Relevant bibliographies by topics / Mice Mice Anxiety

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  1. Journal articles
  2. Dissertations / Theses
  3. Books
  4. Book chapters

Academic literature on the topic 'Mice Mice Anxiety'

Author: Grafiati
Published: 4 June 2021
Last updated: 7 February 2022

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Journal articles on the topic "Mice Mice Anxiety"

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Hurst, Jane L., and Rebecca S. West. "Taming anxiety in laboratory mice." Nature Methods 7, no. 10 (2010): 825–26. http://dx.doi.org/10.1038/nmeth.1500.

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Hasan, Syed Rehan, Manish Sinha, and Nitin Bansal. "Anxiolytic activity of Angiotensin-Receptor-Blocker in Experimental Models of Anxiety in Mice." Journal of Pharmaceutical Technology, Research and Management 2, no. 2 (2014): 189–202. http://dx.doi.org/10.15415/jptrm.2014.22013.

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Avgustinovich, D. F., and N. N. Kudryavtseva. "Partition test measures anxiety in mice." Behavioural Pharmacology 6, SUPPLEMENT 1 (1995): 32. http://dx.doi.org/10.1097/00008877-199505001-00035.

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Schrott, Lisa M., and Linda S. Crnic. "Increased anxiety behaviors in autoimmune mice." Behavioral Neuroscience 110, no. 3 (1996): 492–502. http://dx.doi.org/10.1037/0735-7044.110.3.492.

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Bourin, Michel, Benoit Petit-Demoulière, Brid Nic Dhonnchadha, and Martine Hascöet. "Animal models of anxiety in mice." Fundamental & Clinical Pharmacology 21, no. 6 (2007): 567–74. http://dx.doi.org/10.1111/j.1472-8206.2007.00526.x.

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Raber, Jacob. "Role of Apolipoprotein E in Anxiety." Neural Plasticity 2007 (2007): 1–7. http://dx.doi.org/10.1155/2007/91236.

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Anxiety is most common among Alzheimer's disease (AD) patients with an age at onset under age 65. Apolipoprotein E4 (apoE4) is a risk factor for developing AD at an earlier age and might contribute to this effect. In mice, apoE plays a role in the regulation of anxiety, which might involve histamine receptor-mediated signaling and steroidogenesis in the adrenal gland. In addition, human apoE isoforms have differential effects on anxiety in adult mice lacking apoE and probable AD patients. Compared to wild-type mice, mice lacking apoE and apoE4 mice showed pathological alterations in the central nucleus of the amygdala, which is involved in regulation of anxiety. ApoE4, but not mice lacking apoE, or apoE3 mice showed impaired dexamethasone suppression of plasma corticosterone. Understanding how apoE modulates measures of anxiety might help the developments of therapeutic targets to reduce or even prevent measures of anxiety in health and in dementing illnesses.
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Walther, Thomas, Jörg-Peter Voigt, Akiyoshi Fukamizu, Heidrun Fink, and Michael Bader. "Learning and anxiety in angiotensin-deficient mice." Behavioural Brain Research 100, no. 1-2 (1999): 1–4. http://dx.doi.org/10.1016/s0166-4328(98)00078-3.

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Boccalon, S., B. Scaggiante, and L. Perissin. "Anxiety stress and nociceptive responses in mice." Life Sciences 78, no. 11 (2006): 1225–30. http://dx.doi.org/10.1016/j.lfs.2005.06.027.

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Schmalzigaug, Robert, Ramona M. Rodriguiz, Lindsey E. Phillips, Collin E. Davidson, William C. Wetsel, and Richard T. Premont. "Anxiety-like behaviors in mice lacking GIT2." Neuroscience Letters 451, no. 2 (2009): 156–61. http://dx.doi.org/10.1016/j.neulet.2008.12.034.

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Hölter, Sabine M., Jan Einicke, Bettina Sperling, et al. "Tests for Anxiety-Related Behavior in Mice." Current Protocols in Mouse Biology 5, no. 4 (2015): 291–309. http://dx.doi.org/10.1002/9780470942390.mo150010.

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Dissertations / Theses on the topic "Mice Mice Anxiety"

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Verma, Sujeet. "Live plant and artificial plant settings are able to alleviate anxiety levels in mice an elevated plus-maze study /." Pullman, Wash. : Washington State University, 2009. http://www.dissertations.wsu.edu/Thesis/Spring2009/S_Verma_042409.pdf.

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Thesis (M.S. in horticulture)--Washington State University, May 2009.<br>Title from PDF title page (viewed on July 28, 2009). "Department of Horticulture and Landscape Architecture." Includes bibliographical references (p. 51-58).
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Avrabos, Charilaos. "Brain circuit dynamics related to extremes in trait anxiety in mice." Diss., lmu, 2012. http://nbn-resolving.de/urn:nbn:de:bvb:19-149945.

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Ghosh, Aniruddha. "ELECTROPHYSIOLOGICAL INVESTIGATION OF HIPPOCAMPAL SYNAPTIC PLASTICITY IN DEAF-1 KNOCK-OUT MICE." OpenSIUC, 2016. https://opensiuc.lib.siu.edu/dissertations/1207.

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Intellectual Disability (ID) is a condition in which day-to-day cognitive, intellectual and adaptive functioning is negatively affected including poor performance in memory tests in human subjects. Patients with comorbid anxiety and depression demonstrated adverse memory when subject to a verbal learning test. Abnormal mutation in the human deaf1 gene has been previously reported to be associated with ID. Previous behavioral studies in mice with a brain specific conditional neuronal knock outs (NKO) of deaf 1 gene exhibited memory deficit and anxiety-like behavior. These deaf 1 NKO mice represent a convenient model for the study of the effects of ID on both in vivo and in vitro memory tests. Earlier studies in these deaf 1 NKOs have shown increased levels of anxiety in the Elevated Plus Maze and Open Field - Test along with contextual-memory deficits in Fear-conditioning experiments. In the intact animal, behavioral phenotyping experiments in mice such as Fear conditioning including contextual and cued fear conditioning measures the ability of the animal to learn, remember and associate an aversive experience to environmental cues. Studies in rodent brain slices involving Long-term potentiation (LTP) and long-term depression (LTD) have long been associated to reflect substrates for memory formation and memory loss respectively. While early-LTP (ELTP) typically lasts between 30-60 minutes, late-LTP (LLTP) lasts for hours; though there is much disagreement about the time courses. In vitro LTD was first reported in 1978 and since then has been studied in details. NMDA receptor (NMDAR) and metabotropic glutamate receptor (mGLUR) activation has been implicated in induction of both LTP and LTD among others. The CA1 region of the rodent hippocampus is the most widely explored area for LTP studies especially stratum radiatum (SR). In addition to the commissural fibers, SR receives Schaffer-collaterals (SC) and is an integral part of memory formation. Previous studies have reported that the CA1 region of the hippocampus expresses both NMDAR-LTD and mGluR-LTD. In the present study, we aim to establish whether these mice might show altered hippocampal Long-term Potentiation (LTP) and/or Long-term Depression (LTD) when brain slices from deaf1 NKO mice were subject to electrophysiological studies and if so, whether pharmacological interventions had any effect on it. Using electrophysiological techniques, hippocampal slices from DEAF1 KO mice were tested for possible alterations in LTP when compared to age-matched controls. Both early and late forms of LTP were examined, since these two types of LTP are medicated through different biochemical mechanisms. ELTP was unaltered in the NKO animals compared to their WT littermates. This experiment was followed by investigating LLTP. The control animals, as expected, exhibited a large LTP. The DEAF1 animals, in contrast, showed a paradoxical response to LLTP stimulation. Instead of the increase in response as observed in the control animals, slices from DEAF1 mice decreased to about 80% of baseline at 30 mins post train. This depression (LTD) became greater throughout the 3 hours of post-train recording, at the end of which the responses were approximately 25% of baseline. The mechanisms of this LTD were then explored with focus on glutamate receptors. Based upon existing knowledge in the literature, the possible roles of both NMDA receptors and mGlu receptors (mGluR1 and mGluR5) were explored. Treatment with D-AP5 - a selective NMDAR antagonist on slices from control animals showed no effect on the baseline evoked responses, but LLTP was blocked following D - AP5 treatment. In slices from DEAF1 NKO animals, AP5 did not affect the baseline evoked responses, but it reversed the expected LTD to a robust LLTP. Next, the involvement of mGlu receptors, known to play a role in LTD, was tested. In controls, there was once again no effect on baseline activity but LLTP at both 30 mins and 180 mins P.T was significantly enhanced as compared to aCSF-only treated slices. In slices from DEAF1 mice, similar to the AP5 study, LY367385 did not affect the baseline response, but reversed LTD to LLTP. Following this, the effect of 40 µM MPEP (an mGluR5 antagonist) was tested, and produced similar results. Thus, three receptor antagonists known to impair the expression of LTD in wild-type animals not only prevented its appearance, but lead to a robust enhancement of the response in DEAF1 hippocampus. Further exploration of the mechanics of altered LTP was undertaken by using Synaptic Tagging and Capture (STC) in combination with pharmacology. Results of the STC experiments suggest that there could be a differential effect of plasticity-inducing stimulation on downstream protein targets. Finally, whole-cell patch recordings were performed to examine the biophysical characteristics of individual CA1 pyramidal neurons. Taken together, the results suggest that multiple mechanisms may be involved in the generation and expression of LTD in the DEAF1 mice.
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Helfand, Rebecca S. Diaz-Granados Jamie L. "Taurine depletion in adolescent mice and implications for ethanol withdrawal-induced anxiety." Waco, Tex. : Baylor University, 2007. http://hdl.handle.net/2104/5059.

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Dawson, Neil. "Affective-related endophenotypes in serotonin transporter over-expressing mice." Thesis, University of Edinburgh, 2008. http://hdl.handle.net/1842/4843.

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The affective disorders (anxiety and depression) are common psychiatric disorders that primarily involve disturbances in mood and represent the second leading source of disease burden world-wide. A wide base of evidence supports a significant genetic contribution to these disorders. Polymorphic variation in the promoter region (5-HTTLPR) of the human serotonin transporter (hSERT) gene, which leads to a life-long alteration in serotonin transporter (SERT) expression and functioning, has been implicated in the aetiology of both anxiety and depression. Despite the strong evidence implicating a role for this polymorphism in affective psychopathology the underlying mechanism by which genetically determined SERT bioavailability influences affective functioning are not understood. In these studies I attempt to elucidate the alterations in cerebral, serotonin (5-HT) system and hypothalamo-pituitary-adrenal (HPA) axis functioning which may relate to the effect of the 5-HTTLPR on affective functioning by characterising these parameters in an animal model of genetically increased SERT expression (hSERT over-expressing mice; hSERT OVR). Furthermore, as gender influences both the likelihood of developing affective disorders and the impact of the 5-HTTLPR on affective functioning, with a greater effect being observed in females than in males, we characterise these parameters in mice of both genders. The data presented in this thesis demonstrate that the life-long increase in SERT bioavailability present in hSERT OVR mice produces profound alterations in cerebral, serotonin system and HPA axis functioning. Furthermore, the influence of increased SERT expression upon cerebral and serotonin system functioning is greater in females than in males. Additionally, a number of sexually dimorphic variations in serotonin system functioning were identified. Thus this thesis extends the currently available information regarding the underlying mechanisms by which gender and a life-long alteration in SERT expression may influence the risk of affective psychopathology.
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Turri, Maria Grazia. "Mapping of behavioural quantitative trait loci." Thesis, University of Oxford, 2002. http://ora.ox.ac.uk/objects/uuid:89823fa1-c1d3-49e3-acb9-46da18b12245.

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Anxiety is a common disorder which affects about 25% of the population and whose pathophysiology is still poorly understood. Animal models of disease have been widely used to investigate the molecular basis of human disorders, including psychiatric illnesses. This thesis is about the study of the genetic basis of a mouse model of anxiety. I have carried out a QTL mapping study of behavioural measures thought to model anxiety. I report results from 1,636 mice, assessed for a large number of phenotypes in five ethological tests. Mice belonged to two F2 intercrosses originated by four lines generated in a replicate selection experiment. By comparing mapping results between the two crosses, I have demonstrated that selection operated on the same relatively small number of loci in the four selected lines. Analysis of genetic effect of QTL across phenotypes has allowed me to identify loci with specific roles on different dimensions of anxious behaviour, therefore enhancing our understanding of the anxiety phenotype in mice. For some of these QTL I have also accomplished fine mapping experiments: a locus on chromosome 15 is now contained in an interval of only 3 centimorgans. This work is the basis for further molecular dissection of the genetic loci that underlie anxiety and provides a starting point for the discovery of genes involved in a common psychiatric condition.
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Godbey, Steven J. "Environmental and genetic modulation of morphology, memory, olfactory ability, and anxiety in mice." Tallahassee, Fla. : Florida State University, 2009. http://purl.fcla.edu/fsu/lib/digcoll/undergraduate/honors-theses/244587.

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Thesis (Honors paper)--Florida State University, 2009.<br>Advisor: Dr. Debra Ann Fadool, Florida State University, College of Arts and Sciences, Dept. of Biological Science. Includes bibliographical references.
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Dutton, R. M. "An investigation into the genetic basis of anxiety." Thesis, University of Oxford, 2013. http://ora.ox.ac.uk/objects/uuid:b6f96c9c-8645-4659-b288-c370c2e67654.

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This thesis aimed to investigate the genetic basis of anxiety in mice. The first half describes searches for genetic variation beneath quantitative trait loci (QTLs) and computationally pulls together data from several sources in order to assess how likely each variant is to be responsible for the QTLs. The second half describes the results of the behavioural phenotyping of three knockout mouse models. Examination of the sequence data beneath anxiety-related QTLs mapped from quasi-outbred mice identified 326 variants across eight inbred mouse strains in the coding and promoter regions beneath a prominent QTL for startle behaviour on murine chromosome 15. Variants in the genes Muc19, Gxylt1 and Kif21a were pinpointed as being most likely to contribute towards the phenotypic variation of that QTL. 12 structural variants (SVs) were also identified across the same strains as being potentially causal for at least one QTL when the search was extended to the whole genome. Testing the association between SV genotype and phenotype in an outbred murine population implied that SVs in the genes Fam110c, Fam117a and Gm6320 had similar phenotypic associations across different populations of mice, although the associations in the outbred mice did not achieve statistical significance. From the work with the three knockout mouse models, it was concluded that two of the genes, Eps15 and Car2, do affect anxiety in male animals, with Eps15 deficiency reducing anxiety and Car2 deficiency increasing it. The results for the Dstn mouse model were inconclusive. This model may need to be reengineered onto a less anxious background for future testing. In conclusion, this thesis identified a number of genes and genetic variants, some of which do seem to affect murine anxiety levels. Improved understanding of anxiety in mice will hopefully lead to a better understanding of the causes and treatment of anxiety disorders in humans.
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Ribeiro, Monique Vieira. "Efeitos comportamentais do metilfenidato e da reboxetina em modelo animal de dÃficit de atenÃÃo induzido pela lesÃo por etanol em camundongos." Universidade Federal do CearÃ, 2008. http://www.teses.ufc.br/tde_busca/arquivo.php?codArquivo=3034.

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Conselho Nacional de Desenvolvimento CientÃfico e TecnolÃgico<br>O Transtorno de DÃficit de AtenÃÃo e Hiperatividade (TDAH) à uma desordem do desenvolvimento neurocomportamental que afeta de 3 a 5% das crianÃas em idade escolar. O transtorno à caracterizado pela presenÃa de sintomas como desatenÃÃo, hiperatividade e impulsividade. CrianÃas expostas ao Ãlcool durante o perÃodo gestacional exibem um padrÃo de hiperatividade, dÃficit de linguagem e aprendizado. A Dopamina e a Noradrenalina parecem ter um papel primÃrio na gÃnese do transtorno, o que à confirmado pela resposta ao psicoestimulantes que aumentam suas quantidades na fenda sinÃptica. O psicoestimulante Metilfenidato à a droga de primeira escolha no tratamento do TDAH. MedicaÃÃes nÃo-psicoestimulantes como o inibidor da recaptaÃÃo de noradrenalina Reboxetina, tÃm ganhado forÃa como possÃvel alternativa no tratamento do dÃficit de atenÃÃo. Em ratos, o etanol administrado no perÃodo de neurodesenvolvimento gera disfunÃÃo em circuitos prÃ-frontais, levando a transmissÃo dopaminÃrgica anormal. O objetivo desse trabalho foi avaliar os efeitos comportamentais (memÃria, atenÃÃo, atividade locomotora, depressÃo e ansiedade) do Metilfenidato (MFD) e da Reboxetina (RBX) em modelo de dÃficit de atenÃÃo induzido em camundongos pela lesÃo por etanol. Camundongos Swiss machos e fÃmeas no 10o dia de vida foram submetidos a injeÃÃo de etanol (2 x 2,5g/kg, s.c., 6 h-intervalo) ou soluÃÃo salina (mesmo volume). No 30o dia, iniciaram-se testes comportamentais (T-maze, Y-Maze, esquiva passiva, nado-forcado, plus-maze, caixa claro-escuro e campo-aberto). Os animais receberam MFD (2,5mg/kg) ou RBX (10 mg/kg) por gavagem 30 minutos antes de cada sessÃo de testes.. NÃo se observaram alteraÃÃes histopatolÃgicas em cortes de cÃrtex cerebral dos camundongos lesados por etanol. No T-Maze, o grupo do etanol apresentou significativos (p<0,001, Teste de Kruskal-Wallis) dÃficits de atenÃÃo, necessitando de mais sessÃes para aprender. Os dÃficits foram revertidos pelo MFD e pela RBX. (Cont. 1,5Â0,32, Et 7,18Â0,32, MFD+Et 3,14Â0,88, RBX+Et 1,55Â0,33). Na fase de discriminaÃÃo tardia, os animais lesados tambÃm apresentaram dÃficits de memÃria, com menor nÃmero de acertos quando comparados aos controles. O efeito revertido pelo MFD, mas nÃo pela RBX. (Cont. 25,78Â0,86, Et 21,27Â1,02, MFD+Et 25,14Â1,03, RBX+Et 21,88Â1,00) NÃo houve dÃficits de memÃria aversiva na Esquiva Passiva. No Y-Maze, o grupo do etanol apresentou dÃficits de memÃria de trabalho, revertidos pelo MFD, mas nÃo por RBX. (Cont. 73,28Â4,75, Et 43,53Â4,65, MFD+Et 60,57Â1,92, RBX+Et 54,63Â2,80). No Campo Aberto, o grupo do etanol teve hipoatividade motora, o que foi mitigado por MFD e RBX (Cont. 93,59Â6,38, Et 66,52Â5,87, MFD+Et 98,14Â9,23, RBX+Et 77,3Â7,68) No Claro-Escuro, o grupo do etanol mostrou comportamento ansiogÃnico, permanecendo menos tempo no claro, o que foi revertido pela RBX. (Cont. 149Â5,99, Et 115,4Â4,27, MFD+Et 120,1Â6,81, RBX+Et 149,1Â2,55). No Plus-Maze, o grupo etanol apresentou comportamento ansiogÃnico, revertido pela RBX, mas nÃo pelo MFD (Cont. 88,06Â12,52, Et 50,53Â5,99, MFD+Et 39,86Â12,00, RBX+Et 86,29Â9,49). No Nado-ForÃado, o grupo do etanol teve um comportamento depressivo que nÃo foi melhorado por MFD ou RBX (Cont. 74,17Â23,43, Et 141,8Â19,3, MFD+Et 178,9Â12,43, RBX+Et 118,5Â18,25). ConcluÃmos que camundongos lesados por etanol no perÃodo neonatal apresentam dÃficits de atenÃÃo e memÃria que sÃo adequadamente revertidos por MFD. A RBX permanece como droga de segunda escolha, principalmente em casos onde existem comorbidades como ansiedade.<br>Attention Deficit and Hyperactivity Disorder (ADHD) is a neurobehavioral disorder that affects between 3 - 5% of scholar-aged children. The disorder is characterized by inattention, hyperactivity and impulsivity. Children exposed to alcohol during pregnancy may exhibit hyperactivity, language and learning deficits. Dopamine and Norepinephrine seem to have an important role in the pathophysiology, which is confirmed by the response to psychostimulants, which increase the availability of these neurotransmitters in the synaptic cleft. The psychostimulant Methylphenidate is the gold-standard in the treatment of ADHD. Non-stimulant medications, such as norepinephrine reuptake inhibitor Reboxetine are gaining space as an alternative in the treatment of ADHD. In rats, when ethanol is given during the period of brain development, it may cause pre-frontal circuitsâ dysfunction and abnormal dopaminergic transmission. The aim of this work is to evaluate the behavioral effects (attention, memory, motor activity, anxiety and depression) of Methylphenidate (MPH) and Reboxetine (RBX) in an experimental model of attention deficit induced by ethanol in mice. Male and female Swiss mice on the post-natal day 10 were injected with ethanol (2 x 2,5g/kg, s.c., 6 h-interval) or saline (same volume). On post-natal day 30, behavioral testing was started (T-maze, Y-maze, passive avoidance, forced swim test, open field, plus maze and dark/light box). The subjects received either MPH (2,5mg/kg) or RBX (10 mg/kg) p.o, 30 minutes before each test session. There were no histopathologic changes in cerebral cortex of mice that received ethanol. In the T-maze, ethanol subjects had significant attention deficits, taking a longer time to learn, but these were reversed by MPH and RBX (Cont. 1,5Â0,32, Et 7,18Â0,32, MPH+Et 3,14Â0,88, RBX+Et 1,55Â0,33). During delayed discrimination, ethanol group had memory deficits, with fewer correct choices than controls. MPH ameliorated the deficits, but RBX did not (Cont. 25,78Â0,86, Et 21,27Â1,02, MPH+Et 25,14Â1,03, RBX+Et 21,88Â1,00). There were no deficits in aversive memory during passive avoidance test. In the Y-Maze, ethanol subjects had working memory deficits, that were mitigated MPH, but not by RBX. (Cont. 73,28Â4,75, Et 43,53Â4,65, MPH+Et 60,57Â1,92, RBX+Et 54,63Â2,80) . At the open field, ethanol subjects had motor hypoactivity that was reversed by MPH and RBX (Cont. 93,59Â6,38, Et 66,52Â5,87, MPH+Et 98,14Â9,23, RBX+Et 77,3Â7,68). At the Light/dark paradigm, ethanol subjects displayed anxious behavior, remaining more time in the dark side and this behavior was reversed by RBX only (Cont. 149Â5,99, Et 115,4Â4,27, MPH+Et 120,1Â6,81, RBX+Et 149,1Â2,55). At the Plus-Maze, ethanol subjects had an anxiogenic behavior, remaining less time in the open arms, and this effect was reversed by RBX (Cont. 88,06Â12,52, Et 50,53Â5,99, MPH+Et 39,86Â12,00, RBX+Et 86,29Â9,49). At the forced swimming test, ethanol subjects had prolonged immobility, which was not reversed by MPH or RBX (Cont. 74,17Â23,43, Et 141,8Â19,3, MPH+Et 178,9Â12,43, RBX+Et 118,5Â18,25). In conclusion, mice exposed to ethanol during brain development have attention and memory deficits that are reversed by MPH and partially by RBX. RBX may be used as a second line treatment in subjects that do not respond to stimulants or have comorbid anxiety.
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Lynch, Karl. "The role of 5-HT←3 and 5-HT←4 receptors in social and agonistic behaviour in male mice." Thesis, Queen's University Belfast, 2000. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.343057.

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Books on the topic "Mice Mice Anxiety"

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Gould, Todd D., ed. Mood and Anxiety Related Phenotypes in Mice. Humana Press, 2011. http://dx.doi.org/10.1007/978-1-61779-313-4.

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Gould, Todd D., ed. Mood and Anxiety Related Phenotypes in Mice. Humana Press, 2009. http://dx.doi.org/10.1007/978-1-60761-303-9.

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

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

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Mice. Macmillan, 2012.

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Mood and Anxiety Related Phenotypes in Mice: Characterization Using Behavioral Tests. Humana, 2012.

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Shum, Fanny Wan Fei. Genetic alteration of anxiety and stress like behavior in mice lacking CaMKIV. 2006.

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Concierto de piano. ekare, 2013.

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Klemenhagen, Kristen C., Franklin R. Schneier, Abby J. Fyer, H. Blair Simpson, and René Hen. Adult Hippocampal Neurogenesis, Pattern Separation, and Generalization. Edited by Israel Liberzon and Kerry J. Ressler. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780190215422.003.0006.

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Almost one-third of adult Americans will have an anxiety disorder in their lifetime, with enormous personal, societal, and financial costs. Among the most disabling of these disorders are post-traumatic stress disorder (PTSD), obsessive-compulsive disorder (OCD), social anxiety disorder, generalized anxiety disorder, and panic disorder. Although there are evidence-based treatments for these disorders, as many as 50% of patients do not respond, and there is a considerable need for new therapies. This chapter proposes that the excessive generalization seen in patients with pathological anxiety is due to impaired hippocampal functioning, specifically a deficit in the neural process of pattern separation, which relies upon the dentate gyrus and is sensitive to neurogenesis. Preclinical findings indicate that stimulating DG neurogenesis improves pattern separation and reduces anxiety behaviors in mice. As a result the authors hypothesize that pharmacological or environmental manipulations aimed at stimulating neurogenesis will be beneficial for the treatment of anxiety disorders.
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Hodgkiss, Andrew. Psychiatric consequences of cancer treatments: ‘small molecule’ molecularly targeted agents. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780198759911.003.0008.

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The psychiatric consequences of a range of small-molecule, molecularly targeted systemic treatments for cancer are reviewed. Psychopathology may arise from the endocrine complications of VEGFR/multiple TK inhibitors. The mechanisms by which PI3K/AKT inhibition and proteasome inhibition can provoke anxiety and depressive phenomena in animals and humans are discussed. PARP-1 inhibition impairs memory acquisition in animal models and is neuroprotective. PARP-2 inhibitors display anti-neuroinflammatory properties in mice. The cognitive enhancing, mood stabilizing, and neuroprotective effects of HDAC inhibitors are considered.
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Book chapters on the topic "Mice Mice Anxiety"

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Anisman, Hymie, and Zul Merali. "Learned Helplessness in Mice." In Mood and Anxiety Related Phenotypes in Mice. Humana Press, 2009. http://dx.doi.org/10.1007/978-1-60761-303-9_10.

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Dent, Claire L., and Anthony R. Isles. "Measuring Impulsive Choice Behaviour in Mice." In Mood and Anxiety Related Phenotypes in Mice. Humana Press, 2011. http://dx.doi.org/10.1007/978-1-61779-313-4_21.

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Hascoët, Martine, and Michel Bourin. "The Four-Plate Test in Mice." In Mood and Anxiety Related Phenotypes in Mice. Humana Press, 2011. http://dx.doi.org/10.1007/978-1-61779-313-4_8.

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Park, Jin Ho. "Assessment of Male Sexual Behavior in Mice." In Mood and Anxiety Related Phenotypes in Mice. Humana Press, 2011. http://dx.doi.org/10.1007/978-1-61779-313-4_22.

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Kuti, Orsolya J., and Damon T. Page. "Assessment of Social Approach Behavior in Mice." In Mood and Anxiety Related Phenotypes in Mice. Humana Press, 2011. http://dx.doi.org/10.1007/978-1-61779-313-4_5.

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Kas, Martien J., Ilan Golani, Yoav Benjamini, Ehud Fonio, and Oliver Stiedl. "Longitudinal Assessment of Deliberate Mouse Behavior in the Home Cage and Attached Environments: Relevance to Anxiety and Mood Disorders." In Mood and Anxiety Related Phenotypes in Mice. Humana Press, 2011. http://dx.doi.org/10.1007/978-1-61779-313-4_1.

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Witkin, Jeffrey M. "A Vogel Conflict Test Using Food Reinforcement in Mice." In Mood and Anxiety Related Phenotypes in Mice. Humana Press, 2011. http://dx.doi.org/10.1007/978-1-61779-313-4_10.

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Gafford, Georgette M., and Kerry J. Ressler. "Fear Conditioning and Extinction as a Model of PTSD in Mice." In Mood and Anxiety Related Phenotypes in Mice. Humana Press, 2011. http://dx.doi.org/10.1007/978-1-61779-313-4_11.

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Cohen, Hagit, Michael A. Matar, and Joseph Zohar. "The “Cut-Off Behavioral Criteria” Method: Modeling Clinical Diagnostic Criteria in Animal Studies of PTSD." In Mood and Anxiety Related Phenotypes in Mice. Humana Press, 2011. http://dx.doi.org/10.1007/978-1-61779-313-4_12.

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Franks, Becca, James P. Curley, and Frances A. Champagne. "Measuring Variations in Maternal Behavior: Relevance for Studies of Mood and Anxiety." In Mood and Anxiety Related Phenotypes in Mice. Humana Press, 2011. http://dx.doi.org/10.1007/978-1-61779-313-4_13.

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