Relevant bibliographies by topics / Mice – Nervous system

Academic literature on the topic 'Mice – Nervous system'

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Published: 4 June 2021
Last updated: 7 February 2022

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Journal articles on the topic "Mice – Nervous system"

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Serrano-Caballero, JM, AM Molina, AJ Lora, JM Serrano-Rodriguez, F. Pena, and MR Moyano. "Evaluation of different central nervous system depressors combined with ketamine for anaesthesia in mice." Veterinární Medicína 58, No. 7 (August 20, 2013): 364–72. http://dx.doi.org/10.17221/6917-vetmed.

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The aim of this study was to compare some depressors of the central nervous system combined with ketamine in order to find an adequate scombination for anaesthesia in mice, coupled with a simple, easy to use and reliable method. Forty Swiss OF-1 mice (Mus musculus), 20 females and 20 males with a body weight from 35 to 45 g aged from 12 to 16 weeks, were used to evaluate one of the following central nervous system depressors (CNSD): acepromazine (5 mg/kg), diazepam (5 mg/kg), medetomidine (1 mg/kg), midazolam (5 mg/kg) and xylazine (10 mg/kg) combined with the dissociative anaesthetic ketamine (100 mg/kg) by the intraperitoneal route. Different parameters were evaluated at regular intervals to assess the depth of anaesthesia (time of induction, time of loss and recovery of pedal withdrawal reflex, time of recovery from the anaesthesia), and respiratory and heart rate and oxygen saturation. Most of the assessment times and physiological parameters were exhibited earlier in females than in males but, in most cases, these differences were not significant. The diazepam combination resulted in death in half of the male group. Significant differences for the combination comparison were found for induction, pedal withdrawal reflex and recovery from anaesthesia, as well as for respiratory and heart rate and oxygen saturation. The best results for mice of both genders, i.e. induction, maintenance and recovery from anaesthesia were more stable with &alpha;<sub>2</sub>-agonists than with other combinations (benzodiazepines or acepromazine), which did not reach a good anaesthetic level, that is, an adequate anaesthetic plane with an absence of the pedal withdrawal reflex and the maintenance of stable vital constants. &nbsp;
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Tallini, Yvonne N., Bo Shui, Kai Su Greene, Ke-Yu Deng, Robert Doran, Patricia J. Fisher, Warren Zipfel, and Michael I. Kotlikoff. "BAC transgenic mice express enhanced green fluorescent protein in central and peripheral cholinergic neurons." Physiological Genomics 27, no. 3 (December 2006): 391–97. http://dx.doi.org/10.1152/physiolgenomics.00092.2006.

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The peripheral nervous system has complex and intricate ramifications throughout many target organ systems. To date this system has not been effectively labeled by genetic markers, due largely to inadequate transcriptional specification by minimum promoter constructs. Here we describe transgenic mice in which enhanced green fluorescent protein (eGFP) is expressed under the control of endogenous choline acetyltransferase (ChAT) transcriptional regulatory elements, by knock-in of eGFP within a bacterial artificial chromosome (BAC) spanning the ChAT locus and expression of this construct as a transgene. eGFP is expressed in ChATBAC-eGFP mice in central and peripheral cholinergic neurons, including cell bodies and processes of the somatic motor, somatic sensory, and parasympathetic nervous system in gastrointestinal, respiratory, urogenital, cardiovascular, and other peripheral organ systems. Individual epithelial cells and a subset of lymphocytes within the gastrointestinal and airway mucosa are also labeled, indicating genetic evidence of acetylcholine biosynthesis. Central and peripheral neurons were observed as early as 10.5 days postcoitus in the developing mouse embryo. ChATBAC-eGFP mice allow excellent visualization of all cholinergic elements of the peripheral nervous system, including the submucosal enteric plexus, preganglionic autonomic nerves, and skeletal, cardiac, and smooth muscle neuromuscular junctions. These mice should be useful for in vivo studies of cholinergic neurotransmission and neuromuscular coupling. Moreover, this genetic strategy allows the selective expression and conditional inactivation of genes of interest in cholinergic nerves of the central nervous system and peripheral nervous system.
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Glatzel, Markus, and Adriano Aguzzi. "PrPC expression in the peripheral nervous system is a determinant of prion neuroinvasion." Journal of General Virology 81, no. 11 (November 1, 2000): 2813–21. http://dx.doi.org/10.1099/0022-1317-81-11-2813.

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Transmissible spongiform encephalopathies are often propagated by extracerebral inoculation. The mechanism of spread from peripheral portals of entry to the central nervous system (neuroinvasion) is complex: while lymphatic organs typically show early accumulation of prions, and B-cells and follicular dendritic cells are required for efficient neuroinvasion, actual entry into the central nervous system occurs probably via peripheral nerves and may utilize a PrPC-dependent mechanism. This study shows that transgenic mice overexpressing PrPC undergo rapid and efficient neuroinvasion upon intranerval and footpad inoculation of prions. These mice exhibited deposition of the pathological isoform of the prion protein (PrPSc) and infectivity in specific portions of the central and peripheral sensory pathways, but almost no splenic PrPSc accumulation. In contrast, wild-type mice always accumulated splenic PrPSc, and had widespread deposition of PrPSc throughout the central nervous system even when prions were injected directly into the sciatic nerve. These results indicate that a lympho-neural sequence of spread occurs in wild-type mice even upon intranerval inoculation, while overexpression of PrPC leads to substantial predilection of intranerval over lymphoreticular spread. The rate of transport of infectivity in peripheral nerves was ca. 0·7 mm per day, and prion infectivity titres of sciatic nerves were much higher in tga20 than in wild-type mice, suggesting that overexpression of PrPC modulates the capacity for intranerval transport.
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Osterloh, Anke, Stefanie Papp, Kristin Moderzynski, Svenja Kuehl, Ulricke Richardt, and Bernhard Fleischer. "Persisting Rickettsia typhi Causes Fatal Central Nervous System Inflammation." Infection and Immunity 84, no. 5 (March 14, 2016): 1615–32. http://dx.doi.org/10.1128/iai.00034-16.

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Rickettsioses are emerging febrile diseases caused by obligate intracellular bacteria belonging to the familyRickettsiaceae. Rickettsia typhibelongs to the typhus group (TG) of this family and is the causative agent of endemic typhus, a disease that can be fatal. In the present study, we analyzed the course ofR. typhiinfection in C57BL/6 RAG1−/−mice. Although these mice lack adaptive immunity, they developed only mild and temporary symptoms of disease and survivedR. typhiinfection for a long period of time. To our surprise, 3 to 4 months after infection, C57BL/6 RAG1−/−mice suddenly developed lethal neurological disorders. Analysis of these mice at the time of death revealed high bacterial loads, predominantly in the brain. This was accompanied by a massive expansion of microglia and by neuronal cell death. Furthermore, high numbers of infiltrating CD11b+macrophages were detectable in the brain. In contrast to the microglia, these cells harboredR. typhiand showed an inflammatory phenotype, as indicated by inducible nitric oxide synthase (iNOS) expression, which was not observed in the periphery. Having shown thatR. typhipersists in immunocompromised mice, we finally asked whether the bacteria are also able to persist in resistant C57BL/6 and BALB/c wild-type mice. Indeed,R. typhicould be recultivated from lung, spleen, and brain tissues from both strains even up to 1 year after infection. This is the first report demonstrating persistence and reappearance ofR. typhi, mainly restricted to the central nervous system in immunocompromised mice.
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Girard, Sophie, Thérèse Couderc, Josette Destombes, Danièle Thiesson, Francis Delpeyroux, and Bruno Blondel. "Poliovirus Induces Apoptosis in the Mouse Central Nervous System." Journal of Virology 73, no. 7 (July 1, 1999): 6066–72. http://dx.doi.org/10.1128/jvi.73.7.6066-6072.1999.

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ABSTRACT Poliovirus (PV) is the etiological agent of human paralytic poliomyelitis. Paralysis results from the destruction of motoneurons, a consequence of PV replication. However, the PV-induced process leading to the death of motoneurons is not well known. We investigated whether PV-induced central nervous system (CNS) injury is associated with apoptosis by using mice as animal models. Transgenic mice expressing the human PV receptor were infected intracerebrally with either the neurovirulent PV-1 Mahoney strain or a paralytogenic dose of the attenuated PV-1 Sabin strain. Nontransgenic mice were infected with a mouse-adapted PV-1 Mahoney mutant. DNA fragmentation was demonstrated in CNS tissue from paralyzed mice by visualization of DNA oligonucleosomal laddering and by enzyme-linked immunosorbent assay. Viral antigens and DNA fragmentation detected by the in situ terminal deoxynucleotidyltransferase-mediated dUTP-biotin nick end-labeling technique were colocalized in neurons of spinal cords from paralyzed mice. In addition, morphological changes characteristic of cells undergoing apoptosis were observed in motoneurons by electron microscopy. Thus, we show that PV multiplication and CNS injury during paralytic poliomyelitis are associated with apoptosis.
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Grote, Caleb W., Anna L. Groover, Janelle M. Ryals, Paige C. Geiger, Eva L. Feldman, and Douglas E. Wright. "Peripheral nervous system insulin resistance in ob/ob mice." Acta Neuropathologica Communications 1, no. 1 (2013): 15. http://dx.doi.org/10.1186/2051-5960-1-15.

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Öztürk, Nilgün, K. Hüsnü Can Başer, Süleyman Aydin, Yusuf Öztürk, and Ihsan Çaliş. "Effects ofGentiana luteassp.symphyandraon the Central Nervous System in Mice." Phytotherapy Research 16, no. 7 (October 30, 2002): 627–31. http://dx.doi.org/10.1002/ptr.998.

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Nobel, T. A., A. Nyska, M. Pirak, M. Skolnik, and A. Meshorer. "Epidermoid cysts in the central nervous system of mice." Journal of Comparative Pathology 97, no. 3 (May 1987): 357–59. http://dx.doi.org/10.1016/0021-9975(87)90101-0.

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Hao, Wei, Cuiui Wang, Jia Song, Ping Zhao, and Gang Li. "The effects of nanofatty acids on the nervous system." Materials Express 10, no. 11 (November 1, 2020): 1831–35. http://dx.doi.org/10.1166/mex.2020.1837.

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To investigate the effect of polyunsaturated fatty acids (nanofatty acids) on the nervous system, 90 clean female mice aged 3?5 weeks old were randomly divided into two groups (n = 45). The experimental group was injected with nanofatty acids once every other day for a total of three times, while the control group was injected with the same volume of normal saline. The behavior, weight, plasma, malondialdehyde content in the brain homogenate, and total superoxide disodium alcohol were assessed after the treatments. Mice treated with nanofatty acid were easily provoked, hyperactive, and had significantly reduced body weight as compared to the control mice (P <0.05). These findings suggest that polyunsaturated fatty acid can reduce the levels of lipid peroxidation and the activity of total superoxide dismutase in mice. Our results suggest that nanofatty acid exposure has a protect effect on the nervous system.
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Harroch, S., M. Palmeri, J. Rosenbluth, A. Custer, M. Okigaki, P. Shrager, M. Blum, J. D. Buxbaum, and J. Schlessinger. "No Obvious Abnormality in Mice Deficient in Receptor Protein Tyrosine Phosphatase β." Molecular and Cellular Biology 20, no. 20 (October 15, 2000): 7706–15. http://dx.doi.org/10.1128/mcb.20.20.7706-7715.2000.

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ABSTRACT The development of neurons and glia is governed by a multitude of extracellular signals that control protein tyrosine phosphorylation, a process regulated by the action of protein tyrosine kinases and protein tyrosine phosphatases (PTPs). Receptor PTPβ (RPTPβ; also known as PTPζ) is expressed predominantly in the nervous system and exhibits structural features common to cell adhesion proteins, suggesting that this phosphatase participates in cell-cell communication. It has been proposed that the three isoforms of RPTPβ play a role in regulation of neuronal migration, neurite outgrowth, and gliogenesis. To investigate the biological functions of this PTP, we have generated mice deficient in RPTPβ. RPTPβ-deficient mice are viable, are fertile, and showed no gross anatomical alterations in the nervous system or other organs. In contrast to results of in vitro experiments, our study demonstrates that RPTPβ is not essential for neurite outgrowth and node formation in mice. The ultrastructure of nerves of the central nervous system in RPTPβ-deficient mice suggests a fragility of myelin. However, conduction velocity was not altered in RPTPβ-deficient mice. The normal development of neurons and glia in RPTPβ-deficient mice demonstrates that RPTPβ function is not necessary for these processes in vivo or that loss of RPTPβ can be compensated for by other PTPs expressed in the nervous system.
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Dissertations / Theses on the topic "Mice – Nervous system"

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Tsao, Jack W. "Wallerian degeneration in normal mice and in mutant C57BL/Wld mice." Thesis, University of Oxford, 1994. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.260174.

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Liu, Hern Choon Eugene. "The central nervous system effects of nocistatin : behavioral effects in mice." Thesis, University of Cambridge, 2008. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.611850.

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Andersson, Sandra. "Nuclear receptor functions in the central nervous system clues for knockout mice /." Stockholm, 2006. http://diss.kib.ki.se/2006/91-7140-661-1/.

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Simpson, Matthew Thomas W. "Caspace-3 deficiency rescues peripheral nervous system defect in pRb nullizygous mice." Thesis, University of Ottawa (Canada), 2002. http://hdl.handle.net/10393/6297.

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The retinoblastoma tumour suppressor protein, pRb, is a key regulator of cell cycle and has been implicated in the terminal differentiation of neuronal cells. Mice nullizygous for pRb die by E14.5 from haematopoietic and neurological defects attributed to failed differentiation (Jacks et al., 1992; Lee et al., 1992; Clarke et al., 1992). Previous studies by Macleod et al., (1996) have demonstrated that the loss of p53 protects pRb-deficient central nervous system (CNS) neurons but not peripheral nervous system (PNS) neurons from cell death. Thus, the mechanisms by which PNS neurons undergo apoptosis in response to pRb deficiency remain unknown. In view of the pivotal role of caspase-3 in the regulation of neuronal apoptosis during development, we examined its function in the execution of the widespread neuronal cell death induced by pRb deficiency. Our results support a number of conclusions: First, we show that caspase-3 becomes activated in all neuronal populations undergoing apoptosis. Second, caspase-3 deficiency does not extend the life span of pRb null embryos, as double null mutants exhibit high rates of liver apoptosis resulting in erythropoietic failure. Third, pRb/caspase-3 double mutant neurons of the CNS exhibit widespread apoptosis similar to that seen in pRb mutants alone, thus caspase-3 deficiency does not protect this population from apoptosis. Finally, in contrast to the CNS, neurons of the PNS including those comprising the trigeminal ganglia (TG) and the dorsal root ganglia (DRG) are protected from apoptosis in pRb/caspase-3 double mutant embryos. Examination of the mechanistic differences between these two cell types revealed that CNS neurons invoke compensatory caspase activity that is not found in PNS neurons. These findings suggest that PNS neurons are dependent upon caspase-3 for the execution of apoptosis and that caspase-3 may serve as a key therapeutic target for neuroprotection following injury of this cell type.
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Lamprianou, Smaragda. "Biological role of nervous system tyrosine phosphatases revealed by analysis of KO mice." Paris 6, 2007. http://www.theses.fr/2007PA066107.

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Le but de ma thèse a été de déterminer le rôle biologique des récepteurs tyrosine phosphatases, -RPTPzeta, et RPTPgamma,- dans le système nerveux, par l’utilisation de souris knockout. Alors que notre laboratoire a précédemment mis en évidence le rôle de RPTP dans la réparation et la myélinisation lors de lésions, nous avons démontré qu’une des formes solubles de RPTP inhibe la prolifération des oligodendrocytes précurseurs. De plus, nous avons déterminé un rôle de RPTP dans la croissance axonale en agissant sur la voie de signalisation des neurégulines. Des souris exprimant le gène rapporteur de la -galactosidase sous le contrôle du promoteur de RPTP nous ont permises de localiser RPTP essentiellement dans les neurones pyramidaux et dans tous les organes sensoriels. L’étude du comportement des souris déficientes pour RPTP a révélé un rôle de RPTP dans des fonctions motrices et sensorielles. Nos résultats démontrent des profils d’expression complémentaires de RPTP et RPTP.
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Marsicano, Giovanni. "Physiological role of the cannabinoid receptor 1 (CB1) in the murine central nervous system." n.p, 2000. http://ethos.bl.uk/.

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邱大安 and Tai-on Yau. "Regulation of the mouse hoxb-3 gene in the neural expression domains during embryogenesis." Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2001. http://hub.hku.hk/bib/B31242601.

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Lee, King-yiu. "The Ret gene in the enteric nervous system expression analysis and generation of ret deficient mice /." Click to view the E-thesis via HKUTO, 2004. http://sunzi.lib.hku.hk/hkuto/record/B31449669.

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Stromnes, Ingunn Margarete. "T cell determinants of central nervous system autoimmune disease /." Thesis, Connect to this title online; UW restricted, 2007. http://hdl.handle.net/1773/8333.

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Lee, King-yiu, and 李景耀. "The Ret gene in the enteric nervous system: expression analysis and generation of ret deficient mice." Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2004. http://hub.hku.hk/bib/B31449669.

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Books on the topic "Mice – Nervous system"

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Paxinos, George, Charles Watson, and L. Puelles. The mouse nervous system. Amsterdam: Elsevier Academic Press, 2012.

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Herrup, Karl. Transgenic and ES cell chimeric mice as tools for the study of the nervous system. Amsterdam: Published by Elsevier for the Foundation for the Study of the Nervous System, 1995.

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Tesseur, Ina. Expression of human apolipoprotein E₄ in the central nervous system of transgenic mice: Towards a model for alzheimer's disease. Leuven, Belgium: Leuven University Press, 2000.

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International Conference on Senescence (2nd 2003 Sapporo-shi, Japan). The senescence-accelerated mouse (SAM): An animal model of senescence : proceedings of the 2nd International Conference on Senescence, the SAM model, held in Sapporo, Japan between 21 and 23 July 2003. Edited by Nomura Yasuyuki Ph D, Takeda Toshio 1931-, and Okuma Yasunobu Ph D. Amsterdam: Elsevier, 2004.

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Mood and anxiety related phenotypes in mice: Characterization using behavioral tests. New York, NY: Humana Press, 2009.

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Mood and anxiety related phenotypes in mice: Characterization using behavioral tests. New York, NY: Humana Press, 2011.

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Sidman, Richard L., Margaret C. Green, and Stanley H. Appel. Catalog of the Neurological Mutants of the Mouse. Harvard University Press, 2013.

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Brian, Popko, ed. Mouse models in the study of genetic neurological disorders. New York: Kluwer Academic/Plenum, 1999.

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(Editor), Yasuyuki Nomura, Toshio Takeda (Editor), and Yasunobu Okuma (Editor), eds. The Senescence-Accelerated Mouse (SAM): An Animal Model of Senescence: Proceedings of the 2nd International Conference on Senescene: The SAM Model, Sapporo, ... July 2003, ICS 1260 (International Congress). Elsevier, 2004.

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Desroches, Julie. Peripheral analgesia involves cannabinoid receptors. Edited by Paul Farquhar-Smith, Pierre Beaulieu, and Sian Jagger. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780198834359.003.0034.

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This landmark paper by Agarwal and colleagues was published in 2007, when the exact contribution of the activation of the cannabinoid type 1 receptor (CB1) receptors expressed on the peripheral terminals of nociceptors in pain modulation was still uncertain. At that time, while it was clearly demonstrated that the central nervous system (CNS) was involved in the antinociceptive effects induced by the activation of the CB1 receptor, many strains of mice in which the gene encoding the CB1 receptor was deleted by conditional mutagenesis were used to study the specific role of these receptors in pain. Creating an ingenious model of genetically modified mice with a conditional deletion of the CB1 receptor gene exclusively in the peripheral nociceptors, Agarwal and colleagues were the first to unequivocally demonstrate the major role of this receptor in the control of pain at the peripheral level. In fact, these mutant mice lacking CB1 receptors only in sensory neurons (those expressing the sodium channel Nav1.8) have been designed to highlight that CB1 receptors on nociceptors, and not those within the CNS, constitute an important target for mediating local or systemic (but not intrathecal) cannabinoid analgesia. Overall, they have clarified the anatomical locus of cannabinoid-induced analgesia, highlighted the potential significance of peripheral CB1-mediated cannabinoid analgesia, and revealed important insights into how the peripheral endocannabinoid system works in controlling both inflammatory pain and neuropathic pain.
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Book chapters on the topic "Mice – Nervous system"

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Powell, Henry C. "Cycloleucine Encephalopathy, Rats and Mice." In Nervous System, 77–83. Berlin, Heidelberg: Springer Berlin Heidelberg, 1988. http://dx.doi.org/10.1007/978-3-642-83516-2_13.

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Hirano, Asao, and Masayuki Shintaku. "Aberrant Synaptic Development in Mutant “Weaver” Mice." In Nervous System, 215–21. Berlin, Heidelberg: Springer Berlin Heidelberg, 1988. http://dx.doi.org/10.1007/978-3-642-83516-2_37.

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Duff, Karen. "Transgenic Mice Overexpressing Presenilin cDNAs." In Central Nervous System Diseases, 123–28. Totowa, NJ: Humana Press, 2000. http://dx.doi.org/10.1007/978-1-59259-691-1_7.

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Matsuwaki, Takashi. "Generation and Phenotyping of Progranulin-Deficient Mice." In Progranulin and Central Nervous System Disorders, 139–55. Singapore: Springer Singapore, 2019. http://dx.doi.org/10.1007/978-981-13-6186-9_9.

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Müller, Marcus, and Iain L. Campbell. "Chemokine Actions in the CNS: Insights from Transgenic Mice." In Central Nervous System Diseases and Inflammation, 203–19. Boston, MA: Springer US, 2008. http://dx.doi.org/10.1007/978-0-387-73894-9_10.

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Lehmann-Grube, F. "Persistent Infection of Mice with Lymphocytic Choriomeningitis Virus." In Virus Infections and the Developing Nervous System, 69–83. Dordrecht: Springer Netherlands, 1988. http://dx.doi.org/10.1007/978-94-009-1243-4_6.

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Ragel, Brian T., and Randy L. Jensen. "Intracranial Meningioma in Mice: Noninvasive Bioluminescence Imaging." In Tumors of the Central Nervous System, Volume 7, 79–85. Dordrecht: Springer Netherlands, 2012. http://dx.doi.org/10.1007/978-94-007-2894-3_9.

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Zhao, Zheng, and Yinghe Hu. "Genome-Wide Expression Profiles of Amygdala and Hippocampus in Mice After Fear Conditioning." In Genomics, Proteomics, and the Nervous System, 303–29. New York, NY: Springer New York, 2010. http://dx.doi.org/10.1007/978-1-4419-7197-5_12.

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Trapp, B. D., J. A. Small, and G. A. Scangos. "Dysmyelination in Transgenic Mice Containing the Early Region of JC Virus." In Virus Infections and the Developing Nervous System, 21–35. Dordrecht: Springer Netherlands, 1988. http://dx.doi.org/10.1007/978-94-009-1243-4_3.

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Kasof, G., T. Curran, and J. I. Morgan. "Transgenic mice studies of immediate-early genes: from markers to mutants." In Immediate-Early Genes in the Central Nervous System, 116–31. Berlin, Heidelberg: Springer Berlin Heidelberg, 1995. http://dx.doi.org/10.1007/978-3-642-79562-6_7.

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Conference papers on the topic "Mice – Nervous system"

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Khandoker, Ahsan, Thuraia Al Khoori, Takahiro Minato, Takuya Ito, and Yoshitaka Kimura. "Effect of Chronic Hypoxia on Autonomic Nervous System of Fetal Mice." In 2017 Computing in Cardiology Conference. Computing in Cardiology, 2017. http://dx.doi.org/10.22489/cinc.2017.332-298.

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Lysikova, Ekaterina. "MOLECULAR MECHANISMS OF SUPPRESSION OF THE PROGRESSION OF FUS PROTEINOPATHY IN THE NERVOUS SYSTEM OF TRANSGENIC MICE." In XVII INTERNATIONAL INTERDISCIPLINARY CONGRESS NEUROSCIENCE FOR MEDICINE AND PSYCHOLOGY. LCC MAKS Press, 2021. http://dx.doi.org/10.29003/m2209.sudak.ns2021-17/237-238.

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CRISTEA, AURELIA. "EXPERIMENTAL PHARMACOLOGICAL RESEARCHES CONCERNING VEGETAL EXTRACTS IN HIGH DILUTIONS: I. CHAMOMILLA, IN VIVO, ON CENTRAL NERVOUS SYSTEM, AT THE “SENSITIVE” MICE." In Proceedings of the International School of Biophysics. WORLD SCIENTIFIC, 1998. http://dx.doi.org/10.1142/9789812816887_0011.

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Kolesnikova, Inna, Natalia Budennaya, Yurii Severiukhin, Kristina Lyakhova, Dina Utina, and Victor Gaevsky. "THE EFFECT ON MORPHOLOGICAL CHANGES IN THE CENTRAL NERVOUS SYSTEM AND PHYSIOLOGICAL MEASUREMENTS OF AGED MICE AFTER TOTAL IRRADIATION BY GAMMA RAYS." In XVII INTERNATIONAL INTERDISCIPLINARY CONGRESS NEUROSCIENCE FOR MEDICINE AND PSYCHOLOGY. LCC MAKS Press, 2021. http://dx.doi.org/10.29003/m2165.sudak.ns2021-17/193-194.

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"Evaluation of sympathetic nervous system function in normal and spontaneously hypertensive rat hearts with dynamic SPECT imaging." In 2013 IEEE Nuclear Science Symposium and Medical Imaging Conference (2013 NSS/MIC). IEEE, 2013. http://dx.doi.org/10.1109/nssmic.2013.6829043.

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