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1
Coles, S. K. "Controls of the locomotor system in the rat." Thesis, University of Oxford, 1987. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.233493.
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2
Boulay, Denis. "Etude chez le rat des modifications comportementales et neurochimiques après administrations répétées d'agonistes dopaminergiques indirects : la cocaïne ou le GBR12783." Rouen, 1995. http://www.theses.fr/1995ROUE5042.
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Nous avons recherché si un blocage répété du système de capture de la dopamine par un inhibiteur spécifique de la capture neuronale de dopamine, le GBR12783, pouvait mimer les sensibilisations observées après administrations de cocaïne, inhibiteur non sélectif de la recapture des monoamines. Des administrations répétées de GBR12783 ont induit une sensibilisation à ses effets stimulants moteurs, se développant au cours du temps et pouvant persister plusieurs semaines après la dernière administration. L'expression de cette sensibilisation dépend en partie de la durée des traitements chroniques ; elle est favorisée par le contexte environnemental. Les traitements chroniques par le GBR12783 ne modifient pas les taux tissulaires ni de la dopamine, ni de ses métabolites mesurés 48 heures ou 15 jours après l'arrêt des traitements dans le noyau accumbens et le striatum. Un traitement répété de 15 jours par le GBR12783 ou par la cocaïne diminue la densité du transporteur neuronal de la DA dans la partie coque du noyau accumbens. Cette diminution n'apparaît que 15 jours après l'arrêt des traitements ; elle pourrait participer à la sensibilisation des effets moteurs de ces substances. Des administrations répétées de GBR12783 induisant chez le rat une sensibilisation aux effets moteurs de cet inhibiteur de capture de la dopamine ont sensibilisé également les effets stimulants moteurs d'un dérivé de la neurotensine (résistant à la dégradation par les peptidases): la D tryptophane-11-neurotensine injectée par voie i. C. V. , Sans pour autant modifier la densité des récepteurs de la neurotensine
3
Cohen, Ricky Israel. "Rat brain oligodendrocytes express muscarinic and adrenergic receptors." Thesis, McGill University, 1996. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=42006.
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The aim of the studies underlying this thesis was to characterize the muscarinic and adrenergic receptors expressed in rat brain oligodendrocytes' (OLs); determine if ligand binding alters second messenger levels classically associated with these families of receptors, such as inositol phosphates (InsP), intracellular calcium ( (Ca$ rm sp{2+} rbrack sb{i}),$ and cyclic AMP (cAMP); and the role of neurotransmitters, acetylcholine (Ach) or norepinephrine (NE) on oligodendrocyte growth.CCH (carbachol), a stable Ach analog, caused a concentration and time dependent increase in the accumulation of InsPs and the mobilization of (Ca$ rm sp{2+} rbrack sb{i},$ which was inhibited by atropine, a specific muscarinic antagonist, and was negatively regulated by acute activation of protein kinase C by the phorbol ester TPA. CCH also negatively regulated the $ beta$-adrenergic-stimulated increase in cAMP levels. Using subtype m1 and m2 specific muscarinic receptor oligonucleotide primers RT-PCR confirmed the presence of, at least, these two muscarinic receptor subtypes. CCH caused a time and concentration-dependent increase in c-fos proto-oncogene mRNA levels as determined by Northern blot analysis. The CCH-stimulated c-fos increase was mediated through a non-phorbol ester sensitive PKC isozyme, and was dependent upon intra and extracellular calcium. Moreover, CCH stimulated DNA synthesis in OLPs, as measured by both ($ sp3$H) -thymidine and BrdU incorporation.
Lastly, the NE-stimulated signal transduction pathway was characterized in developing OLPs. Using selective agonists and antagonists, we determined that NE increased the formation of InsPs through $ alpha sb1$ adrenoceptors. We further subclassified the $ alpha sb1$ receptor to the $ rm alpha sb{1A}$ subtype using more selective reagents; WB4101, a selective antagonist for $ rm alpha sb{1A}$ receptors blocked the response to NE, while chloroethylclonidine, an $ rm alpha sb{1B}$ antagonist had no effect. Furthermore, Pertussis toxin, a bacterial toxin that ADP-ribosylates and inactivates certain G-proteins, EGTA, a calcium chelator, or CdCl$ sb2,$ an inorganic calcium channel blocker, all significantly blocked the NE-stimulated InsP formation. Together these results suggest that OLPs express $ alpha sb1$-adrenoceptors characteristic of the $ rm alpha sb{1A}$ subtype.
In toto, these studies demonstrate that developing OLs express functional muscariaic and adrenergic receptors, and suggest that Ach may function as a trophic factor. These results help to define a mechanism whereby neurons, and OLs may use neurotransmitters to communicate both during development and in the mature central nervous system.
4
Cohen, Ricky Israel. "Rat brain oligodendrocytes express muscarinic and adrenergic receptors." Thesis, National Library of Canada = Bibliothèque nationale du Canada, 1997. http://www.collectionscanada.ca/obj/s4/f2/dsk2/tape16/PQDD_0022/NQ29913.pdf.
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Mahalekam, Malani. "Natriuretic peptide receptors in developing and adult rat brain." Thesis, University of Cambridge, 1998. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.368618.
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6
Howard, Helen Clare. "The pharmacological characterisation of oxytocin receptors in the rat brain." Thesis, University of Bristol, 1999. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.299594.
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7
Pasquini, Filoteo. "High resolution radioautographic visualization of delta opioid receptors in rat brain." Thesis, McGill University, 1988. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=64051.
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Smith, Steven Andrew. "The role of Peroxisome proliferator-activated receptors in the rat brain /." St. Lucia, Qld, 2004. http://www.library.uq.edu.au/pdfserve.php?image=thesisabs/absthe17982.pdf.
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9
Gibbins, Jonathan Martin. "The purification of corticotropin-releasing factor (CRF) receptors from rat brain." Thesis, University of Reading, 1995. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.260813.
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10
Schindler, Marcus. "The distribution of somatostatin receptors in the rat and human brain." Thesis, University of Cambridge, 1997. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.627298.
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11
Kelly, Mary D. W. "The ontogeny of delta and kappa opioid receptors in the rat." Thesis, University of Surrey, 1996. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.318690.
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12
Large, Charles Henry. "Characterisation of dopamine D3 receptors in recombinant cell lines and rat brain." Thesis, University of Bristol, 1994. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.388037.
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13
Wang, Li Racine Ronald J. "Expression of EphA receptors and ligands in rat brain following status epilepticus." *McMaster only, 2006.
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14
Mason, Sarah. "Post-mortem neuropharmacological studies of human and rat brain relating to schizophrenia and antipsychotic drug action." Thesis, University of Sheffield, 1995. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.364237.
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15
Nemati, Farshad, and University of Lethbridge Faculty of Arts and Science. "Contribution of brain with or without visual cortex lesion to exploratory locomotion in the rat." Thesis, Arts and Science, 2008. http://hdl.handle.net/10133/665.
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Over the past five decades spatial behavior has been a subject of research
interest in psychology and neuroscience, in part based on philosophical theories
of mental spatial representations. In order to continue uncovering the facts
regarding spatial behavior, the focus of this thesis was on the contribution of
entry point and visual inputs to the organization of exploratory locomotion and
spatial representation in the rat. Despite the contribution of the hippocampus to
spatial abilities, the exploratory locomotion is still visually organized in rats with
damage to the hippocampus. On the other hand, recent studies have
demonstrated a contribution of visual areas to the spatial ability of the rat.
Nevertheless, the contribution of visual cortex to the organization of exploratory
locomotion has not been studied in an open field. The experiments in this thesis
were designed to characterize the organization of exploratory locomotion to the
point of entry and/or visual cues. Rats were started from the edge or center of an
open table near or on which a salient object could be placed. The main findings
were that rats organized their exploratory locomotion to their point of entry and
modified their behavior as they encountered objects. Also, rats with damage to
visual cortex displayed an extra-attachment to the visual objects and in contrast
to controls did not expand their exploratory locomotion with time. The results are
discussed with respect to the centrality of the entry point in the organization of
exploratory locomotion and the neural network that control visual exploration in
the rat.xiii, 220 leaves : ill. ; 29 cm. --
16
Ma, Guofen. "Functional responses of pre- and postsynaptic dopamine D2 receptors in rat brain striatum." Doctoral thesis, Universitat Autònoma de Barcelona, 2014. http://hdl.handle.net/10803/283893.
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El sistema dopaminèrgic has estat molt estudiat en els darrers anys, principalment degut a la seva implicació en diverses patologies com la malaltia de Parkinson, la esquizofrènia o la síndrome de Tourette, així com també en l’abús de drogues. S’han descrit cinc subtipus de receptors per la dopamina (DA), tots els quals pertanyen a la família de receptors acoblats a proteïnes G (GPCRs). D’aquests cinc subtipus, els receptors D2 son la diana principal dels antipsicòtics (antagonistes) i també dels fàrmacs utilitzats en el trastament del Parkinson (agonistes). Malauradament, els efectes antagonistes sobre els receptors D2 comporten importants efectes secundaris indesitjables. Els antipsicòtics de nova generació (com l’aripiprazole) presenten menys efectes secundaris, la qual cosa s’ha atribuït a diferent selectivitat funcional sobre els receptors D2, malgrat que es necessiten més estudis per confirmar aquesta hipòtesi. En el nostre treball, hem observat diferent activitat de l’aripiprazol sobre els auto-receptors D2 en resposta a canvis en les concentracions extracel·lulars de DA, la qual cosa és coherent amb la hipòtesi de que els receptors D2 presenten “selectivitat funcional”. Per altra banda, actualment està cada cop més acceptat el concepte de heteromerització entre diferents GPCRs que co-localitzen en les mateixes mostres tissulars, i representa un nou camp per al disseny de millors teràpies. Així doncs, els estudis dirigits a la identificació de nous heteròmers que impliquin els receptors D2, permet ampliar la farmacologia del sistema dopaminèrgic. En aquesta tesis hemos observat crosstalk funcional entre dos parells de GPCRs: entre D2 i GABAB por un costat, i entre D2 i el receptor-1 de Orexina per un altre. Malgrat que els nostres resultats indiquen que és molt probable que ambdós parells de receptors formin heteròmers, es necessiten mñes dades per a corroborar-ho. La DA és clau pel sistema cerebral de la recompensa, que juga un paper primordial en el fenòmen de l’addicció. Està descrit que la administració crònica de cocaïna altera la densitat i l’afinitat dels receptors D1 i D2, així com també la seva interacció amb altres receptors. En el nostre model de auto-administració de cocaïna en rates, hem trobat canvis en la resposta del sistema dopaminèrgic a l’agonista D2 quinpirole, després de abstinència de curt i també de
llarg termini. En summa, els nostres resultats sobre l’administració de cocaïna destaquen la importància del sistema dopaminèrgic en l’addicció a la cocaïna, i a més, el crosstalk funcional que hem observat entre els receptors D2 i altres GPCRs obre noves possibilitats per al disseny i desenvolupament de nous tractaments per a l’abús de drogues així com també per l’esquizofrènia.El sistema dopaminérgico ha sido ampliamente estudiado en las últimas décadas, principalmente por su implicación en diversas patologías como la enfermedad de Parkinson, la esquizofrenia o el síndrome de Tourette, así como en el abuso de drogas. Se han descrito cinco subtipos de receptores para la dopamina (DA), todos ellos pertenecientes a la familia de receptores acoplados a proteínas G (GPCRs). De estos cinco subtipos, los receptores D2 son la diana principal de los antipsicóticos (antagonistas) y también de los fármacos utilizados en el tratamiento del Parkinson (agonistas). Desafortunadamente, los efectos antagonistas sobre los receptores D2 conllevan importantes efectos secundarios indeseables. Los antipsicóticos de nueva generación (como el aripiprazole) presentan menos efectos secundarios, hecho que se ha atribuido a diferente selectividad funcional sobre los receptores D2, aunque se requieren más estudios para confirmar esta hipótesis. En nuestro trabajo, hemos observado distinta actividad del aripiprazol sobre los autoreceptores D2 en respuesta a cambios en las concentraciones extracelulares de DA, lo cual es coherente con la hipótesis de que los receptores D2 presenten “selectividad funcional”. Por otra parte, actualmente está cada vez más aceptado el concepto de heteromerización entre distintos GPCRs que co-localizan en las mismas muestras tisulares, y representa un nuevo campo para el diseño de mejores terapias. Por ello, los estudios dirigidos a la identificación de nuevos heterómeros que impliquen los receptores D2, permite ampliar la farmacología del sistema dopaminérgico. En esta tesis hemos observado crosstalk funcional entre dos pares de GPCRs: entre D2 y GABAB por un lado, y entre D2 y el receptor-1 de Orexina por otro. Aunque nuestros resultados indican que es muy probable que ambos pares de receptores formen heterómeros, se necesitan más datos para corroborarlo. La DA es crucial en el sistema cerebral de la recompensa, que juega un papel primordial en el fenómeno de la adicción. Está descrito que la administración crónica de cocaína altera la densidad y la afinidad de los receptores D1 y D2, así como también su interacción con otros receptores. En nuestro modelo de auto-administración de cocaína en ratas, hemos encontrado cambios en la respuesta del sistema dopaminérgico al agonista D2 quinpirole, después de la abstinencia de corto y también de largo plazo. En suma, nuestros resultados sobre la administración de cocaína subrayan la importancia del sistema dopaminérgico en la adicción a la cocaína, y además, el crosstalk funcional que hemos observado entre los receptores D2 y otros GPCRs abre nuevas posibilidades para el diseño y desarrollo de nuevos tratamientos para el abuso de drogas así como también para la esquizofrenia.
The dopaminergic system has been the focus of much research during the past several decades mostly because it is believed to be involved in several pathological conditions such as Parkinson’s disease, schizophrenia, Tourette’s syndrome, as well as in drug abuse. All the five subtypes of dopamine (DA) receptors belong to the family of the G-protein coupled receptors (GPCRs). Among them, D2 subtype are the primary target for all known antipsychotic drugs (antagonists) and drugs used to treat Parkinson’s disease (agonists). Unfortunately, the antagonistic effects on D2 receptors also elicit serious side effects. The low liability of side effects of the newest generation of antipsychotics (aripiprazole) is proposed to be based on selective D2 receptor functions, however further evidence is needed to support this hypothesis. In our study, we observed a variable property of aripiprazole on D2 autoreceptors in response to changes of the extracellular DA concentration, which is consistent with the D2 receptor “selective function” opinion. On the other hand, the concept of the heteromerization between colocalized GPCRs has been widely accepted and is suggested to be a new field for therapeutic improvement. Thus, the studies concerning the identification of new pairs of heteromers related to D2 receptors may broaden the pharmacology of the dopaminergic system. In this thesis, we found functional crosstalk in two pairs of GPCRs: between GABAB and D2R, and between orexin-1 and D2R. Although our results indicate the probability of their heteromerization, further studies are still needed. Dopamine is crucial in the brain reward system, which plays an important role in drug addiction. Chronic cocaine administration is widely reported to alter the dopamine D1 and D2 receptor density or affinity, as well as their interaction with other receptors. In our cocaine self-administration model, we found changes in dopamine system in response to the D2R agonist quinpirole in the long-term and short-term withdrawal rats. In conclusion, our results in cocaine administration emphasize the importance of dopamine system in cocaine addiction. Moreover, the functional crosstalk of D2 receptors with others GPCRs may supply new possibilities for developing innovative treatments in drug abuse as well as in schizophrenia.
17
McFadzean, I. "Kappa opioid actions in the rat locus coeruleus in vitro." Thesis, University of Cambridge, 1986. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.233318.
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Intracellular recordings were made from neurones of the rat locus coeruleus (lc) contained within a brain slice maintained in vitro. When applied to the slice in known concentrations, K opioid receptor agonists produced a concentration-dependent, naloxone-reversible depression of the electrically evoked excitatory post-synaptic potential (epsp). This effect of K agonists was observed in the absence of changes in the membrane potential or input resistance of the post-synaptic cell. Similarly, the K agonists had no effect on the tetrodotoxin-resistant action potential waveform. Naloxone antagonised the response to U50488 with an apparent dissociation equilibrium constant (Kd) of 28 nM, consistent with the response being mediated via K opioid receptors. In contrast, u opioid receptor agonists caused a membrane hyperpolarisation concomitant with a fall in neuronal input resistance, and depressed the tetrodotoxin-resistant action potential. These effects were concentration-dependent and antagonised by naloxone; the hyperpolarising action of [D-Ala2 , NMePhe4 , Gly-ol5 ] enkephalin (DAGO) was antagonised by naloxone with a Kd of 1.5 nM. These findings are in agreement with previous reports that u receptor activation increases a potassium conductance in lc neurones. The epsp was depressed, but not abolished, by the excitatory amino acid antagonists, 2-amino-5-phosphonovaleric acid (2APV) and kynurenic acid, suggesting that the epsp was at least partly mediated by an excitatory amino acid. U50488 did not depress the depolarisation produced by local application of L-glutamic acid. In addition to the epsp, a noradrenergic inhibitory post-synaptic potential (ipsp) could be evoked in lc neurones. U50488 depressed the ipsp, but this effect was not reversed by naloxone and therefore not mediated via opioid receptors. U50488 had no effect on the all or nothing depolarising potential which could be evoked in a proportion of lc neurones. The effect of U50488 on the epsp was reduced when experiments were performed in the presence of agents - either barium, quinine or 4-aminopyridine - which block potassium conductances. An in vitro autoradiographic study of 3 H bremazocine binding within the lc revealed that the majority of binding was displaced by a combination of unlabelled DAGO and [D-Ser2 ] Leu enkephalin Threonine (DLSET) and so represented u sites. A significant proportion however, was displaceable by unlabelled U50488 and thus represented K binding sites. It is concluded that K opioid receptors are situated pre-synaptically within the lc and when activated depress excitatory synaptic transmission.
18
Leonard, M. N. "Studies on the potential heterogeneity of D2̲ dopamine receptors from bovine and rat brain." Thesis, University of Nottingham, 1987. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.381474.
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Perron, Amélie. "NTS2 neurotensin receptors : distribution, interactions, and cellular dynamics in model systems and rat brain." Thesis, McGill University, 2006. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=102692.
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Although available evidence suggests that NTS1 receptors play a key role in the transduction of many of the central effects of neurotensin (NT), recent data indicate that the NTS2 subtype may be responsible for mediating NT-induced analgesia. However, little is known about the cellular and molecular mechanisms underlying NTS2 function. It is also unclear whether endogenous NT is an agonist at the NTS2 site and to which second messenger system(s) this receptor is coupled since conflicting data has emerged from studies carried out in systems heterologously expressing the NTS2 receptor. In this context, the overall objective of the present study was to characterize the distribution of the NTS2 protein in rat brain, to further document the role played by NTS2 receptors in antinociception, and to unravel the cellular mechanisms underlying NTS2-mediated transduction of NT's effects. Our immunohistochemical studies revealed that NTS2 receptors are widely expressed within the rat CNS with high densities of labeled neurons and/or processes in descending antinociceptive pathways including the periaqueductal gray (PAG), and the rostroventral medial medulla. Both the full-length and alternatively-spliced isoforms induced a rapid and sustained activation of the mitogen-activated protein kinase (ERK1/2) pathway in both transfected CHO and COS-7 cells upon stimulation with NT. Combined biochemical and confocal microscopic studies revealed that NTS2 receptors were maintained at the cell surface following long-term agonist exposure despite efficient internalization mechanisms. This preservation was neither due to NTS2 neosynthesis nor recycling but rather appeared to involve translocation of spare receptors from intracellular stores as observed in both transfected cells and rat spinal cord neurons. NTS2 was demonstrated to heterodimerize with NTS1 in cells co-transfected with the two receptors. This heterodimerization was found to affect cell surface recruitment of NTS1, making it more similar to that of NTS2. Also, upon prolonged NT stimulation, cell surface NTS1 were more resistant to down-regulation in cells co-expressing NTS1 and NTS2 than in cells expressing NTS1 alone. Such maintenance of NT receptors bioavailability might prove of great importance for the use of NTS2-selective agonists for the treatment of chronic pain.
20
Gerova, Nadezhda [Verfasser]. "Expression of angiotensin receptors in the rat brain after focal cerebral ischemia / Nadezhda Gerova." Berlin : Medizinische Fakultät Charité - Universitätsmedizin Berlin, 2015. http://d-nb.info/1071087770/34.
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21
Prunell, dos Santos Giselle F. "Pathophysiology of subarachnoid hemorrhage in the rat /." Stockholm, 2003. http://diss.kib.ki.se/2003/91-7349-610-3/.
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Gruber, Susanne H. M. "Novel mechanism of action of antipsychotic drugs : effects on neuropeptides in rat brain /." Stockholm : [Karolinska institutets bibliotek], 2002. http://diss.kib.ki.se/2002/91-7349-229-9.
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Alex, Katherine D. "5-HT2C SEROTONIN RECEPTORS: CELLULAR LOCALIZATION AND CONTROL OF DOPAMINERGIC PATHWAYS IN THE RAT BRAIN." Connect to text online, 2007. http://rave.ohiolink.edu/etdc/view?acc%5Fnum=case1164766901.
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Yi, Chenju [Verfasser], and H. J. [Akademischer Betreuer] Schlüsener. "Sweet Taste Receptors in Normal and Pathological Rat Brain / Chenju Yi ; Betreuer: H. J. Schlüsener." Tübingen : Universitätsbibliothek Tübingen, 2011. http://d-nb.info/1161464638/34.
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Woodhall, Gavin Lawrence. "The role of glutamate receptors at the CA3/CA1 Schaffer collateral/commissural synapse of rat hippocampus." Thesis, University of Southampton, 1994. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.295902.
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Chong, Victor Z. Mishra Ram K. "Differential regulation of synapsin II expression by dopamine-D1 and -D2 receptors in the rat brain /." [Hamilton, Ont.] : McMaster University, 2005.
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27
Leventopoulos, Michail. ""Long-term effects of the postnatal environment on brain glia and monoamine receptors in the rat"." Thesis, Roehampton University, 2007. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.515146.
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Evans, Ian Michael. "Maternal hypothyroxinemia and the ontogeny of thyroid hormone nuclear receptors and cholinergic and monoaminergic neurotransmitter systems in developing rat brain." Thesis, University College London (University of London), 2000. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.322515.
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Szigethy, Eva Maria. "Cellular and subcellular radioautographic localization of neurotensin receptors to chemically-identified neuronal subpopulations in the rat brain." Thesis, McGill University, 1989. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=74216.
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Neurotensin (NT) is a putative neurotransmitter, the central actions of which appear to be mediated by specific high affinity binding sites. Radioautographic studies using emulsion-coated sections have selectively localized a major proportion of NT binding sites over nerve cell bodies in the rat midbrain tegmentum and basal forebrain. In the present studies, it was shown that the vast majority of $ sp{125}$I-NT-labeled neurons in the rat midbrain tegmentum were dopaminergic, while those in the magnocellular basal forebrain of both rats and humans were predominantly cholinergic using adjacent-section light microscopic $ sp{125}$I-NT radioautography combined with either tyrosine hydroxylase (TH) immunohistochemistry or acetylcholinesterase (AChE) pharmacohistochemistry. In specific, cell counts demonstrated that 95-100% of TH-immunoreactive neurons in the rat substantia nigra (SN) and 80-90% in the ventral tegmental area (VTA) exhibited dense $ sp{125}$I-NT labeling. In the rat basal forebrain, 65-80% of AChE-positive perikarya in the vertical limb of the diagonal band, 45-60% in the horizontal limb of the diagonal band, and 75-90% in the nucleus basalis magnocellularis demonstrated selective $ sp{125}$I-NT binding sites. Moreover, competition studies using levocabastine, a selective blocker of the low affinity NT binding component, revealed that the vast majority of $ sp{125}$I-NT binding sites labeled in the SN, VTA, and NBM were of the levocabastine insensitive, high affinity type, previously documented to correspond to the physiologically active NT receptor. These data provide an anatomical substrate for NT-dopaminergic interactions in the rat midbrain tegmentum and for NT-cholinergic interactions in the rat and human basal forebrain.Ibotenic acid-induced lesions of the NBM produced a marked reduction in both AChE reactivity and cellular $ sp{125}$I-NT binding suggesting that most of the labeled binding sites detected in this region were indeed associated with cholinergic neurons themselves rather than with impinging afferent terminals. In fact, electron microscopic examination of the distribution of $ sp{125}$I-NT binding sites in the NBM revealed that 84% of labeled sites were inside AChE-positive perikarya and proximal dendrites and presumably represented intracellular receptors undergoing synthesis, transport, and/or degradation. The remainder were evenly dispersed along the plasma membrane of AChE-reactive neurons, but were only rarely concentrated opposite synapsing axon terminals. These latter results are consistent with a paracrine mode of action of NT in influencing the NBM cholinergic system.
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Tiger, Gunnar. "Signal transduction in the brain : modulation of receptor-mediated inositol phospholipid breakdown by potassium and fluoride ions." Doctoral thesis, Umeå universitet, Farmakologi, 1990. http://urn.kb.se/resolve?urn=urn:nbn:se:umu:diva-68968.
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Neurotransmitter receptor types mediating the generation of intracellular signals are of two types; ligand-gated ion channels and G protein coupled receptors. The effector enzyme phosphoinositide-specific phospholipase C (PLC) is modulated by stimulation of G protein coupled receptors, leading to an increased breakdown of inositol phospholipids ("Ptdlns breakdown").In recent years, the receptors in the brain coupled to PLC and modulation of such receptor-mediated Ptdlns breakdown have been characterised. One such modulation is the "potassium effect", whereby an increase in the assay [K+] from 6 to 18 mM potentiates the Ptdlns breakdown response to the muscarinic agonist carbachol in the rat brain. It has been speculated that this effect is one way of enhancing the signal :noise ratio of muscarinic neurotransmission. The mechanisms responsible for the potassium effect have been studied in this thesis.Initial methodological studies indicated that the temperature of the Krebs buffer used after tissue dissection was an important factor regulating the Ptdlns response to receptor stimulation. Expressing the Ptdlns breakdown response as a fraction of the total labelled phosphoinositides was more useful than other ways of expressing the data. Acid extraction of the Lipid fraction was also superior to neutral extraction.Miniprismspreparedfrompig striatum and hippocampus showed qualitative (but not quantitative) similarities with the rat with respect to stimulation by carbachol, noradrenaline and the potassium effect. Dopamine also stimulated Ptdlns breakdown, though probably via a noradrenergic mechanism.The enhancing actions of potassium appeared to be selective for muscarinic Ml-type receptors. Thus glutamate, quisqualate and NaF-stimulated Ptdlns breakdown are not affected by raised [K+].The potassium effect is brought about by two mechanisms. In calcium-free Krebs buffer, the effect could be mimicked by the calcium channel agonist BAY K-8644 and partially antagonised by verapamil. At an assay [Ca2*] of 2.52 mM, however, modulation of calcium uptake had little effect on carbachol-stimulated Ptdlns breakdown at either normal or raised [K+]. The synergy between potassium and carbachol at252 mM Ca?+ is not dependent upon tissue depolarisation perse, since other ways of depolarising the tissue did not enhance the response to carbachol. It is suggested that potassium might have a direct effect on the muscarinic Ml-type receptor - G protein - PLC complex.In order to investigate this possibility, the effect of fluoride ions (which activate G proteins via formation of AlF4) on basal and carbachol-stimulated Ptdlns breakdown was investigated. Fluoride ions inhibited the enhanced breakdown response to carbachol found at raised [K+]. However, this effect is secondary to effects of fluoride on PLC substrate availibility rather than on G protein function.digitalisering@umu
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Ayman, Göher. "Dynamic aspects of the control of excitatory transmission by metabotropic glutamate receptors at cortical synapses of rat brain." Thesis, University of Bristol, 2005. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.414358.
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Nunn, Elizabeth de Fourgerolles. "The characterisation of oestrogen receptors by gel filtration in hormone-sensitive tissues : immature rat uterus, brain and thymus." Thesis, Open University, 1999. http://oro.open.ac.uk/57989/.
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The aims of this project were to investigate the binding characteristics of the cytosolic oestrogen receptor in the uterus, brain and thymus of immature Wistar rats. The specificities of the receptor in the uterus are well established. The specificities of the cytosolic receptor in the uterus and thymus of immature female Wistar rats were tested against a range of steroids and the values found for the thymus compared with those for the uterus. The concentrations and dissociation constant (Kd) of the cytosolic oestrogen receptor were determined in uterus, brain and thymus of male and female rats at 5,18 and 30 days of age. Clomiphene citrate (CC), an oestrogen antagonist/partial agonist, oestradiol (E2), CC+E2 or 4-hydroxyandrostenedione (4-OHA), an aromatase inhibitor, were administered to animals at 15 days in order to study the effects of these compounds on receptor binding characteristics at 30 days. Significant differences in specificity were found between the thymus and uterus, the cytosolic oestrogen receptor in the thymus exhibited significantly higher affinity for corticosterone than it did in the uterus. Male animals were heavier than females at 30 days. Uterus and thymus weights increased exponentially between 5 and 30 days. The tissue-to-body weight ratio increased in uterus between 18 and 30 days and increased in the thymus in both sexes between 5 and 18 days. In males at 30 days, the tissue-to-body weight ratio of the thymus was significantly lower than in females of the same age. Cytosolic oestrogen receptor concentrations in the uterus, brain and thymus differed between some age and/or sex groups. Cytosolic oestrogen receptor concentrations increased exponentially in the uterus between the different age groups. Cytosolic oestrogen receptor concentrations in both thymus and hypothalamus at 5 days were significantly higher in females than in males of the same age group. No differences in cytosolic oestrogen receptor concentrations were found between the sexes in the cortex at 5 and 18 days but at 30 days, receptors were not detectable in this brain area. The Kd for moxestrol, a synthetic oestrogen agonist that is not bound by alphafetoprotein present in the blood of immature rats, was similar in all tissues. E2 and CC+E'-' treatmentsr esulted in decreasedb ody and thymus weight in both sexes,i ncreased uterus weight and decreased thymus weight in both sexes but led to increased uterus weight. CC treatment decreased the concentration of the receptors in the female thymus only-, E2 and CC+E2 treatments decreased the concentratIon of the receptor to levels that were undetectable in hypothalamus and thymus in both sexes, 4-OHA treatment increased thymus weight and cytosolic receptor concentrations in the hypothalamus and thymus of males only. These results suggest that cytosolic oestrogen receptors in uterus, brain and thymus are similar and that sex differences in these tissues are mediated by differential exposure to oestradiol during the early postnatal period. The thymus is crucial to the development of the immune response. The finding that the cytosolic oestrogen receptor differed from the uterus receptor in its affinity for corticosterone and that sex differences in cytosolic oestrogen receptor concentrations were present in the thymus at 5 days could be relevant to the sex dimorphisms that exist in autoirnmune disease manifestation.
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Caberlotto, Laura. "Distribution and regulation of neuropeptide Y and its receptors in the human and rat brain : role in affective disorders /." Stockholm, 1998. http://diss.kib.ki.se/1998/91-628-3310-3.
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Subramaniam, Sabarinath. "Studies on the expression of synaptic terminal proteins and neurotransmitter receptors in the rat brain following amphetamine-induced behavioral sensitization." Thesis, National Library of Canada = Bibliothèque nationale du Canada, 2000. http://www.collectionscanada.ca/obj/s4/f2/dsk3/ftp04/mq64462.pdf.
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Lecours, Maurice. "Electrophysiological Investigations on the Role of Selected Serotonin Receptors and the Serotonin Transporter on Serotonin Transmission in the Rat Brain." Thèse, Université d'Ottawa / University of Ottawa, 2013. http://hdl.handle.net/10393/30400.
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This study assessed the in vivo effects of various serotonin (5-HT) receptor modulators on 5-HT neurotransmission in the rat hippocampus. Vortioxetine, humanized-vortioxetine, and escitalopram blocked the 5-HT transporter, but similar to ipsapirone did not dampen the sensitivity of postsynaptic 5-HT1A receptors. Long-term administration of all treatments increased the tonic activation of postsynaptic 5-HT1A heteroreceptors, an effect common to all antidepressants. Vortioxetine decreased the function of the terminal 5-HT1B autoreceptor under high but not a low degree of activation, thus showing that its partial agonism led to increased 5-HT release and that long-term administration results in the desensitization of terminal 5-HT1B autoreceptors.
Vortioxetine overcame the effects of 5-HT1B and 5-HT3 receptor agonists. This study was unable to determine the involvement of 5-HT7 receptor antagonism exerted by vortioxetine affects 5-HT neurotransmission. Therefore, vortioxetine would appear to exert different actions, via transporter and receptor activity, on the serotonergic system in the hippocampus, consistent with its unique pharmacological profile.
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Apaydin, Serpil. "Effect Of Lipids On Binding Characteristics Of Opioid Receptors." Phd thesis, METU, 2005. http://etd.lib.metu.edu.tr/upload/3/12605971/index.pdf.
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Effect of lipids on binding characteristics of opioid receptors in membranes prepared from rat brain were studied. Lipid concentrations causing changes in specific binding of [3H]Endomorphin-1 (ProE1), an opioid agonist highly specific to mu-type opioid, [3H]Ile5,6deltorphin II (DIDI), an agonist ligand highly specific to delta type receptor and [3H]Naloxone (Nlx), a universal opioid receptor antagonist were determined. Inhibition of [3H]ProE1, [3H]DIDI and [3H]Nlx specific binding was also examined by homologous displacement experiments in the presence and absence of lipids. In order to understand whether the changes occurring in the specific binding is due to changes in equilibrium dissociation constant (KD) or maximum number of binding sites (Bmax), the equilibrium binding experiments were performed.
Arachidonic acid (AA) inhibited binding of both agonist and antagonist ligand in a dose dependent manner with IC50 values of 0.15, 0.1, and 0.6 mM for [3H]ProE1, [3H]DIDI and [3H]Nlx, respectively. Kd values were not affected while Bmax values decreased 38 % and 76 % for mu, and delta receptor subtypes, respectively. For [3H]Nlx, Bmax values decreased 20 and 56 % in the absence and presence of 100 mM NaCl, respectively.
Cholesteryl hemisuccinate (CHS) enhances (100 % of control) ligand binding at mu-sites however no effect was encountered at delta sites. Furthermore, CHS also enhances (50 % of control) the binding of antagonist ligand in the absence of NaCl. Bmax values were increased by 70 % for mu sites and 40% for antagonist ligand binding site. Under similar conditions Kd values were not affected.
Phosphatidic acid (PA) and phosphatidylcholine (PC) exhibited negligible effect on ligand binding. PA decreased specific binding of ProE1 and DIDI by 16 and 10 %, respectively. Specific binding of antagonist ligand Nlx decreased 11 % in the presence of NaCl whereas in the absence of NaCl specific binding is very close to control. In the presence of PC specific binding of both agonist and antagonist ligands were around control values.
In this study modulatory effect of lysophospholipids, lysophosphatidic acid and lysophosphatidylcholine on opioid binding sites were evaluated for the first time. Both lysophospholipids exhibited similar effects: decreasing specific binding in receptor subtype independent manner between 0.1 to 1 mM range. Kd values were not significantly affected, while remarkable decrease (45-75 %) in Bmax values were observed.
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Dwyer, Daniel, and na. "Serotonin as a Mediator of Fatigue During Exercise and Training." Griffith University. School of Health Science, 2004. http://www4.gu.edu.au:8080/adt-root/public/adt-QGU20040521.130535.
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Exercise has been shown to cause an increase in the concentration of brain serotonin (5-hydroxytryptamine, 5-HT) in humans and experimental animals. The increase in brain serotonin coincides with the onset of fatigue and is referred to as "central fatigue". Experiments in humans and animals involving serotonin receptor agonists have demonstrated reductions in exercise performance by simulating the exercise-induced increase in endogenous serotonin. Conversely, the administration of serotonin receptor antagonists has been shown to extend exercise performance in experimental animals, but not in humans. Although the relationship between the concentration of brain serotonin and exercise performance is well described in the literature, the precise effect of central fatigue on muscle function per se is unclear. Furthermore, there appear to be differences in serotonergic function between trained and untrained cohorts. However, it is not clear whether the differences are due to a training adaptation or if the differences are inherent in the individual. In addition, the time course of these adaptations and the mechanisms of adaptation are not known. The initial purpose of this thesis was to determine whether six weeks of endurance exercise training had any effect on central serotonin receptor sensitivity in Wistar rats. The rats ran on a treadmill 4 times per week with 2 exercise tests of endurance performance per week. Receptor sensitivity was determined indirectly, at the end of each training week, by the reduction in endurance performance, under the influence of a 5-HT1a agonist, (m-Chlorophenylpiperazine, m-CPP). Improved tolerance to the fatiguing effects of the serotonin agonist would suggest desensitisation of central serotonin receptors, probably 5-HT1a receptors. Two groups of controls were used to examine, i) the effect of the injection per se on exercise performance and ii) changes in serotonin receptor sensitivity associated with maturation, in the absence of any exercise training. In the training group, undrugged exercise performance significantly improved by 47% after 6 weeks of training (mean ± SEM, 4518 ± 729 s vs. 6640 ± 903 s, p=0.01). Drugged exercise performance also increased significantly from week 1 to week 6 (306 ± 69 s to 712 ± 192 s, p=0.004). Control group results indicated that the dose of m-CPP alone caused fatigue during exercise tests and that maturation was not responsible for any decrease in receptor sensitivity. Endurance training appears to stimulate an adaptive response to the fatiguing effects of increased brain serotonin, which may enhance endurance exercise performance. The purpose of the second set of experiments described in this thesis was to investigate changes in serotonin receptor sensitivity in response to exercise training in human subjects. Twelve male volunteers completed 30 minutes of stationary cycling at 70% of VO2peak, on 3 days per week, for 9 weeks. Serotonin receptor sensitivity was assessed indirectly by measuring the prolactin response to a serotonin receptor agonist (buspirone hydrochloride), using a placebo controlled, blind cross-over design. A sedentary group of control subjects were also recruited to control for possible seasonal variations in serotonin receptor sensitivity. Endurance capacity was also assessed as time to exhaustion while cycling at 60% of VO2peak. The exercise training caused a significant increase in aerobic power (VO2peak, 3.1±0.16 to 3.6±0.15 L.m-1, p< 0.05) and endurance capacity (93±8 to 168±11 min, p<0.05), but there was no change (p>0.05) in the prolactin response to a serotonin agonist. However, 25% of the subjects in the training group demonstrated a decrease in receptor sensitivity, as indicated by a decrease in prolactin response. These results suggest that while the exercise training caused an increase in aerobic power and endurance capacity, there was no measurable change in 5-HT receptor sensitivity. In addition, it is possible that changes in receptor sensitivity may take longer to occur, the training stimulus used in the present investigation was inadequate or that changes occurred in other 5-HT receptor subtypes that were not assessed by the present methodology. The third set of experiments described here, investigated the changes in neuromuscular function under the influence of a serotonin receptor agonist (buspirone hydrochloride). Subjects were administered the agonist or a placebo in a blind cross over design. Measures of neuromuscular function included reaction time (RT), hand eye coordination (HEC), isometric neuromuscular control (INC), maximal voluntary isometric contractile force (MVIC-F), isometric muscular endurance capacity (IMEC) and various electromyographic (EMG) indices of fatigue in biceps brachii. A preliminary experiment was conducted to determine a drug dose that did not cause sedation of the research subjects. The agonist caused a significant (p<0.05) decrease in MVIC-F, INC and IMEC. There was a non significant (p = 0.08) decrease in EMG amplitude during the MVIC-F trial with the agonist, compared to the effect of the placebo. The median EMG frequency during the IMEC test was also significantly less with the agonist, when compared to the placebo effect. There was a decline in RT and HEC, although this was not significant. These findings indicate that a serotonin receptor agonist causes a decrease in neuromuscular function during isometric muscle contractions. The decrements in muscle function reported in this study may help to explain previous reports of an association between increased brain serotonin concentration and a reduction in endurance performance. Although the present study does not exclude the possibility that an increase in brain serotonin does cause fatigue by affecting organs peripheral to the brain, it provides evidence of fatigue within the central nervous system. Further examination of the effect of a serotonin agonist on muscle function during non-isometric muscle contractions is warranted.
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Roulston, Carli L. (Carli Lorraine) 1973. "Localization of both type 2 angiotensin II receptors and a non-angiotensin II binding site by [125 I] CGP42112 in rat brain stem." Monash University, Dept. of Pharmacology, 2001. http://arrow.monash.edu.au/hdl/1959.1/8844.
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Beauvais, Geneviève. "Molecular and cellular bases for the protective effects of dopamine D1 receptor antagonist, SCH23390, against methamphetamine-induced neurotoxicity in the rat brain." Phd thesis, Université René Descartes - Paris V, 2012. http://tel.archives-ouvertes.fr/tel-00691924.
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Methamphetamine (METH) is a potent psychostimulant known to cause cognitive abnormalities and neurodegenerative changes in the brains of METH abusers. One approach for developing therapies for METH abuse is to understand the molecular mechanisms of toxicity of the drug. Investigations in our laboratory and elsewhere have shown that single intraperitoneal injections of METH (30-40 mg/kg of body weight) can cause damage to striatal and cortical monoaminergic systems and induce neuronal apoptosis in the striatum of rodents via activation of endoplasmic reticulum (ER) and mitochondrial death pathways. Hence, the purpose of this thesis was to investigate if toxic binge METH injections can cause ER- and mitochondria-induced stress in the rat striatum. Recent studies have suggested that dopamine (DA) D1 and D2 receptors might mediate neuronal apoptosis in the striatum after single toxic METH doses. We therefore hypothesized that signaling through these two types of DA receptors might activate toxic effects of the binge METH regimen. The role of DA D1 or D2 receptors in METH-induced cell death pathways was thus examined by using pharmacological inhibitors of these receptors. In this dissertation, I report that binge METH regimen caused differential changes in immediate early genes (IEGs) that are known to influence synaptic changes in the brain. METH-induced changed in the expression of the IEGs were dependent on DA D1 receptor stimulation. The second study examined the effects of binge METH on the expression of ER stress- and mitochondrial dysfunction-responsive genes. Pretreatment with the DA D1 receptor antagonist, SCH23390, caused complete inhibition of METH-induced ER and mitochondrial stresses whereas the DA D2 receptor antagonist, raclopride, provided only partial blockade. SCH23390 also blocked METH-induced hyperthermia whereas raclopride failed to do so. Interestingly, both antagonists attenuated METH-induced dopaminergic and serotonergic deficits in the striatum. Moreover, SCH23390 but not raclopride blocked METH-induced serotonergic deficits in cortical tissues. I also found that METH treatment induced upregulation of activin βA mRNA, increased TGF-β and phosphorylated Smad2 proteins in the rat striatum. SCH23390 pretreatment completely blocked all these effects whereas raclopride did not block METH-induced increases in TGF-β expression.
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Bhindi, Amar. "Immuno-histochemical study of somatostatin receptors and the Golgi-associated protein PIST in the rat brain - the cellular and sub-cellular distributions, and their potential implications in receptor regulation." Thesis, McGill University, 2013. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=114438.
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Somatostatin (SOM) is a neuropeptide fulfilling numerous physiological and neuro-modulatory functions throughout the body and brain. Its actions are mediated through a family of G Protein-coupled receptors (GPCRs), designated sst1-5, which are differentially regulated. While in vitro studies have previously demonstrated that the co-expression of several SOM receptor subtypes in cell lines has influence over receptor regulation and trafficking, this has yet to be confirmed in situ. Moreover, SOM receptors carry on their C-terminal ends, PDZ-binding motifs that mediate dynamic interactions between the receptors and various scaffolding and accessory proteins that also contain PDZ-binding motifs. For example, the "Protein Interacting Specifically with Tc10", abbreviated PIST, is a Golgi-associated chaperone that has been implicated in the cell surface targeting of sst5. The goal of my Master's thesis is to clarify, in situ, the regional and sub-cellular distributions of the sst2a and sst5 receptors, as well as the PDZ protein PIST, in the rat Basal Forebrain (BF). In the first portion of my thesis, I set out to identify, using stereology based quantification methods, neuronal populations co-expressing sst2a and sst5. Within the BF, 72% of SOM receptor expressing neurons co-expressed both sst2a and sst5. However, when qualitatively analyzed at the sub-cellular level, sst2a and sst5 did not co-localize to the same organelle compartments. In the second part of my project, I semi-quantitatively examined the sub-cellular distribution of PIST in nuclei of the BF. I found that the majority of immuno-labeled neurons (57% within the Olfactory Tubercle, 84% in the Ventral Pallidum and 82% in the horizontal limb of the diagonal band of Broca) presented a dispersed and granular pattern of of PIST distribution, where the chaperone localized primarily to punctate organelles that were separate from markers for the Trans-Golgi. Finally, I employed stereology-based methods to quantify the proportions of sst5-containing neurons that co-express the PIST chaperone. Though sst5 and PIST were found co-expressed in 46% of immuno-labeled neurons of the BF, their sub-cellular distributions indicated no overt signs of co-localization at the organelle level. In summary, past in vitro studies have shown that the intracellular trafficking of SOM receptors may be regulated through the expression of multiple SOM receptor subtypes, as well as through interactions with PDZ-motif containing chaperones, like PIST. My anatomical project suggests that the regional and subcellular distributions of SOM receptors and PIST in situ may be conducive to these models of regulation.La Somatostatine (SOM) est un neuropeptide ayant de nombreuses fonctions physiologiques et neuro-modulatrices dans tout le corps et le cerveau. Ses actions sont contrôlées par une famille de récepteurs couplés aux protéines-G (GPCR), désignés sst1-5, et qui sont régulés différemment. Alors que des études in vitro ont déjà démontré que la co-expression de plusieurs sous-types du récepteur SOM dans des lignées cellulaires a une influence sur la régulation et le trafic du récepteur, cela reste encore à être confirmé in situ. De plus, les récepteurs SOM contienent, aux C-terminaux, des motifs de liaison PDZ qui interviennent dans les interactions dynamiques entre les récepteurs et des protéines d'échafaudages, et des accessoires qui contiennent également des motifs de liaison PDZ. Par exemple, le chaperon «Protein Interacting Specifically with Tc10», PIST, une est protéine associée à l'appareil de Golgi, et impliqué dans le ciblage, au niveau de la surface-cellulaire, des récepteurs neuropeptidique, tel que le sst5. Le but de ma thèse de maîtrise est de clarifier in situ la répartition régionale et sous-cellulaire de sst2a et sst5, ainsi de que PIST, dans le cerveau antérieur basal (BF) chez le rat. Dans la première partie de ma thèse, j'ai identifié, en utilisant des méthodes de quantifications stéréologiques, les populations neuronales qui co-expriment sst2a et sst5. Dans le BF, 72% des neurones exprimant des récepteurs SOM ont co-exprimé sst2a et sst5. Cependant, quand ils ont été analysés qualitativement au niveau sous-cellulaire, sst2a et sst5 n'ont pas été trouvés co-localisés dans les mêmes organelles.Dans la deuxième partie de mon projet, j'ai examiné semi-quantitativement la distribution sous-cellulaire de PIST dans les noyaux du BF. J'ai trouvé que la majorité des neurones immuno-marqués (57% dans le tubercule olfactif, 84% dans le pallidum ventral et 82% dans la branche horizontale de la bande diagonale de Broca) ont présenté une distribution de PIST dispersée et granulaire qui ressemble à des compartiments vésiculaires et qui sont séparés des marqueurs du trans-Golgi. Finalement, j'ai employé des méthodes stéréologiques pour quantifier les proportions des neurones contenant le sst5 qui co-expriment le chaperon PIST. Bien que sst5 et PIST ont été trouvés co-exprimés dans 46% des neurones immuno-marqués de la BF, leurs distributions sous-cellulaires n'indiquent pas des signe de co-localisation au niveau des organelles. En résumé, des études precédentes in vitro ont montré que le trafic intracellulaire des récepteurs SOM peut être régulé par l'expression de plusieurs sous-types de récepteurs SOM, ainsi que par des interactions avec des chaperons-PDZ comme PIST. Mon projet anatomique in situ suggère que la répartition régionale et sous-cellulaire des récepteurs SOM et PIST favorise ces modèles de régulation.
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Uys, Joachim De Klerk. "The effects of early life trauma on the neurochemistry and behaviour of the adult rat." Thesis, Link to the online version, 2006. http://hdl.handle.net/10019/1249.
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Lafaille, Francine. "Characterization of [125I]7-amino-8-iodo-ketanserin binding and comparative effects of long-term treatment with anxiolytic and antidepressant drugs on serotonin type 2 and beta-adrenergic receptors in rat brain." Thesis, McGill University, 1991. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=60548.
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Changes to 5-HT$ sb2$ receptors in rat brain following antidepressant and anxiolytic treatment were investigated. The B$ sb{ rm max}$ of ($ sp{125}$I) AMIK was found to be decreased significantly in rat fronto-parietal cortex after 21 days administration of antidepressant drugs including desmethylimipramine (30%), buspirone (47%) and adinazolam (17%). The anxiolytic drug, diazepam, which is devoid of intrinsic antidepressant action, did not significantly change the binding parameters. In comparison to 5-HT$ sb2$ receptors, the beta-adrenoceptors labelled by ($ sp{125}$I) cyanopindolol in membrane binding were decreased only by desmethylimipramine, with a 17% reduction in B$ sb{ rm max}$. Data from in-vitro quantitative autoradiography suggests that ($ sp{125}$I) AMIK binding to 5-HT$ sb2$ receptors is decreased in frontal and parietal cortices following 21 days administration of DMI, amitryptiline, gepirone and adinazolam. The results from the present study strongly suggest that the 5-HT$ sb2$ receptor is involved in depressive disorders. Since some of the antidepressant drugs tested possess anxiolytic activity after prolonged administration, 5-HT$ sb2$ receptors may also be important in anxiety disorders.
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Balaños, Guzman Carlos Alberto. "The effects of the kappa agonist U-50,488 on morphine-induced place preference conditioning and Fos immunoreactivity in the preweanling and periadolescent rat." CSUSB ScholarWorks, 1995. https://scholarworks.lib.csusb.edu/etd-project/1074.
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The effects of the kappa opioid agonist U-50,488 on morphine-induced condtioned place preference (CPP), locomotor activity and Fos immunoreactivity and assessed in 10-, 17- and 35-day old rats. It was predicted that kappa agonist treatment would block the unconditioned and conditioned behaviors produced by morhine (a mu opioid receptor agonist).
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Degoulet, Mickaël. "Implication de la neurotransmission glutamatergique dans la sensibilisation comportementale à court terme aux amphétamines." Thesis, Aix-Marseille 2, 2010. http://www.theses.fr/2010AIX20673.
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Bien que la neurotransmission glutamatergique joue un rôle pivot dans le développement et l’expression de la sensibilisation comportementale aux amphétamines, le rôle spécifique de certaines structures glutamatergiques qui projettent sur l’aire tegmentale ventrale et/ou le noyau accumbens n’est pas encore bien caractérisé. Nous montrons que l’hippocampe dorsal, la partie prélimbique du cortex préfrontal et l’amygdale basolatérale joue un rôle prépondérant dans les réponses locomotrices induites par l’administration aiguë (développement de la sensibilisation) et chronique (expression de la sensibilisation) d’amphétamines, suggérant les réponses locomotrices aux amphétamines impliquent un ensemble de structures glutamatergiques corticolimbiques. Par la suite, nous nous sommes intéressés au rôle de la neurotransmission glutamatergique associée aux récepteurs NMDA dans le noyau accumbens, qui est considéré comme le noyau clé de l’expression de la sensibilisation, sur le développement à court terme de la sensibilisation aux amphétamines. De plus, nous montrons le développement de la sensibilisation à court terme aux amphétamines requiert l’activation concomitante de certains récepteurs NMDA au glutamate et nicotiniques à l’acétylcholine dans le noyau accumbens. De plus, l’activation concomitante de ces récepteurs sous tend également la libération de dopamine induite par les amphétamines dans le noyau accumbens. L’ensemble de ces données montre que la neurotransmission glutamatergique, et les structures glutamatergiques qui projettent sur l’aire tegmentale ventrale et/ou le noyau accumbens, joue un rôle majeur dans la sensibilisation comportementale à court terme aux amphétaminesAlthough it is well admitted that the glutamatergic neurotransmission plays a pivotal role in the development and expression of behavioral sensitization to amphetamine, the specific role of glutamatergic structures that project to the ventral tegmental and/or the nucleus accumbens is less well studied. We showed that the dorsal hippocampus, the prelimbic part of the prefrontal cortex and the basolateral amygdala play a critical role in both acute (development of sensitization) and chronic (expression of sensitization) locomotor responses induced by amphetamine, suggesting that behavioral responses to amphetamine are mediated by circuitry of corticolimbic glutamatergic structures. Next, we investigated the role of glutamatergic NMDA receptors contained in the nucleus accumbens, which is seen as the key structure for the expression of sensitization, in the development of short term sensitization to amphetamine. Interestingly, we showed that, contrasting with the current dichotomous thinking that has attributed specialized functions to the ventral tegmental area and the nucleus accumbens, respectively in the development and the expression of behavioral sensitization, concomitant activation of certain types of NMDA and nicotinic receptors in the nucleus accumbens is also required for the development of short term sensitization. Furthermore, we showed that concomitant activation of these receptors sustained the amphetamine-induced dopamine release in the nucleus accumbens. All these data show that glutamatergic neurotransmission, and glutamatergic structures which project onto mésoaccumbens system, plays a major role in short-term behavioral sensitization to amphetamine
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Tsai, Ping-Ju, and 蔡秉儒. "Lysophosphatidic acid receptors mediate the reduction of rat brain infarct volume." Thesis, 2011. http://ndltd.ncl.edu.tw/handle/30148483572729274704.
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碩士國立中山大學
生物科學系研究所
99
Abstract Stroke is a potentially lethal cerebrovascular event. Many research studies devoted to the treatment of stroke. In a recent study, sphingosine-1-phosphate (S1P) has the function of reducing the brain infarct volume. However, no study has yet demonstrated that lysophosphatidic acid (LPA) has this function. LPA and S1P are thought to be the two functionally important LPLs with high structural similarity. Although the neuroprotective function of S1P in TIA rat was confirmed, the effects of LPA on the brain damage after ischemic stroke of animal remain unclear. In this study we evaluated the neuroprotective effects of LPA1/3 receptor agonist (VPC31143; VPC) on rat brains subjecting to permanent middle cerebral artery occlusion (PMCAO). A reliable surgical model of rat PMCAO was first established. Thereafter, the animals were divided into control, vehicle, high-dose VPC, and low-dose VPC groups. The vehicle group received intraperitoneal (i.p.) injection of 3% bovine serum albumin (BSA; 1 ml/kg) 30 minutes after PMCAO surgery. The high-dose VPC and the low-dose VPC group respectively received 0.8 mg/kg and 0.25 mg/kg of i.p. injection of VPC (in 3% BSA) 30 minutes after PMCAO surgery. The mortality rate, infarct volume ratio, and the neurobehavioral outcome were measured 24 hours after PMCAO and statistically analyzed for the difference between treatments. Analyses of the experimental results showed that VPC treatment significantly reduced the mortality rate and the infarct volume ratio of the rats 24 hours after PMCAO. The neurobehavioral scores also showed the improved outcome in stroke rats treated with VPC. The beneficial effect of VPC to the ischemic brain was thought to be mediated through the PI3K signal transduction pathway. Further studies at the transcriptional and the translational levels will further confirm this postulation.
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Jensen, Abigail M. "Cellular and molecular characterization of glutamate receptors in rat brain glia." 1992. http://catalog.hathitrust.org/api/volumes/oclc/28727758.html.
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Waldvogel, Henry J. "GABAA receptors in the basal ganglia of the rat, baboon and the human brain." 2000. http://hdl.handle.net/2292/3329.
Full textAbstract:
Whole document restricted, see Access Instructions file below for details of how to access the print copy.The regional, cellular and subcellular distribution of GABAA receptors was investigated in the striatum and globus pallidus of the rat, baboon and human brain using receptor autoradiography, and multiple immunohistochemical labelling techniques at the light, confocal and electron microscopic levels using antibodies to the α1, α2, α3, β2,3 and γ2-subunits of the GABAA receptor complex. The results demonstrated that GABAA receptors in the striatum showed considerable subunit heterogeneity in their regional (primate brain) and cellular distribution (rodent and primate brain). At the regional level in the baboon and human brain, GABAA receptors in the striosome compartment contained the α2, α3, β2,3 and γ2-subunits while receptors in the matrix compartment contained the α1, α2, α3, β2,3 and γ2-subunits In general terms in both the rodent and the primate brain, up to six different types of neurons were identified in the striatum. There was considerable species diversity in the cell types. Two main types of neurons (type 1 and type 2) immunoreactive for the subunits α1,β2,3,γ2 were identified in the striatum. They were GAD positive and were classified according to their cellular morphology and staining properties; rat type 1 neurons were GAD positive only, while human type 1 neurons were GAD and parvalbumin positive. Type 2 neurons were identified in both the rat (GAD positive only) and in human (GAD and calretinin positive). All three mammalian species showed the presence of type 3 neurons which were large neurons with few spines and immunoreactive for subunits α1,3,β2,3,γ2. Type 4 neurons were calbindin positive and immunoreactive for subunits α2,3,β2,3,γ2. The remaining neurons were immunoreactive for ChAT and the α3-subunit (type 5), or immunoreactive for neuropeptide Y with no GABAA receptor subunit immunoreactivity (type 6). The globus pallidus contained three types of neurons; type 1 neurons contained parvalbumin and type 2 contained parvalbumin and calretinin and both were immunoreactive for subunits α1,β2,3, γ2 while type 3 neurons were medium-sized calretinin neurons immunoreactive for the subunits α1,β2,3,γ2 At the ultrastructural level in the globus pallidus, α1 and β2,3-subunits were localised on large neurons (types 1 and 2) and were found at three types of synaptic terminals. These results show that the subunit composition of GABAA receptors displays considerable regional and cellular variation in the striatum, but is more homogeneous in the globus pallidus.
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"Gonadal hormones, glutamate receptors and morphine-induced immediate early genes in the rat brain." Tulane University, 1999.
Find full textAbstract:
Studies have suggested sex differences in the neural response to drugs of abuse. Previous studies have shown that morphine induces immediate early gene (IEG) expression in the brain and this is reduced by administration of the N-methyl-D-aspartate receptor antagonist, dizocilpine maleate (MK-801). This study looked at the role played by glutamate in morphine-induced IEG expression in the brain and determined if this IEG induction is sexually dimorphic. These experiments also tested if gonadal hormones modulate glutamate receptors and alter behavioral and IEG responses to morphine and MK-801 In this dissertation, the following findings are reported. Morphine induced c-Fos expression in the dorsomedial caudate-putamen (CPu) and in the midline-intralaminar nuclei of the thalamus. Morphine caused a significantly greater expression of c-Fos in the CPu in intact males than in females, and castration with or without hormone-replacement did not eliminate this sex difference. MK-801 inhibited the morphine-induced IEG expression in the CPu in a sexually dimorphic manner, and this sex difference was eliminated by castration of males and restored by administration of gonadal steroids. Ovariectomy with or without estrogen replacement did not alter the ability of MK-801 to completely block the morphine-induced IEG expression in the CPu. MK-801 alone caused a robust induction of c-Fos in the midline-intralaminar thalamic nuclei in females as opposed to a negligible induction in males and this sex difference was independent of gonadal steroids. Significant behavioral sex differences were also seen in response to MK-801, with females showing far greater hyperactivity as compared to males; gonadal hormones did not appear to influence these behavioral responses. Ovariectomy decreased immunoreactivity of the GluR2 subunit of the AMPA receptor in the striatum, whereas no changes were seen in immunoreactivity of the NR1 subunit of the NMDA receptor These results suggest that the responses to both morphine and NMDA receptor antagonists differ between the sexes and emphasize that glutamate is involved in morphine-induced immediate early gene expression in the brain. These findings indicate that sex differences in response to morphine and MK-801 may be mediated by sex-steroid dependent and independent mechanisms and thus have important implications in treatment outcomes of drug addictionacase@tulane.edu
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Kirouac, Gilbert J. "An in vitro autoradiographic investigation of dopamine receptors in the brain of the spontaneously hypertensive rat." 1992. http://hdl.handle.net/1993/17507.
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Wu, Chun-Hung, and 吳俊宏. "Distribution of neuropeptide FF (NPFF) receptors in correlation with morphine-induced reward in the rat brain." Thesis, 2010. http://ndltd.ncl.edu.tw/handle/70427526970631831291.
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博士國防醫學院
生命科學研究所
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Neuropeptide FF (NPFF) exhibited anti-/pro-opioid effects when centrally injected. It was proved to bind to its own receptors, namely NPFF1 and NPFF2 receptors, but did not bind to opioid receptors. In our previous study, we found that intra- cerebroventricularly (i.c.v.) injected NPFF suppressed morphine-induced conditioned place preference (CPP) in rats, which indicated that NPFF may play a role in the modulation of morphine-induced reward. In the present study, we further investigated the action site of NPFF to attenuate morphine-induced reward. Bilateral intra-VTA (ventral tegmental area) and intra-NAc (nucleus accumbens) injections of NPFF both blocked the CPP caused by morphine in rats. This suggests that NPFF may act at both VTA and NAc to inhibit the sensitization of the mesocorticolimbic dopaminergic pathway. Neurochemical analyses support that NPFF may act through the inhibition of the mesocorticolimbic dopaminergic activity increased by morphine, which is believed to cause rewarding. In addition, we also determined the distribution of NPFF receptors in the CNS (central nervous system) of rat. Our results showed that both NPFF receptors were abundantly expressed in VTA and spinal cord but less in NAc. The NPFF2 receptor was demonstrated to have two forms of variants in many brain regions, including the VTA and the NAc. However, these variants were not observed in the spinal cord. In fluorescent immunohistochemical staining, our results revealed that NPFF1 and NPFF2 receptors could be expressed at the TH (tyrosine hydroxylase)- or GAD67 (glutamic acid decarboxylase-67)-positive neurons in VTA, whereas some of them were present in the TH- or GAD67-negative neurons. This implies a possible function of NPFF to modulate dopaminergic neurons directly and a possible indirect action of NPFF on GABAergic neurons to modulate dopamine release. Taken together, our study should be helpful for clarifying the possible mechanisms of NPFF system to modulate morphine-induced reward.