent form the image, while Últimas Conversas, on the contrary, includes a confessional prologue that moves the director from the margins to the center of his films. This article examines the ways in which these works stand out in the filmography of a director who offers new insights into the notion of cinematic authorship
Appropriate Similarity Measures for Author Cocitation Analysis
Get PDFWe provide a number of new insights into the methodological discussion about author cocitation analysis. We first argue that the use of the Pearson correlation for measuring the similarity between authors’ cocitation profiles is not very satisfactory. We then discuss what kind of similarity measures may be used as an alternative to the Pearson correlation. We consider three similarity measures in particular. One is the well-known cosine. The other two similarity measures have not been used before in the bibliometric literature. Finally, we show by means of an example that our findings have a high practical relevance.information science;Pearson correlation;cosine;similarity measure;author cocitation analysis
PURINERGIC SUPERSENSITIVITY FOLLOWING SYMPATHECTOMY ADDS FURTHER SUPPORT TO CO-TRANSMISSION IN THE RAT VAS-DEFERENS
No full textAdrenergic and purinergic compounds contract the longitudinal muscles of the rat vas deferens. Whereas ATP and related purinergic analogs produced contractions of greater magnitude in the prostatic half as compared to that of the epididymal end, the magnitude of the .alpha.1-adrenoceptor-induced responses was larger in the epididymal than in the prostatic half of the rat ductus. Chemical sympathectomy following a 48 hr 6-hydroxydopamine-treatment (6-OHDA) caused a leftward displacement of the concentration-response curves for adrenergic and purinergic drugs, this effect being more evident in the prostatic segment. Sympathectomy caused a significant increase in the maximal response induced by ATP and adrenergic compounds which was more evident in the prostatic half of the rat ductus. The denervation-induced supersensitivity was stimulus-specific since angiotensin II and acetylcholine showed no significant change in potency. In the case of bradykinin, there ws a manifest increase in the maximal response of the prostatic segment of the ductus of the chemically denervated tisses. In addition, denervation also caused an increase in the potency of prazosin and phentolamine as .alpha.1-adrenoceptor blocking agents; denervation did not change the potency of yohimbine as an .alpha.2-adrenoceptor blocker
KAPPA-OPIATES AND URINATION - PHARMACOLOGICAL EVIDENCE FOR AN ENDOGENOUS ROLE OF THE KAPPA-OPIATE RECEPTOR IN FLUID AND ELECTROLYTE BALANCE
No full textCENTRAL EFFECTS OF MORPHINE, LEVORPHANOL, ( - )-METHADONE AND THE OPIOID-LIKE PEPTIDES BETA-ENDORPHIN AND D-ALANINE2-METHIONINE ENKEPHALINAMIDE ON URINE VOLUME OUTFLOW AND ELECTROLYTES
No full textThe intraventricular injection of 10-30 nmol of morphine, (-)-methadone or levorphanol caused a reduction in the volume of the urine output in rats previously hydrated with 0.5% NaCl. The decrease in urine outflow was associated with a dose-dependent reduction in the concentration of urine Na+ and K+. Two opioid-like peptides: .beta.-endorphin and D-alanine2 methionine enkephalinamide shared this morphine action. On a molar basis, .beta.-endorphin was about 100 times more potent than morphine to cause an equivalent antidiuresis. Naloxone injected i.p. antagonized the response of centrally administered morphine or .beta.-endorphin on urine formation and composition. (+)-Methadone or dextrorphan injected into the cerebral ventricles were considerably less active than their corresponding stereoisomers. N-methyl morphine injected i.p. was completely inactive up to doses that caused signs of toxicity; when injected into the lateral cerebral ventricles, it produced a decrease in the urine outflow and a reduction in the concentration of urine electrolytes. The pattern of changes in urine electrolytes produced by morphine and surrogates as well as the opioid-like peptides was in marked contrast to that caused by the i.p. administration of vasopressin. Whereas the i.p. administration of antidiuretic hormone caused oliguria and a large increase in the urine concentration of Na+ and K+, all the opiates produced at comparable antidiuresis a marked reduction in urine electrolytes. The opiates and the opioid-like peptides may selectively activate central opiate receptors to produce changes in urine formation and composition. Results are discussed in relation to probable central opiate mechanisms controlling the production and formation of urine
EXCITATORY NEUROTENSIN RECEPTORS ON THE SMOOTH-MUSCLE OF THE RAT FUNDUS - POSSIBLE IMPLICATIONS IN GASTRIC-MOTILITY
No full textPicomolar concentrations of neurotensin caused concentration-dependent contractions of the longitudinal musculature of the fundus of the rat stomach. The EC50 [concentration giving 50% effectiveness] of neurotensin was .apprx. 1.5 nM. On a molar basis neurotensin was about 5-10 times more potent than 5-hydroxytryptamine (5-HT) and .apprx. 80 times as active as acetylcholine in producing similar contractions. Studies with structurally related peptides indicated that whereas the carboxy terminal portion of neurotensin was essential for biological activity, a substantial part of its amino terminus end could be removed without affecting its potency. The EC50 for the neurotensin fragment 8-13 was identical to that of neurotensin, its 1-8 or 1-11 fragments were completely inactive. Tetrodotoxin did not modify the potency of neurotensin or structurally related analogs suggesting that the neurotensin receptor is probably located on the smooth muscle membrane. In addition, the potency of neurotensin in contracting the fundus was not modified by pretreatment with atropine, methysergide or diphenhydramine. Fade to the contractile response of neurotensin was followed by the development of tachyphylaxis; densensitization was concentration-dependent and characterized by a shift in the agonist concentration-response curve to the right and downwards. Desensitization with a priming concentration of neurotensin (.apprx. EC50) caused a substantial blockade of its excitability. There was cross-densensitization between neurotensin and the contractile activity of neurotensin 8-13 or xenopsin, but not with angiotensin II, bradykinin, substance P, acethylcholine, 5-HT or histamine. Pretreatment of the fundus strip with verapamil 0.3-1 .mu.M antagonized in a concentration-dependent fashion the neurotensin-induced contractions but not the muscular contractions caused by acetylcholine. Neurotensin activates a specific excitatory receptor probably located on the cell membrane of the smooth muscles of the rat fundus. This receptor is somehow related to a voltage-dependent Ca channel, sensitive to verapamil
INVOLVEMENT OF POSTJUNCTIONAL PURINERGIC MECHANISMS IN THE FACILITATORY ACTION OF BRADYKININ IN NEUROTRANSMISSION IN THE RAT VAS-DEFERENS
No full textTo investigate the nature of the bradykinin-induced potentiation of electrically driven muscle twitches in the isolated vas deferens, bradykinin, noradrenaline and adenosine 5''-triphosphate (ATP) concentration-response curves were made with control, reserpinized and chemically sympathectomized rats. Bradykinin potentiated the ATP- but not the noradrenaline-induced contractions in the epididymal and prostatic segments of the ductus. The epididymal segment of the ductus did not respond to transmural electrical stimulation following reserpine treatment. Bradykinin potentiated the muscular contractions caused by exogenous ATP but not by noradrenaline. In contrast, the transmurally evoked twitches of the prostatic portion of the ductus remained almost unaltered; bradykinin increased the motor effect of ATP without modifying the potency of noradrenaline. All neuronally induced contractile activity was absent in sympathetomized rats; bradykinin potentiated the contractile effect of ATP without altering the noradrenaline-induced contractions. These results suggest that bradykinin potentiates the ATP-evoked contractions by acting postjunctionally
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