Academic literature on the topic 'Selectively bred mice'

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Journal articles on the topic "Selectively bred mice"

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Smolen, Andrew, Toni N. Smolen, and Jennifer L. van de Kamp. "Sensitivity of inbred and selectively bred mice to ethanol." Alcohol 4, no. 1 (January 1987): 57–62. http://dx.doi.org/10.1016/0741-8329(87)90061-9.

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Ewalds-Kvist, S. Béatrice M., Ritva-Kajsa Selander, and N. Kenneth Sandnabba. "Sex-Related Coping Responses in Mice Selectively Bred for Aggression." Perceptual and Motor Skills 84, no. 3 (June 1997): 911–14. http://dx.doi.org/10.2466/pms.1997.84.3.911.

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Sex differences in strategies of coping with novel situations were studied in three strains of mice with regard to metabolism and open-field and maze activity as well as learning-induced adjustment. The 140 mice were selectively bred for high (Turku Aggressive [TA]) and low (Turku Nonaggressive [TNA]) levels of aggressiveness and originated from a Swiss albino stock normally distributed [N] for aggressiveness. The results indicated that TNA sex differences are more similar to those of the control N mice as compared to those of TA mice. In maze learning, however, the sex differences of TA mice are more in agreement with those of the N strain. Recordings of metabolism and open-field as well as maze activity were correlates of both gender and strain. Sex differences in learning-induced open-field coping behavior were unrelated to strain.
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Kvist, Béatrice. "Learning in Mice Selectively Bred for High and Low Aggressiveness." Psychological Reports 64, no. 1 (February 1989): 127–30. http://dx.doi.org/10.2466/pr0.1989.64.1.127.

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Male mice selectively bred for aggressiveness (TA) and nonaggressiveness (TNA) were compared on maze performance and passive avoidance behavior The two lines performed the learning tasks in separate ways but the significant differences in performance were probably due to factors other than the brightness of one particular line.
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Buckman, Jennifer F., and Charles K. Meshul. "Immunocytochemical analysis of glutamate and GABA in selectively bred mice." Brain Research 760, no. 1-2 (June 1997): 193–203. http://dx.doi.org/10.1016/s0006-8993(97)00281-3.

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Nehrenberg, Derrick L., Ramona M. Rodriguiz, Michel Cyr, Xiaodong Zhang, Jean M. Lauder, Jean-Louis Gariépy, and William C. Wetsel. "An anxiety-like phenotype in mice selectively bred for aggression." Behavioural Brain Research 201, no. 1 (July 2009): 179–91. http://dx.doi.org/10.1016/j.bbr.2009.02.010.

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Meek, T. H., B. P. Lonquich, R. M. Hannon, and T. Garland. "Endurance capacity of mice selectively bred for high voluntary wheel running." Journal of Experimental Biology 212, no. 18 (August 28, 2009): 2908–17. http://dx.doi.org/10.1242/jeb.028886.

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Crabbe, John C., Lauren C. Kruse, Alexandre M. Colville, Andy J. Cameron, Stephanie E. Spence, Jason P. Schlumbohm, Lawrence C. Huang, and Pamela Metten. "Ethanol Sensitivity in High Drinking in the Dark Selectively Bred Mice." Alcoholism: Clinical and Experimental Research 36, no. 7 (February 8, 2012): 1162–70. http://dx.doi.org/10.1111/j.1530-0277.2012.01735.x.

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Mathes, Wendy Foulds, Derrick L. Nehrenberg, Ryan Gordon, Kunjie Hua, Theodore Garland, and Daniel Pomp. "Dopaminergic dysregulation in mice selectively bred for excessive exercise or obesity." Behavioural Brain Research 210, no. 2 (July 2010): 155–63. http://dx.doi.org/10.1016/j.bbr.2010.02.016.

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Kosobud, Ann E., Stephen J. Cross, and John C. Crabbe. "Neural sensitivity to pentylenetetrazol convulsions in inbred and selectively bred mice." Brain Research 592, no. 1-2 (October 1992): 122–28. http://dx.doi.org/10.1016/0006-8993(92)91666-3.

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Steward, Michael W., Carolynne Stanley, and Maria D. Furlong. "Antibody affinity maturation in selectively bred high and low-affinity mice." European Journal of Immunology 16, no. 1 (1986): 59–63. http://dx.doi.org/10.1002/eji.1830160112.

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Dissertations / Theses on the topic "Selectively bred mice"

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Knapman, Alana. "Cognitive Deficits and their Underlying Structural and Functional Alterations in Mice Selectively Bred for High Stress Reactivity." Diss., lmu, 2010. http://nbn-resolving.de/urn:nbn:de:bvb:19-125411.

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Heinzmann, Jan-Michael [Verfasser], and Rainer [Akademischer Betreuer] Landgraf. "Central and peripheral aspects of hypothalamic-pituitary-adrenal (HPA) axis dysfunction : insights from mice selectively bred for extremes in stress reactivity / Jan-Michael Heinzmann. Betreuer: Rainer Landgraf." München : Universitätsbibliothek der Ludwig-Maximilians-Universität, 2012. http://d-nb.info/1028191367/34.

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Green, Alexis Suzanne. "Intravenous Self-Administration of Alcohol in Selectively Bred High- and Low- Alcohol Preferring Mice." Thesis, 2011. http://hdl.handle.net/1805/2612.

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Indiana University-Purdue University Indianapolis (IUPUI)
Genetic vulnerability to alcoholism is theorized to be caused by multiple interacting genetic loci, each with a small to modest effect combining under certain environmental influences to contribute to vulnerability to ethanol dependence. Animal models such as selectively bred rodent lines can be used to address this hypothesis of genetic vulnerability. High-drinking lines are implicitly assumed by many to be evidence of high ethanol reinforcement without consideration for variables such as differential pre- and post ingestive effects, low response to alcohol or novelty-seeking. Therefore, it is an open question as to whether animal studies support the idea that genetic differences in free-choice drinking are correlated with genetic differences in other assessments of ethanol-reinforced behavior, including those utilizing operant and classical conditioning. Thus, the present study utilizes selectively bred High- and Low- Alcohol Preferring mice tested for operant intravenous alcohol administration to address the hypothesis that High Alcohol Preferring mice would show evidence of greater alcohol reinforcement than their selectively bred opposite, Low Alcohol Preferring mice. Evidence for greater reinforcement was supported by High Alcohol Preferring mice voluntarily pressing a lever to administer an intravenous dose of alcohol in a two lever choice paradigm, administering higher doses of intravenous alcohol, and tracking the location of the active alcohol lever during a lever reversal procedure in comparison to Low Alcohol Preferring mice. This study supports the High- and Low- Alcohol Preferring mice as a useful genetic model of alcohol-related vulnerability even when utilizing a route of administration that bypasses the digestive system.
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Carron, Claire R. "A Novel Risky Decision-Making Task in High and Low Alcohol Preferring Mice." Thesis, 2018. http://hdl.handle.net/1805/17957.

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Indiana University-Purdue University Indianapolis (IUPUI)
Deficits in impulse control and decision-making have been implicated in the development and maintenance of alcohol use disorders (AUDs). Individuals with AUD often make disadvantageous choices under conditions of probabilistic risk. The Iowa Gambling Task (IGT) is often used to measure risky decision-making, in which impaired individuals tend to favor large, infrequent rewards even when punished for these choices, rather than smaller, safer, and more advantageous rewards. It remains poorly understood if these deficits are behaviors under genetic control and if ethanol intoxication may alter decision-making. High and Low Alcohol Preferring (HAP3 and LAP3, respectively) mice were trained on a novel gambling task to investigate these possible influences. In Experiment 1, HAP3s and LAP3s responded for a 0.1% saccharin solution, choosing between a risky and a safe option. Importantly, choosing the risky option was meant to be ultimately disadvantageous. In Experiment 2, these same HAP3 mice responded for saccharin or saccharin plus 10% ethanol. Contrary to hypothesis, LAP3s preferred the risky option more than HAP3s. Alcohol increased preference for the risky lever, but only in male mice. HAP3 preference for the safe lever may be explained by higher motivation to obtain sweet rewards, or higher overall avidity for responding. Ethanol-induced changes in male risk behavior may be explained by higher androgen levels, but further investigation is required. Similarly, continued research is necessary to optimize a risky decision-making task for both lines, and thus investigate possible genetic differences in risk acceptance that correlate with differences in alcohol intake.
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Knapman, Alana [Verfasser]. "Cognitive deficits and their underlying structural and functional alterations in mice selectively bred for high stress reactivity / Alana Knapman." 2010. http://d-nb.info/100997419X/34.

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(5931026), Claire Carron. "A Novel Risky Decision-Making Task in High and Low Alcohol Preferring Mice." Thesis, 2019.

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Abstract:

Deficits in impulse control and decision-making have been implicated in the development and maintenance of alcohol use disorders (AUDs). Individuals with AUD often make disadvantageous choices under conditions of probabilistic risk. The Iowa Gambling Task (IGT) is often used to measure risky decision-making, in which impaired individuals tend to favor large, infrequent rewards even when punished for these choices, rather than smaller, safer, and more advantageous rewards. It remains poorly understood if these deficits are behaviors under genetic control and if ethanol intoxication may alter decision-making. High and Low Alcohol Preferring (HAP3 and LAP3, respectively) mice were trained on a novel gambling task to investigate these possible influences. In Experiment 1, HAP3s and LAP3s responded for a 0.1% saccharin solution, choosing between a risky and a safe option. Importantly, choosing the risky option was meant to be ultimately disadvantageous. In Experiment 2, these same HAP3 mice responded for saccharin or saccharin plus 10% ethanol. Contrary to hypothesis, LAP3s preferred the risky option more than HAP3s. Alcohol increased preference for the risky lever, but only in male mice. HAP3 preference for the safe lever may be explained by higher motivation to obtain sweet rewards, or higher overall avidity for responding. Ethanol-induced changes in male risk behavior may be explained by higher androgen levels, but further investigation is required. Similarly, continued research is necessary to optimize a risky decision-making task for both lines, and thus investigate possible genetic differences in risk acceptance that correlate with differences in alcohol intake.

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Book chapters on the topic "Selectively bred mice"

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Nagao, Mototsugu, Jonathan Lou S. Esguerra, Anna Wendt, Akira Asai, Hitoshi Sugihara, Shinichi Oikawa, and Lena Eliasson. "Selectively Bred Diabetes Models: GK Rats, NSY Mice, and ON Mice." In Methods in Molecular Biology, 25–54. New York, NY: Springer US, 2020. http://dx.doi.org/10.1007/978-1-0716-0385-7_3.

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McCarty, Richard. "Stress and Schizophrenia." In Stress and Mental Disorders: Insights from Animal Models, 225–66. Oxford University Press, 2020. http://dx.doi.org/10.1093/med-psych/9780190697266.003.0008.

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Developing animal models of schizophrenia is challenging because of the uniquely human nature of some of the classic symptoms of the disorder (e.g., hallucinations, delusions, disordered thought). Several efforts have been guided by the neurodevelopmental hypothesis of schizophrenia and have included exposure of animals to stressful stimulation. Other animal models have involved prenatal exposure to maternal immune activation or drugs that disrupt neuronal development, followed by stress during adolescence or in early adulthood to unmask vulnerabilities. Neonatal hippocampal lesions have been employed in other animal models of schizophrenia. Another profitable approach has been to selectively breed laboratory mice or rats for their susceptibility to dopaminergic drugs. A more recent approach has been to develop laboratory mice with targeted alterations in risk genes for schizophrenia that were previously identified in clinical studies. In many cases, the effects of these risk genes are unmasked by exposure of animals to stressful stimulation during specific stages of postnatal development.
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Reports on the topic "Selectively bred mice"

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Coyner, Jennifer L. Differential Expression of Phosphorylated Mitogen-Activated Protein Kinase (pMAPK) in the Lateral Amygdala of Mice Selectively Bred for High and Low Fear. Fort Belvoir, VA: Defense Technical Information Center, June 2013. http://dx.doi.org/10.21236/ad1012913.

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