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1
Smith, Nigel. "Plasma protein binding of noradrenaline." Thesis, University of Nottingham, 1990. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.252951.
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Scriven, Anthony James Ivor. "Plasma noradrenaline and cardiovascular sympathetic activity." Thesis, Imperial College London, 1990. http://hdl.handle.net/10044/1/46541.
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Haywood, S. A. "GnRH network : noradrenaline and sex steroids." Thesis, University of Cambridge, 2000. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.603906.
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The first studies in this thesis use <I>in situ</I> hybridisation to investigate if temporal changes occur in cellular GnRH gene expression during the preovulatory phase of the oestrous cycle and further investigation gene expression in other neurotransmitter systems in the GnRH network within the preoptic area and the brainstem. It is evident from these studies that, during the oestrous cycle, transcriptional changes within GnRH, enkphalin, nitric oxide synthase and noradrenaline containing neural populations, in the preoptic area and brainstem respectively, are small, and are perhaps not pertinent to the imminent LH surge. Nevertheless, it is already established that sex steroid dependent changes in GnRH secretion are associated with an increased in noradrenergic activity. The second study, using immunocytochemical techniques, focuses on this relationship and demonstrates, for the first time, the presence of progesterone receptors (PR) in up to 35% of noradrenaline cells in caudal regions of the nucleus tractus solitarii (A2 cell group). Moreover, this study shows that dynamic fluctuations in sex steroid receptors occur during the oestrous cycle, with the highest percentage of A2 neurones expressing PR and oestrogen receptor (ERα) on proestrous morning with a nadir on dioestrous afternoon. Further studies in steroid-primed female rats provide evidence that this is predominantly an oestrogen-inducing effect on PR expression. Finally, using retrograde tracing techniques combined with dual-labelling immunocytochemistry I show that approximately 5-12% of A cells in the brainstem project to the vicinity of the GnRH perikarya located in the rostral preoptic area (rPOA) and that the majority of these projecting A2 neurones express PR.
4
Field, Brent A. "The effects of noradrenaline on cortical signal processing /." view abstract or download file of text, 2000. http://wwwlib.umi.com/cr/uoregon/fullcit?p9978587.
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Thesis (Ph. D.)--University of Oregon, 2000.<br>Typescript. Includes vita and abstract. Includes bibliographical references (leaves 140-159). Also available for download via the World Wide Web; free to University of Oregon users.
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Kelly, Christopher Brendan. "Noradrenergic function in anxiety and depressive states." Thesis, Queen's University Belfast, 1994. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.261770.
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Roberts, Veronica J. "Corticosterone modulation of noradrenaline stimulated cyclic AMP formation in hippocampus." Thesis, University of Ottawa (Canada), 1985. http://hdl.handle.net/10393/4949.
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Brice, Carolyn F. "Caffeine : consumption, behavioural effects and the role of central noradrenaline." Thesis, University of Bristol, 2000. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.302061.
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Popovik, Elvira. "The role of noradrenaline in the development of rat neocortex." Thesis, University of Bristol, 2003. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.289632.
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DONG, WEN-XIN. "Metabolisme pre-synaptique peripherique de la noradrenaline chez le rat." Paris 6, 1997. http://www.theses.fr/1997PA066067.
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Nous avons etudie le metabolisme pre-synaptique de la noradrenaline (na) chez l'animal entier ; cette voie metabolique etant la voie la plus importante pour la na synaptique. Un dosage radio-enzymatique, approprie pour mesurer les concentrations plasmatiques des derives desamines de la na (3,4-dihydroxyphenyl glycol : dhpg et 3,4-dihydroxymandelique acide : doma) a ete developpe et valide au plan physiologique. Une reduction de l'activite sympathique par la clonidine ou la guanethidine provoque une baisse de la na mais aussi du dhpg ; la reponse du doma est moins claire. Dans une deuxieme etape, nous avons evalue le modele du rat anesthesie, demyele et stimule a 2. 5 hz. Nous avons mesure une baisse du trop-plein synaptique de la na chez le rat demyele, avec retour a la normale quand le rat est stimule. Une correlation a ete calculee entre la concentration plasmatique de la na et celle du dhpg et entre la na et la pression arterielle moyenne suggerant un equilibre synaptique physiologique. Nous avons active la recapture neuronale de la na en perfusant de la na exogene. Le dhpg plasmatique augmente en parallele avec celle de la na ; le doma augmente aussi, mais l'amplitude est moins eleve que celui du dhpg. Quand le metabolisme pre-synaptique est bloque partiellement par la desipramine, le niveau plasmatique du dhpg s'en trouve reduit, mais pas celui du doma. L'inhibition de la monoamine oxydase par la clorgyline (mao-a) ou le deprenyl (mao-b) induit une baisse significative du dhpg (-85%:clorgyline;-74%:deprenyl) et du doma (-30%:clorgyline;-24%:deprenyl). Une inhibition conjointe des mao-a et b conduit a une disparition presque totale du dhpg, mais n'augmente pas la baisse du doma. Globalement, nos resultats demontrent la possibilite d'explorer le metabolisme pre-synaptique de la na chez l'animal entier, le niveau du dhpg pouvant etre un assez bon marqueur de cette voie metabolique.
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MAIGNAN, EMMANUELLE. "Systeme sympathique : la cinetique de la noradrenaline chez le rat." Paris 6, 2001. http://www.theses.fr/2001PA066331.
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L'objectif de ce travail a ete d'etudier la physiologie du systeme sympathique chez le rat par la technique de la dilution isotopique (di). Nous avons mesure la cinetique de la noradrenaline (na), definie par son trop plein synaptique (tps) et sa clairance metabolique (cm). Nous montrons que l'anesthesie provoque des alterations majeures et heterogenes de la cinetique de la na. Nous avons d'abord retenu que l'etat experimental qui s'imposait etait le rat conscient, non restreint. Dans ce contexte, son tps est environ 10 fois plus eleve que celui de l'homme, suggerant une activite sympathique beaucoup plus elevee. On peut y associer une sensibilite membranaire presynaptique egalement differente entre ces deux especes. La liberation de la na, mesuree par son tps, peut etre amplifiee par un mecanisme encore mal defini, mais resume par l'expression hypothese adrenaline. Nos resultats montrent bien que l'adrenaline (ad) stimule les recepteurs beta 2-adrenergiques presynaptiques conduisant a une augmentation du tps. Cependant, chez le rat, les niveaux circulants d'ad doivent etre 100 fois superieurs a ceux necessaires chez l'homme pour obtenir le meme effet. Cette liberation peut etre encore plus amplifiee par un niveau d'ad, en lui-meme inefficace, lorsque l'inhibition de la liberation de la na, est partiellement bloquee par la yohimbine. Une stimulation du tps peut etre aussi induite par le formoterol, un beta 2-agoniste de synthese. Notre travail a aussi ete consacre a l'etude de la cm de la na. Nous avons constate qu'une variation experimentale de la na plasmatique ne modifie pas le niveau de la cm de la na tant que l'hemodynamique systemique n'est pas alteree. On peut se demander si les mecanismes, autres que la recapture neuronale, ont vraiment une efficacite dans l'elimination d'un exces de na. Quand la pression arterielle augmente, la cm diminue, demontrant le role predominant de l'hemodynamique dans l'homeostase de la na. Par ailleurs, nous avons etudie la cinetique de la na dans des situations suggerant une hyper- (rats shr) ou une hypoactivite (hypervolemie centrale) sympathique et aussi dans des conditions physiologiques plus particulieres : le rat age ou le rat presentant une surrenalectomie bilaterale. Globalement, nos resultats demontrent l'interet majeur d'explorer l'activite sympathique chez le rat conscient par la technique de di.
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Kennett, Alexandra. "Nicotinic acetylcholine receptor modulation of noradrenaline release in the rodent brain." Thesis, University of Bath, 2011. https://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.557794.
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Cognitive function in the brain is controlled by neurotransmitters whose release is tightly controlled. When normal levels are perturbed deficits in function can be observed both in humans and in animal models. The cholinergic system, acting via muscarinic or nicotinic receptors, modulates neurotransmitter release. The aim of this thesis was to investigate the identity of the nicotinic acetylcholine receptor (nAChR) subtypes involved in modulating noradrenaline (NA) release, in rodent frontal cortex (FC) and hippocampus (HC). Comparisons were made both in vitro and in vivo using pharmacological tools. In vitro, acute application of nicotinic agonists evoked release of previously loaded [3H]-NA from prisms of rat FC and HC. There was a 2000-fold more potent response to β2* selective nAChR agonist 5-iodo-A85380 in FC than HC. A greater response to choline in HC than FC, combined with a lack of response to selective α7 ligands supports α3β4* nAChRs as the main mediator of nicotinic stimulated NA release in vitro in HC. A proportion of the release in each region was mediated via a potentially excitatory action of GABA. The profile of responses was unchanged after the acute or chronic administration of nicotine in vivo. In vivo microdialysis experiments were designed to test whether the nAChR subtype differences in vitro were representative of differences in vivo. 5-iodo-A85380 administered by reverse dialysis increased NA levels to a greater extent in FC than HC, supporting differences in the nAChR composition involved in NA regulation between these two regions. Targeted stimulation of these different nAChR subtypes could allow exploitation of this disparity to improve function with novel compounds such as those described in Chapter 2. Overall the studies described in this thesis show that there are differences in the subtype of nAChRs involved in NA release from terminal fields of FC and HC both in vitro and in vivo.
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Abebe, Worku. "Noradrenaline-induced vascular contractility and phosphoinositide metabolism in streptozotocin-diabetic rats." Thesis, University of British Columbia, 1990. http://hdl.handle.net/2429/30549.
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Alterations in the reactivity of blood vessels to neurotransmitters and circulating hormones have been suggested to cause, or contribute to, some of the cardiovascular complications associated with diabetes mellitus. Previous studies have demonstrated that aortae and mesenteric arteries from male rats with streptozotocin (STZ)-induced diabetes of 12 weeks duration are more responsive to the contractile effects of noradrenaline (NA). The increased responsiveness of the diabetic arteries to NA has been reported to result from stimulation of α₁-adrenoceptors. Contraction of vascular smooth muscle induced by NA via α₁-adrenoceptors has been shown to be associated with enhanced metabolism of phosphoinositides. The purpose of the present study was to investigate whether the enhanced contractile responses of aortae and mesenteric arteries from diabetic rats to NA are associated with alterations in phosphoinositide metabolism. Therefore, we compared changes in contractility and phosphoinositide metabolism in response to NA in aortae and mesenteric arteries from male rats with STZ-induced diabetes of 12-14 weeks duration and their age-matched controls. To further investigate the specificity and mechanisms of alterations in these responses, experiments were also conducted using portal veins, and selective α₁-adrenoceptor agonists, potassium chloride and a direct activator of protein kinase C (PKC).
Maximum contractile responses but not sensitivities of aortae and mesenteric arteries from diabetic rats to NA were significantly enhanced compared with responses of arteries from control rats. In contrast,
responses of portal veins from control and diabetic rats to NA were not different from each other. In addition, contractile response of diabetic arteries to KCl were not altered. Contractile responses of both aortae and mesenteric arteries in Ca²⁺-free medium to maximum concentrations of NA, PE and METH were significantly greater in preparations from diabetic than from control rats. Following readdition of Ca²⁺, responses of diabetic arteries to the α-adrenoceptor agonists were also significantly greater than controls. In the absence of extracellular Ca²⁺, contractions of diabetic aortae to a submaximum concentration of NA (10⁻⁶M) were also significantly increased compared with control, while the responses of diabetic mesenteric arteries to this concentration of NA were not significantly different from those of control preparations. Upon readdition of Ca²⁺, contractile responses of both arteries from diabetic rats were significantly greater than those from controls. These data indicate that the maximum contractile responses of diabetic aortae and mesenteric arteries to α₁-adrenoceptor stimulation are associated with increased release of intracellular Ca²⁺. However, α₁-adrenoceptor-mediated Ca²⁺ influx may also be enhanced in arteries from diabetic rats particularly in response to submaximum concentrations of NA.
A maximum concentration of NA (10⁻⁵M) induced a rapid, transient decrease in the level of [³²P]-phosphatidylinositol 4,5-bisphosphate ([³²P]-PtdIns(4,5)P₂), and a time-dependent increase in the formation of [³²P]-phosphatidic acid ([³²P]-PA) and [³H]-inositol phosphates in aortae from both control and diabetic rats. The increase in [³H]-inositol phosphate production was selectively blocked by prazosin. In
both types of aortic preparations, NA also induced a rapid, transient and concentration-related elevation of inositol 1,4,5-trisphosphate (Ins(l,4,5)P₃) content during contraction. The breakdown of [³²P]-PtdIns(4,5)P2, and formation of [³²P]-PA, [³H]-inositol phosphates and Ins(l,4,5)P₃ in response to the maximum concentration of NA were significantly greater in diabetic than in control aortae.
Stimulation of α₁-adrenoceptors by a maximum concentration of NA (3x10⁻⁵M) in mesenteric arteries resulted in a time-dependent increase in the formation of [³H]-inositol phosphates in both control and diabetic rats. NA also caused a rapid and concentration-dependent elevation of Ins(l,4,5)P₃ content in mesenteric arteries from both groups of animals. The increases in [³H]-inositol phosphates and Ins(l,4,5)P₃ levels in diabetic mesenteric arteries in response to the maximum concentration of NA were significantly higher than in control preparations. In contrast, Ins(l,4,5)P₃ production in mesenteric arteries in response to a submaximum concentration of NA (10⁻⁶M) was not significantly different between control and diabetic preparations.
NA also induced a time-dependent increase in the production of [³H]-inositol phosphates in both control and diabetic portal veins. The NA-induced formation of [³H]-inositol phosphates was not significantly different control and diabetic portal veins with a short period of exposure (0.5 min) to the agonist suggesting that the extent of occurrence of early biochemical events including the hydrolysis of PtdIns(4,5)P₂ in response to NA is similar in both types of portal veins.
The role of PKC in mediating enhanced contractile responses of aortae and mesenteric arteries from diabetic rats to NA was also investigated. The PKC inhibitor, staurosporine abolished the difference in the magnitude of contraction observed between control and diabetic arteries in response to NA. Maximum contractile responses of mesenteric arteries but not aortae or portal veins from diabetic rats to the PKC activator, PDB, were significantly enhanced compared with controls. The enhanced contractile responses of diabetic mesenteric arteries to PDB were abolished in the presence of staurosporine, in the presence of Ca²⁺-channel blockers, or in the absence of extracellular Ca²⁺.
These results indicate that phosphoinositide metabolism is enhanced in aortae and mesenteric arteries from STZ-induced diabetic rats in response to NA, via α₁-adrenoceptor stimulation. The enhancement may contribute to the increased contractile responsiveness of these vessels to NA. In addition, increased activation of PKC-mediated processes, which are dependent on the presence of extracellular Ca²⁺, may further contribute to the enhanced contractile responses of diabetic mesenteric arteries to NA. However, increased influx of extracellular Ca²⁺ by other mechanisms may also contribute to the enhanced contraction of diabetic arteries to submaximum concentrations of NA. Diabetes does not seem to induce such changes in portal veins.<br>Pharmaceutical Sciences, Faculty of<br>Graduate
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Wang, Yushan. "Release of glutamate, noradrenaline and adenosine from rat parietal cortical slices." Thesis, National Library of Canada = Bibliothèque nationale du Canada, 2000. http://www.collectionscanada.ca/obj/s4/f2/dsk1/tape4/PQDD_0009/NQ60669.pdf.
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McCance, Alastai J. "Systemic and cardiac noradrenaline kinetics in ischaemic heart disease in man." Thesis, University of Oxford, 1989. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.235891.
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Siyamak, Ahmed Y. "Studies of the effects of nutritional factors on noradrenaline-induced thermogenesis." Thesis, University of Nottingham, 1990. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.291275.
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Tse, Wai Shing. "The role of noradrenaline in different aspects of human social behaviour." Thesis, University of Birmingham, 2002. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.272325.
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Dunk, Christopher Robert. "The uptake of noradrenaline by human red blood cells and ghosts." Thesis, University of Leicester, 1989. http://hdl.handle.net/2381/34331.
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A study has been made of the transport of noradrenaline into human red cells and resealed ghosts. In cells uptake appeared to obey the kinetics of simple diffusion, whilst in metabolically inert ghosts, uptake was identified as a low affinity high capacity saturable transport mechanism. Uptake was markedly temperature sensitive but not dependent upon cellular metabolism, consistent mth facilitated diffusion rather than active transport of noradrenaline. Non-competitive inhibition of uptake was achieved by a variety of structurally related compounds when present at either the inner or outer membrane surface. The ionic requirements for noradrenaline transport by red cells and ghosts have been examined. VJhen external sodium was replaced isosmotically by N-methyl-D-glucamine the apparent affinity for uptake by ghosts was modestly inhibited. Replacement of external sodium by potassium was ineffective, suggesting a requirement for both sodium and/or potassium. Specific sodium transport inhibitors were without effect and it was shown that the mechanism has no requirement for calcium or magnesium. Replacement of external chloride by either nitrate or methylsulphate stimulated red cell noradrenaline accumulation, but was ineffective in ghosts. It is suggested that anion substitution may act secondarily on transport by affecting binding and/or catecholamine metabolism. Noradrenaline uptake was inversely proportional to external hydrogen ion concentration, suggesting that lipophilic substrate is favoured for transport. It is concluded that noradrenaline transport does not occur via the "uptake 1" or "uptake 2" pathways characterised in other tissues. It has been shown that the slowly metabolised noradrenaline analogue, guanethidine, is accumulated by red cells. Guanethidine transport is saturable, sodium and chloride independent, and inhibition studies reveal separate routes of entry for this compound and noradrenaline. Noradrenaline has no effect upon red cell cation transport. Therefore, abnormalities reported in clinical disorders, such as essential hypertension, are not attributable to increased plasma noradrenaline concentration.
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Singh, Lakhbir. "Modulation of a 5-hydroxytryptamine-related behaviour by noradrenaline and gaba." Thesis, Aston University, 1985. http://publications.aston.ac.uk/12471/.
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gov, Clearys@ninds nih, and Susannah Cleary. "From chromaffin cells to Phaeochromocytoma : insight into the sympathoadrenal cell lineage." Murdoch University, 2007. http://wwwlib.murdoch.edu.au/adt/browse/view/adt-MU20080526.105525.
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Chromaffin cells are a modified post-ganglionic sympathetic neuron, which synthesise and secrete catecholamines. The neoplastic transformation of chromaffin cells is demonstrated by the tumour phaeochromocytoma, a functional tumour that recapitulates the normal role of chromaffin cells by synthesising, storing and releasing excess catecholamines. Within this thesis we have explored several aspects of chromaffin cell and phaeochromocytoma tumour biology, including the specific expression of key sympathoadrenal markers such as the noradrenaline transporter (NAT), neuropeptide Y (NPY) and chromogranin A (CGA) in normal human and mouse chromaffin cells versus phaeochromocytomas of human and mouse origin.
Catecholamine-mediated signalling in chromaffin cells is terminated by the sequestration of extracellular catecholamines back into the cell via the noradrenaline transporter (NAT). Following observations that within the rat adrenal medulla, NAT is expressed in PNMT-positive chromaffin cells we explored whether this pattern of expression is also present in the human adrenal medulla. While we successfully established that NAT and PNMT are co localised, we also found that all human adrenal chromaffin cells are PNMT-positive. In the rat, NAT is also observed within the cytoplasm and has been suggested to be associated with secretory vesicles, thus using the secretory vesicle marker, CGA, we demonstrate that NAT is associated with secretory vesicles. However, in contrast to our findings within the normal chromaffin cells, in situ NAT expression in human phaeochromocytoma tumour samples was distorted, with observed changes including the level and type of staining observed, and disruptions to the strict NAT-CGA association observed in the normal adrenal.
Continuing our theme of NAT, we investigated if pre treating the phaeochromocytoma PC12 cell line with the chemotherapy drug cisplatin had an effect on the expression of NAT, to give an indication of the efficacy of this compound in the treatment of metastatic phaeochromocytoma with radiolabelled 131Iodometabenzylguanidine (131I-MIBG), a noradrenaline analogue which can be incorporated into phaeochromocytoma tumour cells though uptake through NAT. The premise of this study is derived from previous work in which neuroblastoma cells pre-treated with cisplatin were more responsive to (131I-MIBG) accumulation due to increased activity and expression of the transporter. Thus we treated PC12 cells for 24-hours in a range of cisplatin concentrations and measured the effect on NAT expression. However, unlike the findings in neuroblastoma cells, in our study, we did not observe an effect of cisplatin pretreatment on NAT activity or expression in PC12 cells.
Upto 30% of phaeochromocytoma arise as apart of a hereditary syndrome. The von Hippel-Lindau (VHL) syndrome, due to germline mutations to the VHL gene, and Multiple Endocrine Neoplasia type 2 (MEN 2), due to germline mutations to the RET gene represent two examples of hereditable endocrine disorders where phaeochromocytoma is a presenting feature. Notable differences in clinical presentation and tumour biology have been identified in phaeochromocytomas from patients with VHL and MEN 2. These differences prompted us to explore whether these observations extend to the chromaffin granule constituents, NPY and CGA.
Patients with MEN 2 disease have a greater incidence of hypertension than patients with VHL disease, MEN 2 are characterised by an adrenergic phenotype (produce predominantly-adrenaline), whereas VHL phaeochromocytomas are noradrenergic (produce predominantly-noradrenaline). Neuropeptide Y, which has powerful vasoactive properties capable of significantly elevating blood pressure, is stored and released with catecholamines and is thought to be associated with PNMT-positive chromaffin cells. Thus, we questioned whether the differences in the symptomatology between VHL and MEN 2 patients may be related to differences in NPY expression between the two groups, and whether any differences in NPY relate to adrenaline and/or PNMT content, or are linked to hereditary factors. Thus we compared tumour samples from four cohorts of patients: (i) adrenergic versus noradrenergic phenotype, (ii) hereditary versus no hereditary syndrome. Results demonstrated that although tumour NPY levels (mRNA and peptide) correlate with PNMT expression and/or adrenaline content, when NPY expression was compared between groups of patients (adrenergic vs noradrenergic; hereditary versus nonhereditary) difference in NPY levels were only significant between VHL and MEN 2 tumour and not between sporadic adrenergic and noradrenergic Immunohistochemistry also supported the above observations. Hence, we concluded that NPY expression in all groups of phaeochromocytoma examined in this study, this effect is not related to tumour biochemical phenotype but rather appears to be a specific unique trait of VHL phaeochromocytomas.
Continuing our theme of the possible differential expression of chromaffin granule constituents between VHL and MEN 2 patients, we also investigated CGA levels in plasma and tumour samples. Given, VHL tumours possess less chromaffin granules than MEN 2 tumours, and CGA has been implicated as a key director of secretory vesicle biogenesis we investigated whether CGA was differentially expressed between VHL and MEN 2 tumours. We found CGA expression was significantly greater in MEN 2 tumours (mRNA; 3-fold, and protein; 20-fold), with western blot confirming this trend. We also found that plasma CGA was greater in MEN 2 patients but not significantly, consequently, we explored the co-variables tumour size and tumour secretory activity (measured by plasma catecholamine concentrations), which influence plasma CGA and found that tumour size and plasma CGA are related but there was no influence of genotype on this relationship. In contrast, plasma CGA was significantly related to tumour secretory activity and the effect of genotype on this relationship narrowly missed significance, but when we expressed plasma CGA as a ratio of plasma catecholamines, plasma CGA was 2-fold greater in MEN 2 patients than VHL patients. Thus despite the tendency of phaeochromocytomas from VHL disease to readily and continuously release their catecholamine stores, plasma CGA levels still appeared to be higher in MEN 2 patients.
Finally, we examined whether the expression of NPY, Leu- enkephalin (Leu-Enk), NAT and the vesicular monoamine transporters type 1 and 2 (VMAT1 and VMAT2,), in normal mouse adrenal glands, and in histologically-confirmed adrenal phaeochromocytomas generated by injected nude mice with a phaeochromocytoma (MPC) cells line. The results of this study established that similar to the rat and human NAT expression is preferentially localised with PNMT within mouse chromaffin cells, while VMAT1 and NPY are found in both PNMT-negative and PNMT-positive cell populations, although expression of NPY was reduced in PNMT-negative cells. In contrast, both VMAT2 and Leu-Enk were found in PNMT-negative noradrenergic cells, and VMAT2 was present in all noradrenergic chromaffin cells while Leu-Enk was observed in a subpopulation of noradrenergic chromaffin cells. In contrast to the normal adrenal but similar to our findings in human phaeochromocytoma, the pattern of marker expression within adrenal phaeochromocytoma lesions of MPC-injected mice are severely disrupted related to both the level of expression of the respective markers, and association with PNMT within the tissue. Thus, the experimentally generated phaeochromocytoma mouse model provides a valuable tool in studying human phaeochromocytoma.
The data presented in this thesis further validate the heterogeneity observed in many aspects of phaeochromocytoma tumour biology, including the expression several chromaffin cell markers such as NAT, NPY and CGA. The altered expression of these markers may contribute to the clinical picture of these tumours, particularly relating to hereditary phaeochromocytoma from VHL and MEN 2 disease.
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Powers, Jennifer Lynn. "Cellular and enzymatic studies with novel adrenergic analogs and effectors." Diss., Georgia Institute of Technology, 1993. http://hdl.handle.net/1853/30262.
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Mctavish, Sarah F. B. "The use of tyrosine depletion to evaluate central catecholamine function in animals and man." Thesis, University of Oxford, 2001. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.365879.
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Phillips, Marc Antony. "An investigation of monoaminergic mechanisms in the regulation of pupil size and the acoustic startle reflex in man." Thesis, University of Nottingham, 2000. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.324546.
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Link, Jeanne Meyers. "Mixed-mode chromatographic separation and whole column radiation detection to improve sensitivity in radiometabolite analysis : application to (Carbon-11)-meta-hydroxyephedrine in plasma /." Thesis, Connect to this title online; UW restricted, 1998. http://hdl.handle.net/1773/8578.
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Bawa, Samiti. "Human platelets : studies on uptake and release of noradrenaline associated with serotonin." Thesis, King's College London (University of London), 2006. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.428700.
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Paeger, Lars [Verfasser], and Peter [Akademischer Betreuer] Kloppenburg. "The Role of Noradrenaline in Energy Homeostasis / Lars Paeger. Gutachter: Peter Kloppenburg." Köln : Universitäts- und Stadtbibliothek Köln, 2013. http://d-nb.info/1052993265/34.
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Sánchez, Soto Marta. "Noncanonical Neurotransmitter Activation of Catecholamine Receptors." Doctoral thesis, Universitat de Barcelona, 2017. http://hdl.handle.net/10803/400298.
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From the D2‐like receptors (D2,D3, D4), only D4 receptor (D4R) has been described as “promiscuous” since it can be activated both by dopamine (DA) and norepinephrine (NE) and function as a noradrenergic receptor in the brain. However, there is no evidence for the other D2‐like receptors. In addition, D4R has a large number of polymorphisms, one of the variants, D4.7, has been associated with several neuropsychiatric disorders. The first aim of this thesis was to study the possible activation of D2‐like recptors (including the three main D4 variants, D2 short, D2 long and D3) by radiolabeled ligand binding and BRET‐based functional assays. Our results indicate that first, NE binds and activates D2‐like receptors and second, there are no differences in the signaling of D4R variants. In addition, the potency of DA and NE depends not only on the receptor but also on the G protein subtype.
The catecholamine NE is implicated in important brain functions and it binds to three receptor families. The α2A receptor (α2AR) is expressed in many brain regions and is particularly enriched in the striatum together with α2C (α2CR). The low levels of NE in the striatum led us to question what is the role of α2R there and hypothesize whether DA could provide the endogenous neurotransmitter of α2R in the striatum. Therefore, the second aim of this thesis was to study the activation of α2AR and α2CR by DA and dopaminergic ligands through radiolabeled binding experiments, activation of different subtypes of G protein and adenylyl cyclase inhibition. Surprisingly, the potencies of α2AR and α2CR for DA are very similar or even higher than for some D2‐like receptors. Thus, we can hypothesize that the DA in the striatum should reach enough concentration to activate α2AR and α2CR. In addition, these receptors are also targets for compounds previously described as D2‐like agonists. Particularly striking is the ability of the D3R and D4R agonists, 7‐OH‐PIPAT and RO‐105824 to bind and activate with high affinity α2AR i α2CR. Similar to the previous part, the efficacy and potency of ligands depends on the receptor and the G protein subtype.
Finally, is its well accepted that G protein‐coupled receptors (GPCRs) form homo‐, heteromers and high order oligomers. Since we had shown that DA and NE bind and activate D2‐like receptors and α2R, we wanted to study the activation of G protein mediated by the complexes formed by D4R variants, D4.4R and D4.7R, and D2R or α2R. In order to do that we used CODA‐RET (complemented donor‐acceptor resonance energy transfer) a technique that allows the study of the function of a signaling complex formed by two defined GPCRs and a subunit of the heterotrimeric G protein. Our results indicate that, although they physically interact, D4.7R is not implicated in the G protein activation when is forming complexes with D2R or α2AR. Also, there are no differences in the potency or efficacy of the endogenous neurotransmitters DA and NE with D4.4R and D4.7R monomers or homodimers, but the association with D2R or 2AR discloses differences between the two D4R variants. Finally, we found important differences in the potency and efficacy dopaminergic ligands for the different receptor complexes that could be important for some neuropsychiatric diseases.<br>Dels receptors D2‐like de dopamina (D2, D3, D4) només el D4 (D4R) s’ha descrit com a “promiscu” ja que pot ser activat tant per dopamina (DA) com per noradrenalina (NE); en canvi, no hi ha evidències de que això sigui cert per la resta de receptors D2‐like. A més, el D4R és un receptor molt polimòrfic i una de les seves variants, la D4.7, s’ha associat a desordres psiquiàtrics. El primer objectiu va ser estudiar la possible activació dels receptors D2‐like (D2S, D2L, D3 i les tres variants més prevalents de D4) per NE mitjançant estudis d’unió de radiolligands i assajos funcionals de BRET. Els resultats mostren que primer, la NE s’uneix i activa els receptors D2‐like i segon, no hi ha diferències en la senyalització de les variants de D4R. El receptor α2A (α2AR) adrenèrgic s’expressa en moltes zones cerebrals i està particularment enriquit a l’estriat junt amb el receptor α2C (α2CR). Els baixos nivells de NE a l’estriat donen peu a la possibilitat de que la DA sigui el neurotransmissor endogen de α2AR i α2CR. Per tant, el segon objectiu de la tesi va ser estudiar l’activació de α2AR i α2CR per DA i lligands dopaminèrgics mitjançant estudis d’unió de radiolligands, activació de diferent proteïnes G i inhibició d’adenilat ciclasa. Sorprenentment les potències de α2AR i α2CR per la DA són molt similars o inclús més altes que per alguns receptors D2‐ like. Per tant és probable que els nivells de DA a l’estriat siguin suficients per activar α2R. A més, aquests receptors també són activats per compostos prèviament descrits com agonistes dels receptors D2‐like com ara el 7‐OH‐PIPAT (D3R) i el RO‐105824 (D4R). A més, tant l’eficàcia com la potència dels lligands depèn del receptor i del subtipus de proteïna G. Per últim, els GPCRs poden formar dímers, heteròmers o entitats superiors. A la tercera part vam voler comparar l’activació de proteïna G per DA i NE mitjançant complexes entre dues de les variants de D4R, D4.4R i D4.7R amb D2R i α2AR. Els resultats indiquen que hi ha diferències en l’activació dels diferents complexes que podria tenir importància en malalties com RLS i Parkinson. A més, donen suport a la teoria de que les diferències entre les variants de D4R es troben en la seva interacció amb altres receptors.
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Pedrini, Denise Leda. "Avaliação da adrenalina, noradrenalina e cortisol sob a formação do biofilme, produção de ácido e expressão de fatores de virulência pelo Streptococcus mutans." Universidade de Taubaté, 2012. http://www.bdtd.unitau.br/tedesimplificado/tde_busca/arquivo.php?codArquivo=568.
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Avaliar o efeito in vitro da adrenalina, noradrenalina e cortisol sobre a formação do biofilme, produção de ácido e expressão de fatores de virulência por S. mutans. Método: Para a formação do biofilme foi realizada uma monocultura de S. mutans (UA159) em discos de hidroxiapatita (HA) associados à adrenalina, noradrenalina e cortisol por cinco dias. Após esse período, foi realizada a contagem bacteriana (ufc/ml) para cada grupo experimental. A avaliação da queda do pH (produção de ácidos) foi realizada a cada 12 horas até o final do experimento (cinco dias). Para a avaliação da expressão de fatores de virulência, RNA total de biofilme maduro (cinco dias) foi extraído, e a análise da expressão de genes relacionados com a virulência do S. mutans (gtfB, gtfC, gtfD, brpA e ldh) foi realizada através de RT-qPCR. Resultados: As catecolaminas (adrenalina e noradrenalina) e também o cortisol aumentaram significativamente a formação de colônias de S. mutans em relação ao grupo controle. Uma queda no valor do pH foi observada nas 12 primeiras horas em todos os grupos. Após este período, os valores se mantiveram praticamente estáveis até o final do experimento (120h), não havendo diferença estatística entre o grupo controle e os grupos testes. Em relação ao efeito das catecolaminas/cortisol sobre a expressão de genes de virulência do S. mutans, não se observou diferença estatística significativa entre os diferentes grupos. Conclusões: Os achados do presente estudo demonstraram que a adrenalina, noradrenalina e cortisol aumentam a formação do biofilme (in vitro), sem alterar o pH (produção de ácidos) e expressão dos genes de virulência avaliados.<br>To evaluate the in vitro effect of adrenaline, noradrenaline and cortisol on biofilm formation, acid production and expression of virulence factors by S. mutans. Methods: Biofilm formation was performed by a monoculture of S. mutans (UA159) in discs of hydroxyapatite (HA) associated with adrenaline, noradrenaline and cortisol for five days. Further, bacterial count was performed (cfu / ml) for each experimental group. Evaluation of the reduction in pH (acid production) was conducted then every 12 hours until the end of treatment (five days). For evaluation of the virulence factors of mature biofilm, total RNA (five days) was extracted and the analysis of expression of genes related to the virulence of S. mutans (gtfB, gtfC, gtfD, brpA and ldh) was performed by RT-qPCR. Results: Catecholamines (adrenaline and noradrenaline) and cortisol tested in this study significantly increased the formation of colonies of S. mutans in the control group. In all groups (control, adrenaline, noradrenaline and cortisol) the highest reduction in pH was observed during the first 15 minutes, with no statistical difference between the control and test group. PH measurements were performed until the 5th day of the experiment at intervals of 12h. Continuous reduction was observed during the first 12 hours in all groups after this period, the values remained almost stable until the end of the experiment (120h). There was no statistical difference between the control and test groups. Regarding the effect of catecholamine / cortisol on the expression of virulence genes of the S. mutans, there was no statistically significant difference among the groups and the control group. Conclusions: The findings of this study demonstrated that adrenaline, norepinephrine and cortisol increase the formation of biofilm (in vitro), without changing the pH (initial and in biofilm) and expression of genes evaluated.
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Santos, Luiz Marcelo Oliveira. "Mecanismos adrenérgicos no núcleo retrotrapezóide no controle respiratório." Universidade de São Paulo, 2015. http://www.teses.usp.br/teses/disponiveis/42/42136/tde-24022016-153800/.
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O núcleo retrotrapezóide (RTN) é uma região bulbar envolvida na respiração. Estudos prévios mostraram a presença de varicosidades catecolaminérgicas na região do RTN. O objetivo deste estudo foi investigar a fonte de catecolaminas e os efeitos promovidos pela ativação dos receptores adrenérgicos no RTN. Uma densa projeção neuronal do grupamento A7 para o RTN foi revelada usando o traçador retrógrado Fluorogold. Foi registrada a atividade eletromiográfica do diafragma (DiaEMG) e do abdominal (AbdEMG) de ratos Wistar anestesiados. A injeção de noradrenalina promoveu uma inibição da DiaEMG, sem alterar a AbdEMG; este efeito foi atenuado pela injeção prévia de ioimbina e não foi afetado pela injeção de prazosina e propranolol no RTN. A injeção de fenilefrina no RTN aumentou a DiaEMG e gerou AbdEMG; estes efeitos foram bloqueados por injeções prévias de prazosina no RTN. Os resultados deste estudo suportam a ideia de que o RTN recebe projeções adrenérgicas da ponte que modula a atividade dos neurônios do RTN por meio da ativação dos receptores adrenérgicos α -1 e α- 2.<br>The retrotrapezoid nucleus (RTN) is a medulla region involved in breathing. Previous studies showed the presence of catecholaminergic varicosities in the RTN region. The aim of this study was to investigate the source of cathecolamines and the effects produced by the activation of adrenergic receptors in the RTN. A dense neuronal projection from A7 to RTN was revealed using retrograde tracer FluorGold. In anaesthetized male Wistar rats, diaphragm (DiaEMG) and abdominal (AbdEMG) muscle activities were recorded. Injection of noradrenaline produced an inhibition of DiaEMG, but did not change AbdEMG; These effects was attenuated by pre-injection of yohimbine and were not affect by injection of prazosin and propranolol into the RTN. Injection of phenilephrine into the RTN increased DiaEMG and was also able to generate AbdEMG; these responses were eliminated by pre-injections of into the RTN. These results support the idea that RTN has pontine adrenergic inputs that modulate RTN neurons activity through activation of α - 1 and - α -2 adrenergic receptors.
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Bergen, Hugo Theodore. "The role of norepinephrine in the neuroendocrine regulation of luteinizing hormone release in the rat." Thesis, University of British Columbia, 1988. http://hdl.handle.net/2429/28623.
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An excitatory role for norepinephrine (NE) in the regulation of luteinizing hormone (LH) release was first suggested when it was demonstrated that noradrenergic receptor antagonists were able to block ovulation. More recently it has been proposed that NE has both an excitatory role and an inhibitory role in the neuroendocrine regulation of LH release. The excitatory effects may be mediated by alpha-adrenergic receptors and the inhibitory effects may be mediated via beta-adrenergic receptors. These experiments were performed to better understand the role of NE, the receptor type through which NE exerts its effects, and the role of the two major NE pathways in the brain, on LH secretion in the rat. To further understand the role of NE in pulsatile LH release, NE or one of its agonists was infused into the third ventricle of ovariectomlzed rats pretreated with an adrenergic antagonist. In the second set of experiments ascending noradrenergic pathways were electrically stimulated to determine their effect on pulsatile LH release. These experiments demonstrated that the inhibitory effect of NE on pulsatile LH release is blocked when alpha-1- or alpha-2- receptors are blocked but not when beta-receptors are blocked. Electrical stimulation experiments in unprimed ovariectomlzed rats demonstrated that activation of the dorsal noradrenergic tract (DNT) but not the ventral noradrenergic tract (VNT) inhibited pulsatile LH release.
Another series of experiments were performed to determine the role NE in the regulation of LH release in the steroid-primed ovariectomlzed rat. These experiments demonstrated that activation of alpha- or beta-adrenergic receptors inhibited the LH surge when adrenergic agonists are infused during the rising phase of the surge. In a similar manner electrical stimulation of either the DNT or VNT inhibited LH release if stimulation occured during the rising phase of the surge. The inhibitory effects of the DNT appear to be via activation of alpha-adrenergic receptors since inhibition was prevented by an alpha-adrenergic antagonist. Under a variety of steroidal conditions and stimulation parameters, activation of the DNT or VNT did not enhance LH release. The lone exception to this was stimulation of the VNT in anaesthetized, steroid-primed ovariectomized rats pretreated with an alpha-adrenergic antagonist. In this case stimulation of the VNT did enhance LH release over non-stimulated and electrically stimulated, saline-treated controls. These results suggest that LH release is enhanced by stimulation of the VNT only when alpha-adrenergic receptors are blocked.
In conclusion, it is evident from these studies that activation of alpha-adrenergic receptors either by intraventricular
infusion of NE or alpha-agonists, as well as electrical stimulation of noradrenergic tracts inhibits LH secretion. This suggests that the inhibitory effects of NE may be more of a factor in the regulation of LH release than has been previously proposed. In conclusion, NE, in addition to its well established excitatory role, may also have an important inhibitory role in the regulation of LH release. It appears that both inhibitory and excitatory effects of NE on LH release may be mediated by both alpha- and beta-receptors.<br>Medicine, Faculty of<br>Cellular and Physiological Sciences, Department of<br>Graduate
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Evans, Richard James. "Neuronal control mesenteric arteries." Thesis, University of Oxford, 1990. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.279879.
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Houghton, Andrea Karen. "Peptide and monoamine modulation of a withdrawal reflex in the rabbit." Thesis, University of Nottingham, 1995. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.294717.
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Burton, Claire Louise. "Norepinephrine, iron and Escherichia coli." Thesis, University of Nottingham, 2000. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.342475.
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VIGIER, THIERRY. "Comparaison de l'adrenaline et de la noradrenaline dans le traitement du choc septique post-operatoire." Nantes, 1993. http://www.theses.fr/1993NANT248M.
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Wehrwein, Erica Ariece-Dorothy. "Norepinephrine transporter in the autonomic innervation of the heart and its role in hypertension." Diss., Connect to online resource - MSU authorized users, 2008.
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Sirivelu-Prabhakar, Madhu. "Immune stress and reproduction insights into the role of norepinephrine and gaba /." Diss., Connect to online resource - MSU authorized users, 2008.
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Thesis (Ph. D.)--Michigan State University. Dept. of Comparative Medicine and Integrative Biology, 2008.<br>Title from PDF t.p. (viewed July 31, 2009). Includes bibliographical references (p. 165-198). Also issued in print.
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Mahmood, Samira Rashid. "Vascular calcium adenosine triphosphatase as a site of noradrenaline and hypotensive drug action." Thesis, Heriot-Watt University, 1985. http://hdl.handle.net/10399/1626.
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Hughes, Zoe Alexandra. "Modulation of extracellular noradrenaline in rate cortex by selective serotonin reuptake inhibitors (SSRIs)." Thesis, University College London (University of London), 1998. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.300168.
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Clark, Andrew J. M. "On the action of noradrenaline microinjected into the paraventricular nucleus of rat hypothalamus." Thesis, University of St Andrews, 1990. http://hdl.handle.net/10023/14704.
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The microinjection of noradrenaline (NA) into the hypothalamic paraventricular nucleus (PVN) of the rat results in feeding. This response was shown; contrary to previous reports; to be mediated through both a-1 and a-2 NA receptors. Selective blockade of these two receptor sub-types, in conjunction with re-uptake blockade was used to examine the individual contributions of each receptor type to the whole response. It is suggested that the previously reported a-2 receptor specificity of the response to microinjected NA is a result of the location of these receptors. The post-synaptic a-1 receptor being located close to the pre-synaptic re-uptake mechanism, whilst the post-synaptic a-2 receptor is located outside the synapse and thus away from the re-uptake mechanism. The re-uptake mechanism acts to create a concentration difference of microinjected NA between the two receptor sub-types, resulting in a higher concentration and thus a preferential action at a-2 receptors. The involvement of the paraventricular NA system in stress induced eating was examined using a tail pinch procedure. Microinjection of NA antagonists into PVN prior to the onset of the pinch had no effect on the duration or latency of the eating response, thus there was no evidence for the involvement of this system in tail pinch elicited feeding. Further to the suggestion that the NA a-2 receptor is extra-synaptic whilst a-1 is intrasynaptic, the actions of NA were examined at a second site. NA microinjected into the ventral striatum elicited a vigorous locomotor response, although the origins of this showed a clear priming effect. However, this response was unaffected by prior microinjection of NA a-antagonists, preventing an analysis of receptor involvement comparable with that performed in PVN.
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Airo, Juha. "Role of cerebral dopamine and noradrenaline in locomotor sensitization to morphine in mice." Helsinki : University of Helsinki, 1999. http://ethesis.helsinki.fi/julkaisut/mat/farma/vk/airio/.
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Moreira, Marilia Francisco. "Sensibilidade adrenergica de atrios direitos isolados de ratos normo ou hiperlipidemicos sedentarios ou submetidos a natação." [s.n.], 2005. http://repositorio.unicamp.br/jspui/handle/REPOSIP/314100.
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Previous issue date: 2005<br>Resumo: Lipídios provenientes da dieta têm um importante efeito no sistema de sinalização transmembrana presente nas células cardíacas. Um vez ingeridos em excesso ocorre aumento no conteúdo de colesterol na membrana da célula cardíaca o qual afeta a atividade da adelilil ciclase ligada ao receptor ß e conseqüentemente as respostas cronotrópicas e inotrópicas às catecolaminas causando arritmogênese. O objetivo desta tese foi analisar os efeitos de sessões de natação com o objetivo de prevenir os efeitos de dieta hiperlipídica sobre a sensibilidade de átrios direitos isolados a agonistas adrenérgicos. Ratos Wistar machos adultos foram usados após uma semana de adaptação em salas climatizadas 22±2ºC e com ciclo claro-escuro de 12 h (luzes acendendo as 6:30 da manhã). Os experimentos foram realizados de acordo com os princípios para utilização de animais em pesquisa e educação e adotado pelo COBEA (Colégio Brasileiro de Experimentação Animal). Os animais foram randomicamente divididos em dois grupos, sedentários (S) e que praticaram exercício (T). O exercício constou de sessões de natação na freqüência de 5 dias na semana com 50 minutos de duração durante 20 dias (4x5 dias) em tanque de água com temperatura de 34 ± 2oC. Estes dois grupos foram ainda subdivididos em 2 subgrupos, o que recebia ração padrão (N) e outro que recebia a dieta rica em lipídios (H). O átrio direito foi isolado e curvas cumulativas dose-resposta a noradrenalina (NA) e isoprenalina (ISO) foram obtidas, na ausência ou presença de inibição da recaptação neuronal e extraneuronal. Não houve alteração na freqüência cardíaca basal ou resposta máxima aos agonistas nos átrios isolados dos diferentes grupos experimentais (NS, NT, HS e HT). O programa de exercício físico proposto induziu em ratos que ingeriram dieta padrão uma subsensibilidade à noradrenalina e uma supersensibilidade a isoprenalina. Os átrios direitos isolados de ratos sedentários que ingeriram dieta rica em lipídios apresentaram, após quatro semanas, subsensibilidade a noradrenalina e nenhuma alteração na sensibilidade a isoprenalina. A associação da dieta rica em lipídios com o programa de exercício físico preveniu as alterações observadas tanto pela dieta hiperlipídica como pelo programa de exercício isoladamente. Os valores pD2 para NA foram: 7,44±0,09 (NS); 6,65±0,17* (HS); 6,52±0,25* (NT); 7,15±0,04**# (HT) e para ISO foram: 8,37±0,12 (NS); 8,52±0,10 (HS); 8,94±0,09* (NT); 8,55±0,08 (HT). Onde as diferenças significativas (p<0.05 ANOVA seguida de Tukey) foram indicadas como segue: * vs NS; ** vs NT, # vs HS. Este programa de exercício físico induziu alterações na resposta atrial semelhantes àquelas observadas no modelo de choques nas patas (três sessões diárias), ou seja, diminuição na resposta mediada pelos adrenoceptores ß1 (NA) e aumento na resposta mediada pelo adrenoceptor ß2 (ISO). A dieta hiperlipídica oferecida aos ratos durante 4 semanas induziu subsensibilidade a noradrenalina e esta resposta é provavelmente devida a alterações na membrana lipídica e alta atividade adrenérgica relatada neste modelo animal. O motivo da ausência de alterações cardíacas quando da associação dieta hiperlipídica e exercício físico precisa sem investigado<br>Abstract: Dietary lipids has an important effect on transmembrane signaling system in the heart increasing the cardiac membrane cholesterol content, which in time affect ß-adrenoceptor/adenylyl cyclase activity and the inotropic and chronotropic responses to catecholamines causing arrhytmogenesis.The aim of this work was to analyze the effect of swimming, to prevent the effects of high fat-CHO diet on the sensitivity to adrenergic agonists in rat isolated right atria. Adult male Wistar rats were used after one week of adaptation in acclimated room at 22±2ºC and 12h light-dark cycle (lights on at 6:30 a.m.). The experiments were carried out in accordance with the principles for the use of animals in research and education and adopted by COBEA (Brazilian College for Animal Experimentation). The animals were randomly divided into two groups, sedentary (S) and exercised (T) with a swimming sessions, 5 days a week (50 min. session) during 20 days (4x5 days) in a water glass tank with temperature at 34 ± 2oC. These two groups were divided into two subgroups; one of them fed a standard chow (N) and the other, a high fat-CHO diet (H). The atrium was isolated as described before and cumulative concentration-response curves to noradrenaline (NA) and isoprenaline (ISO) were obtained, in the absence or presence of inhibitors of neuronal and extraneuronal uptake. There was no alteration in the basal heart rate or maximal response to the agonists in isolated atria rats from different groups (NS, NT, HS and HT). The physical exercise program in rats fed with standard chow induced right atria subsensitivity to noradrenaline and supersensitivity to isoprenaline. Atria isolated from rats fed with high fat-CHO diet showed subsensitivity to noradrenaline and no alterations on the sensitivity to isoprenaline. Association of high fat-CHO diet and this physical exercise program prevented the alterations induced by the diet or the exercise values were: 7.44±0.09 (NS); 6.65±0.17* (HS); 6.52±0.25* (NT), 7.15±0.04**(HT) and ISO pDprograms alone. The NA pD2 # 2 values were: 8.37±0.12 (NS); 8.52±0.10 (HS); 8.94±0.09* (NT), 8.55±0.08 (HT). Significant differences (p<0.05 ANOVA plus Tukey test) were indicated as follows: *compared to the NS group, **compared to the NT group, #compared to the HS group. The uptake inhibition did not alter the responses obtained. This exercise program induced alterations in the right atria response similar to those induced by foot shock stress, it means, decrease on ß1-adrenoceptor mediated (NA) response and increase on ß2-adrenoceptor mediated (ISO) response. High fat-CHO diet offered during four weeks induced subsensitivity to noradrenaline, this response is probably due to alterations on the lipid membrane content and high adrenergic activity reported in this animal model. The absence of effects on atria response observed in rats submitted to high fat-CHO diet and exercise program needs to be investigated.<br>Mestrado<br>Fisiologia<br>Mestre em Biologia Funcional e Molecular
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Lima, Ronald de Albuquerque. "Comparação dos efeitos microcirculatórios da vasopressina e da noradrenalina associadas à reposição volêmica durante o choque hemorrágico. Estudo experimental em hamster." Universidade do Estado do Rio de Janeiro, 2009. http://www.bdtd.uerj.br/tde_busca/arquivo.php?codArquivo=1030.
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Objetivos: Este trabalho teve como objetivos avaliar in vivo os efeitos microcirculatórios e a sobrevida de animais submetidos ao choque hemorrágico tratados com vasopressina e noradrenalina associadas à reposição volêmica com solução de NaCl 0,9% .
Desenho do estudo: Estudo prospectivo, randomizado, controlado, intervencionista em modelo animal.
Materiais e métodos: Utilizou-se hamsters machos do tipo sírio dourado, com idade entre 6 e 8 semanas e massa corporal entre 60 e 80 gramas. Os animais foram anestesiados para colocação de uma câmara dorsal. Após 5 a 7 dias, foram re-anestesiados para implante de cânulas na carótida e na veia jugular. No dia seguinte realizou-se o experimento. Os animais sofreram choque hemorrágico por meio da retirada de 40% da volemia, definida como 7% do peso corporal, e mantidos em choque por uma hora. Após, os animais foram aleatoriamente divididos em três grupos : Grupo SF0,9% (N = 6) - recebeu solução de NaCl 0,9% em volume de duas vezes o volume de sangue retirado; Grupo VP recebeu solução de NaCl 0,9% em volume de duas vezes o volume de sangue retirado, associado à infusão contínua durante uma hora de vasopresssina (0,0001 UI/kg/min por uma hora); e Grupo Nora. recebeu solução de NaCl 0,9% em volume de duas vezes o volume de sangue retirado, associado à infusão contínua de solução de noradrenalina (2 g/kg/min por uma hora). Foram avaliados os diâmetros das arteriolas e vênulas e a densidade capilar funcional (DCF) no momento basal, após o choque e após o tratamento. Os parâmetros laboratoriais observados foram: pH, HCO-3, BEx, paO2, paCO2 e lactato durante as três fases do experimento. Após o término do tratamento, foi visualizado o rolamento e adesão de leucócitos , assim como a sobrevida dos animais durante setenta e duas horas.
Resultados: A terapia com reposição volêmica por si ou associada à vasopressina ou à noradrenalina não alterou valores relativos à gasometria arterial ou lactato em relação ao choque. A terapia com vasopressina associada à reposição volêmica manteve a densidade capilar funcional após ressuscitação do choque hemorrágico, (97% do valor basal da mediana), enquanto tratamento com solução de NaCl 0,9% apenas, não obteve o mesmo resultado (70% do valor basal da mediana). A noradrenalina associada à reposição volêmica piorou a densidade capilar funcional após o tratamento (44% do valor basal da mediana). A sobrevivência em setenta e duas horas foi significativamente menor no grupo da noradrenalina do que no grupo da vasopressina (33% em relação ao grupo Vaso). Ao final do experimento não foi observada diferença estatisticamente significativa relativa à adesão ou rolamento de leucócitos.
Conclusão: Durante o choque hemorrágico, o tratamento com infusão de solução de NaCl 0,9% associada à vasopressina mantém a DCF, enquanto que o tratamento com solução de NaCl 0,9% somente ou associada à noradrenalina pioram a DCF. O tratamento com vasopressina melhora a sobrevida dos animais, em comparação ao tratamento com noradrenalina. Embora a adesão leucocitária não esteja significativamente alterada entre os grupos, houve uma tendência em obtermos uma adesão menor no grupo da vasopressina.<br>Objectives: The goal of this work was to evaluate in vivo the microcirculatory effects and survival of animals subjected to hemorrhagic shock treated with vasopressin or noradrenalin associated to volume infusion associated with NaCl 0,9%
Study design: Prospective, randomized, controlled, intervencionist study in animal model.
Materials and methods: Golden Syrian hamsters were used, aging between 6 and 8 weeks with body mass ranging from 60 to 80 grams. Animals were anesthetized for dorsal chamber implant. After 5 to 7 days there was a new anesthesia for carotid artery and jugular vein catheter implantation. Next day the experiment took place. Animals suffered a hemorrhagic shock by withdrawal of 40% of blood volume, defined as 7% of body weight, and kept in shock condition for 1 hour. After, animals were randomly divided in three groups. SF0,9% group (N=6) received NaCl 0,9% two times the shed volume; VP group (N=6) received NaCl 0,9% two times the shed volume plus continuous infusion for one hour of vasopressin solution (0,0001UI/kg/min for one hour); Nora group received NaCl 0,9% two times the shed volume plus continuous infusion of noradrenalin solution (2mcg/kg/min for one hour). Arteriolar diameter, venular diameter and functional capillary density (FCD) were evaluated in baseline, after shock and after treatment. Laboratory parameters observed were: pH, HCO-3, BEx, paO2, paCO2 and lactate during all three phases of experiment. After end of treatment, leucocyte rolling and adhesion were visualized, as well as animal survival during seventy two hours.
Results: Volume infusion by itself or associated with vasopressin or noradrenalin didnt altered blood gas analysis values or lactate related to hemorrhagic shock. Vasopressin therapy associated with volume infusion sustained functional capillary density after hemorrhagic shock resuscitation (97% of baseline median values), while treatment with NaCl 0,9% only, didnt obtained the same result (70% of baseline median values). Noradrenalin associated to volume infusion worsened the functional capillary density after treatment (44% of baseline median values). Survival in seventy two hours were significantly lower in noradrenalin group comparing to vasopressin group (33% relating to Vaso group). In the end of experiment wasnt observed any significantly statistical difference relative to leucocyte rolling or adhesion.
Conclusion: During hemorrhagic shock, treatment with NaCl 0,9% infusion associated with vasopressin sustains FCD, while treatment with NaCl 0,9% only or associated to noradrenalin worsens FCD. Treatment with vasopressin solution improves survival comparing to noradrenalin infusion treatment. Although leucocyte adhesion wasnt significantly altered among groups, there was a trend in observe lesser adhesion in vasopressin group.
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Birch, P. J. "The role of presynaptic receptors in the regulation of noradrenaline synthesis in rat hippocampus." Thesis, University of Oxford, 1985. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.370237.
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Mason, Kathryn. "Modulation of central noradrenaline efflux by pharmacological and novel environmental stimuli : a microdialysis study." Thesis, University College London (University of London), 1997. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.264181.
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Crawford, Andrew Raymond. "Iodoreboxetine : the development of a novel SPECT brain imaging tracer for the noradrenaline transporter." Thesis, University of Glasgow, 2013. http://theses.gla.ac.uk/4226/.
Full textAbstract:
The noradrenaline system is extensively innervated throughout the brain, implicated in the aetiology of a wide range of psychiatric conditions, and the pharmacological modulation of the noradrenaline system has had a positive influence upon the alleviation of symptoms for those suffering psychiatric or neurological disease. Clinical imaging of the brain with technologies such as Single Photon Emission Computed Tomography (SPECT) can provide clinicians and researchers with valuable information for elucidating disease aetiology, monitoring patient condition, and also confirming the mechanism of action for drug development through occupancy studies. However, to date, there is no SPECT brain imaging tracer for the noradrenaline transporter in regular clinical use. This thesis is a body of work to develop a novel SPECT brain imaging tracer for the noradrenaline transporter with compounds that are iodinated forms of reboxetine, the selective noradrenergic reuptake inhibitor and clinically used antidepressant. From the compounds synthesised and tested, the one which demonstrated the best pharmacological affinity and selectivity for the noradrenaline transporter was NKJ-64. This same compound also displayed many of the HPLC-derived properties predicting in vivo molecular behaviour that are associated with successful brain imaging tracers. Therefore, NKJ-64 was recommended for radiolabelling and further study. PCP MODEL OF THE METABOLIC HYPOFRONTALITY OBSERVED IN SCHIZOPHRENIA: The metabolic hypofunction observed in the prefrontal cortex of schizophrenic patients is mimicked in a rat model via repeated, low-dose phencyclidine administration. The neural mechanisms underlying this hypofrontality are unclear. Whilst dopaminergic transmission is classically associated with aberrant activity in schizophrenia, modulation of noradrenergic neurotransmission is correlated with the alleviation of negative symptoms. Furthermore, the noradrenaline transporter rather than the dopamine transporter functions as the dominant dopaminergic reuptake mechanism in the prefrontal cortex. It was hypothesised that repeated phencyclidine administration in the rat would induce a down-regulation of the NAT. Ligands labelled with [3H] were used for autoradiographic imaging of the noradrenaline, dopamine, and serotonin transporters in phencyclidine-treated and control groups, and [35S]-labelled oligonucleotide probes specific for the mRNA of each transporter were used for in situ hybridisation. The binding densities of the noradrenaline and dopamine transporters were unaltered in the model, however significant selective reductions of serotonin transporter binding sites were measured. The densities of mRNA for all three monoamine transporters were unaltered, so the unaltered densities of noradrenaline and dopamine transporter binding sites and the changes in serotonin transporter binding densities were not the result of altered gene expression. Although the noradrenaline transporter was not directly affected in this model of one particular aspect of schizophrenia and the model is not ideal for demonstrating the capability of a SPECT tracer for the NAT, this does not imply that the noradrenaline transporter is uninvolved in the disease aetiology of schizophrenia or of diminished importance to future schizophrenia studies. The aforementioned correlation of noradrenaline transporter modulation to the alleviation of negative symptoms emphasises the importance of acquiring the clinical ability to assess the density and/or occupancy of the noradrenaline transporter by developing a useful SPECT brain imaging tracer for this site. PHARMACOLOGICAL CHARACTERISATION OF POTENTIAL SPECT BRAIN IMAGING TRACERS FOR THE NORADRENALINE TRANSPORTER: In vivo imaging of the noradrenaline transporter was previously limited to peripheral tracers such as metaiodobenzylguanidine (MIBG), which does not cross the blood-brain barrier, and neuroligands such as radiolabelled desiprimine, which demonstrated problematically high nonspecific binding. Recent efforts in the literature have focused upon modified reboxetine analogues, and some progress was made with the S,S-isomer of iodophenoxy-ring reboxetine, referred to as both INER and IPBM in publication (Tamagnan et al. 2007; Kanegawa et al. 2006). Synthesised iodophenyl-ring compounds in S,S-, R,R-, S,R-, and R,S-isomers were evaluated for their affinity for the NAT. The R,S-isomer demonstrated a very similar level of binding to the S,S-isomer and so this was explored in an iodophenoxy isomer to determine if improvement upon the characteristics of lead iodinated reboxetine compounds in the literature was possible. The R,S-isomer iodophenoxy reboxetine analogues were synthesised with the iodine in the ortho, meta, and para positions of the phenoxy ring and assigned the designations NKJ-64, NKJ-67, and NKJ-68, respectively. NKJ-64 has strong affinity and selectivity for the noradrenaline transporter, with a KD of 8.4 ± 1.7 nM, a 6-fold selectivity for the noradrenaline transporter over the serotonin transporter, and a 63-fold selectivity for the noradrenaline transporter over the dopamine transporter. From the compounds synthesised and tested, NKJ-64 has the most suitable pharmacology to be developed further as a SPECT brain imaging tracer for the noradrenaline transporter and has an affinity in the same order of magnitude as iodinated compounds in the literature, such as the aforementioned INER/IPBM. USING HIGH-PERFORMANCE LIQUID CHROMATOGRAPHY (HPLC) TO PREDICT IN VIVO CHARACTERISTICS OF TRACER CANDIDATES: The development of any candidate tracer compound must include an evaluation of its in vivo properties. To streamline this process and select only the most viable compounds for further testing, predictors of in vivo molecular characteristics are used to conserve research effort. Measures such as lipophilicity, phospholipophilicity, and plasma protein binding, used to estimate the potential for blood-brain barrier penetration, nonspecific binding, and the likelihood of serum availability would be very time-intensive to determine via traditional bench-top methodologies. High-performance liquid chromatography (HPLC) is a quick, precise, and reliable technique that is a rapid and high-throughput automatable process with exceptional precision that does not rely on the bench-top proficiency of an individual experimenter. The optimisation of gradient elution protocols and formulae to interpret sample retention times on commercially available columns into reproducible standardised units has allowed for the efficient evaluation of tracer candidate compounds. The iodinated reboxetine compounds were compared to examples of both successful and failed neuroimaging tracers. Generally, the evaluations of the successful and failed neuroimaging tracers validated the combined methodologies of the HPLC-derived predictors of in vivo molecular behaviour. In applying these methodologies to the synthesised iodoreboxetine compounds, NKJ-64 displayed many of the HPLC-determined properties that are consistent with successful tracers.
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CANDITO, VALLAURI MIRANDE. "Etude circadienne de substances neuro-hormonales circulantes dans la depression : noradrenaline, tryptophane, serotonine, cortisol." Aix-Marseille 2, 1989. http://www.theses.fr/1989AIX22966.
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Homar, Ruano Patricia C. "Oligomerización de receptores α₁ᴀ adrenérgicos y receptores dopaminérgicos en el SNC: implicación en la modulación de la atención". Doctoral thesis, Universitat de Barcelona, 2020. http://hdl.handle.net/10803/668694.
Full textAbstract:
La atención es el proceso cognitivo básico que nos otorga la capacidad de seleccionar aquella información interna o externa que va a ser relevante para la toma de decisiones y el control del comportamiento. Múltiples regiones cerebrales interconectadas entre ellas forman una compleja red de circuitos neuronales capaces de activar y modular diversas funciones cognitivas, como la atención. Concretamente, la corteza prefrontal (PFC) es un punto neurálgico de estos circuitos que, a través de distintas regiones funcionales, orquesta prácticamente todos los aspectos del comportamiento y la cognición humana. A su vez, la PFC y sus conexiones se encuentran finamente regulados por complejos sistemas de neurotransmisores capaces de responder a demandas internas o externas provocando la activación o la inhibición de la atención y las respuestas cognitivas y/o motoras apropiadas. Entre estos sistemas de neurotransmisores destaca el sistema catecolaminérgico. La noradrenalina (NE) y la dopamina (DA) actúan cooperativamente para ejercer efectos complementarios en el refuerzo y la regulación de las conexiones de la PFC mediante la activación diferencial de distintas familias de receptores acoplados a proteína G (GPCRs), los cuales son importantes dianas terapéuticas para el tratamiento de diversos trastornos neuropsiquiátricos. Actualmente, está plenamente aceptado que los GPCRs pueden interaccionar entre sí para generar tanto homo- como heterooligómeros que representan una nueva entidad funcional con características bioquímicas y farmacológicas únicas, por lo que los heterómeros de GPCRs se consideran posibles dianas farmacológicas. Múltiples estudios han reportado la capacidad de los receptores de DA para formar complejos oligoméricos, lo que sugiere un papel clave del proceso de oligomerización en la regulación de la señalización DAérgica.
El objetivo de esta Tesis ha sido evaluar si los efectos complementarios de la DA y la NE en la PFC y en el estriado son, en parte, regulados por interacciones intramoleculares en complejos formados por sus receptores. Nuestros resultados ponen de manifiesto la capacidad del receptor adrenérgico α1A para formar heterodímeros funcionales con los receptores de dopamina, D4 y D1ike en células vivas y en PFC y estriado de rata. Los receptores en estos complejos actúan como moduladores alostéricos del otro protómero, produciendo modificaciones en las potencias de activación de sus proteínas G canónicas y alterando su selectividad funcional. Funcionalmente, los heterodímeros D4R-α1AR y D1R-α1AR exhiben un patrón común de modulación negativa bidireccional tras la coactivación de los receptores tanto con agonistas, como con antagonistas de la pareja. Lo que indica que la interacción molecular entre receptores catecolaminérgicos de distinta familia actúa atenuando la respuesta de los
protómeros en el complejo. Además, se ha descrito diferencias funcionales clave entre la variante más común del receptor D4, D4.4R, y la variante vinculada al trastorno por déficit de atención e hiperactividad (TDAH), D4.7R. Estas diferencias funcionales resultaron ser dependientes de su heteromerización con α1AR. Los receptores D4, D1 y α1A participan diferencialmente en la modulación de la atención, las funciones ejecutivas y del control motor. Dado que estos procesos se encuentran afectados en distintas patologías neuropsiquiátricas como, por ejemplo, en los trastornos del neurodesarrollo, como el TDAH, el síndrome de Gilles de la Tourette, el trastorno obsesivo compulsivo o los trastornos del espectro autista, nuestros resultados sugieren que los heterodímeros de estos receptores pueden ser dianas terapéuticas prometedoras para el tratamiento de trastornos neuropsiquiátricos. Los resultados de esta Tesis ponen de manifiesto la relevancia de la heteromerización de receptores adrenérgicos y dopaminérgicos en la PFC y el estriado para modular los efectos complementarios de las catecolaminas. Así, estos heterodímeros constituyen un nivel superior, y más complejo de la regulación de la señalización catecolaminérgica.<br>Attention is defined as a set of cognitive processes that select certain relevant information while enabling the inhibition of irrelevant inputs. The prefrontal cortex (PFC) via its extensive connection to sensory cortices and subcortical regions plays a pivotal role in top-down attentional modulation and other complex cognitive processes as executive functions. The catecholamines, dopamine (DA) and norepinephrine (NE), act cooperatively as neuromodulators of the PFC networks activity. Thus, alterations of DA and NE signaling has been linked to several disorders comorbid to attentional and cognitive deficits including neurodevelopmental disorders as attention-deficit hyperactivity disorder (ADHD), autism, Tourette’s syndrome and obsessive compulsive disorder (OCD). DA and NE mediate its physiological effects acting through different G protein-coupled receptors (GPCRs), which are important pharmacological targets to the above mentioned disorders. A large number of GPCRs have been described to interact with another receptors forming homodimers, heterodimers and higher order oligomers with different pharmacological and functional properties than of its individual components, being new and more specific drug targets. The aim of this Thesis has been to determine whether the coordinate effects of DA and NE in PFC modulation are mediated by molecular interactions between its receptors. We have proven that DA, D4 and D1like, receptors are forming functional heterodimers with α1A adrenergic receptors in living cells as well as in rat PFC and striatum. The heterodimers characterization demonstrated that the receptors within D4R-α1AR and D1R-α1AR complexes acts as allosteric modulators of the partner, modifying its activation potencies of cognate G proteins and its functional selectivity. Functionally, the complexes display a common negative cross-modulation pattern upon receptors coactivation, indicating that the molecular interaction between DA and NE receptors are attenuating the protomers response in the complex. Moreover, we have described pivotal functional differences between the common D4 receptor variant, D4.4R, and the ADHD related variant, D4.7R, upon its heterodimerization with α1AR. D4, D1 and α1A receptors are involved in attention and executive processes modulation and in motor control. Given that these processes are impaired in different neuropsychiatric pathologies, as neurodevelopmental disorders, our results suggest that D4R-α1AR and D1R-α1AR heterodimers could be targeted for the therapeutic treatment of such neurological disorders.
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Carpes, Pâmela Billig Mello. "Participação da via NTS-PGI-LC-hipocampo (núcleo do trato solitário- núcleo paragigantocelular-Locus coeruleus-hipocampo) na consolidação da memória de reconhecimento de objetos." reponame:Biblioteca Digital de Teses e Dissertações da UFRGS, 2010. http://hdl.handle.net/10183/24681.
Full textAbstract:
Existem crescentes evidências sobre a contribuição da liberação de noradrenalina (NA) central na consolidação das memórias. Teoricamente, o Núcleo do Trato Solitário (NTS) recebe informações e diversos estímulos periféricos, que são então projetados ao Núcleo Paragigantocelular (PGi). Este, por sua vez, utiliza neurotransmissores, predominantemente excitatórios, para influenciar a ativação do Locus Coeruleus (LC). Então, o LC envia projeções noradrenérgicas ao hipocampo e à amígdala, influenciando os processos mnemônicos. Aqui nós demonstramos que a inibição pelo muscimol do NTS, PGi ou LC até 3 horas após o treino na tarefa de reconhecimento de objetos (RO) impede a consolidação da memória medida 24 h após o treino. Adicionalmente, a infusão de timolol, um antagonista de receptores β-adrenérgicos, na região CA1 do hipocampo também impede a consolidação deste tipo de memória. A infusão de NA na região CA1 do hipocampo não altera a retenção da memória, mas, reverte o prejuízo causado pela inibição do NTS, PGi ou LC. A infusão de NMDA no LC após a inibição do NTS ou PGi também reverte essa amnésia. Concomitantemente, verificamos que a inibição NTS, PGi ou LC bloqueia o aumento da expressão do fator neurotrófico derivado do cérebro (BDNF, do inglês brain-derived neurotrophic factor) que ocorre 120 min após o treino na tarefa de reconhecimento de objetos na região CA1 do hipocampo. Também a infusão de NA na região CA1 do hipocampo após a inibição do NTS, PGi ou LC ou de NMDA no LC após a inibição do NTS ou PGi promovem novamente o aumento do BDNF120 min após o treino no RO. Com isso conclui-se que a ativação da via NTS-PGi-LC-Hipocampo é necessária para que ocorra consolidação da memória de RO, na qual desempenha um papel o BDNF hipocampal.<br>There is evidence of the contribution of brain noradrenaline release (NA) to memory consolidation. The Nucleus of the Solitary Tract (NTS) receives information originated by peripheral stimuli and projects to the Paragigantocellularis Nucleus (PGi), which influences the Locus Coeruleus (LC) through excitatory neurotransmitters. The LC sends noradrenergic projections to the hippocampus and amygdala, influencing the memory processes. Here we show that inhibition by muscimol of NTS, PGi or LC up to 3 h after object recognition training impairs the consolidation of the memory measured 24 h later. Additionally, the infusion of timolol in the CA1 region of hippocampus also inhibits consolidation of this type of memory. The infusion of NA into the CA1 region of hippocampus does not alter memory consolidation of this task, but reverts the deleterious effect of NTS, PGi or LC inhibition. The infusion of NMDA in LC after inhibition of NTS or PGi also reverts the amnesia. Concomitantly, the inhibition of NTS, PGi or LC blocks the increase of brain-derived neurotrophic factor (BDNF) expression in CA1 that occurs 120 min after training in the object recognition task. Further, the infusion of NA in CA1 after inhibition of NTS, PGi or LC; or of NMDA in LC after inhibition of NTS or PGi promotes the BDNF increase seen 120 min after object recognition training. Thus, it is concluded that the activation of NTSPGi- LC-Hippocampus pathway is necessary for consolidation of the object recognition memory, and hippocampal BDNF is involved in this process.
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Conde, Gillian L. "Modulation of noradrenergic inputs to the preoptic area of the rat brain by oestradiol." Thesis, University of Cambridge, 1994. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.338066.
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Branger, Caroline. "Développement de molécules pour l'exploration des transporteurs des monoamines." Tours, 1995. http://www.theses.fr/1995TOUR3305.
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Bouret, Sébastien. "Vers une compréhension du rôle du système noradrenergique dans les processus cognitifs : étude électrophysiologique des interactions fonctionnelles entre le locus coeruleus et le cerveau antérieur chez le rat en comportement." Paris 6, 2004. http://www.theses.fr/2004PA066022.
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