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Journal articles on the topic 'Mice – Physiology'

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Published: 4 June 2021

Last updated: 25 January 2023

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1

Modaresi, Mehrdad, and Mansoureh Emadi. "The Effects of Rosemary Extract on Spermatogenesis and Sexual Hormones of Mice under Heat Stress." Trends Journal of Sciences Research 3, no. 2 (September 7, 2018): 69–74. http://dx.doi.org/10.31586/physiology.0302.02.

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2

Choudhury, Chinmoy, Meenakshi Bawari, and G. D. Sharma G. D. Sharma. "Biochemical Screening of The Effect of a Plant Extract on Albino Mice Physiology." International Journal of Scientific Research 2, no. 8 (June 1, 2012): 38–39. http://dx.doi.org/10.15373/22778179/aug2013/13.

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3

James, Jeanne F., Timothy E. Hewett, and Jeffrey Robbins. "Cardiac Physiology in Transgenic Mice." Circulation Research 82, no. 4 (March 9, 1998): 407–15. http://dx.doi.org/10.1161/01.res.82.4.407.

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4

Kale, Ajit, Ivo Amende, Katrina Piskorski, Victor Chu, Jose M. Otero, Peter Mueller, and Thomas G. Hampton. "Non-invasive Physiology in Conscious Mice." Alternatives to Laboratory Animals 32, no. 1_suppl (January 2004): 195–201. http://dx.doi.org/10.1177/026119290403201s33.

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5

VERKMAN, A. S. "Lessons on Renal Physiology from Transgenic Mice Lacking Aquaporin Water Channels." Journal of the American Society of Nephrology 10, no. 5 (May 1999): 1126–35. http://dx.doi.org/10.1681/asn.v1051126.

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Abstract. Several aquaporin-type water channels are expressed in kidney: AQP1 in the proximal tubule, thin descending limb of Henle, and vasa recta; AQP2, AQP3, and AQP4 in the collecting duct; AQP6 in the papilla; and AQP7 in the proximal tubule. AQP2 is the vasopressin-regulated water channel that is important in hereditary and acquired diseases affecting urine-concentrating ability. It has been difficult to establish the roles of the other aquaporins in renal physiology because suitable aquaporin inhibitors are not available. One approach to the problem has been to generate and analyze transgenic knockout mice in which individual aquaporins have been selectively deleted by targeted gene disruption. Phenotype analysis of kidney and extrarenal function in knockout mice has been very informative in defining the role of aquaporins in organ physiology and addressing basic questions regarding the route of transepithelial water transport and the mechanism of near isoosmolar fluid reabsorption. This article describes new renal physiologic insights revealed by phenotype analysis of aquaporin-knockout mice and the prospects for further basic and clinical developments.

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6

Sieck, Gary C. "Physiology in Perspective: Of Mice and Men." Physiology 34, no. 1 (January 1, 2019): 3–4. http://dx.doi.org/10.1152/physiol.00049.2018.

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7

Lindsey, Merry L., Zamaneh Kassiri, Jitka A. I. Virag, Lisandra E. de Castro Brás, and Marielle Scherrer-Crosbie. "Guidelines for measuring cardiac physiology in mice." American Journal of Physiology-Heart and Circulatory Physiology 314, no. 4 (April 1, 2018): H733—H752. http://dx.doi.org/10.1152/ajpheart.00339.2017.

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Cardiovascular disease is a leading cause of death, and translational research is needed to understand better mechanisms whereby the left ventricle responds to injury. Mouse models of heart disease have provided valuable insights into mechanisms that occur during cardiac aging and in response to a variety of pathologies. The assessment of cardiovascular physiological responses to injury or insult is an important and necessary component of this research. With increasing consideration for rigor and reproducibility, the goal of this guidelines review is to provide best-practice information regarding how to measure accurately cardiac physiology in animal models. In this article, we define guidelines for the measurement of cardiac physiology in mice, as the most commonly used animal model in cardiovascular research.Listen to this article’s corresponding podcast at http://ajpheart.podbean.com/e/guidelines-for-measuring-cardiac-physiology-in-mice/ .

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Gordon, C. J. "Thermal physiology of laboratory mice: Defining thermoneutrality." Journal of Thermal Biology 37, no. 8 (December 2012): 654–85. http://dx.doi.org/10.1016/j.jtherbio.2012.08.004.

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Rao, Shobha, and A. S. Verkman. "Analysis of organ physiology in transgenic mice." American Journal of Physiology-Cell Physiology 279, no. 1 (July 1, 2000): C1—C18. http://dx.doi.org/10.1152/ajpcell.2000.279.1.c1.

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The increasing availability of transgenic mouse models of gene deletion and human disease has mandated the development of creative approaches to characterize mouse phenotype. The mouse presents unique challenges to phenotype analysis because of its small size, habits, and inability to verbalize clinical symptoms. This review describes strategies to study mouse organ physiology, focusing on the cardiovascular, pulmonary, renal, gastrointestinal, and neurobehavioral systems. General concerns about evaluating mouse phenotype studies are discussed. Monitoring and anesthesia methods are reviewed, with emphasis on the feasibility and limitations of noninvasive and invasive procedures to monitor physiological parameters, do cannulations, and perform surgical procedures. Examples of phenotype studies are cited to demonstrate the practical applications and limitations of the measurement methods. The repertoire of phenotype analysis methods reviewed here should be useful to investigators involved in or contemplating the use of mouse models.

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10

Gassmann, Max, and Thierry Hennet. "From Genetically Altered Mice to Integrative Physiology." Physiology 13, no. 2 (April 1998): 53–57. http://dx.doi.org/10.1152/physiologyonline.1998.13.2.53.

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Transgenic and gene-targeted mice permit the study of the function(s) of the single gene(s) in a whole organism, thereby relating molecular biology and integrative physiology. To demonstrate the potential of transgenic models, we present in this review some physiologically relevant information obtained from genetically engineered mice.

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Cepas, Vanesa, Pedro González-Menéndez, Alejandro Álvarez-Artime, Juan Carlos Mayo, and Rosa María Sáinz. "SOD2 levels alter reproductive physiology in mice." Free Radical Biology and Medicine 96 (July 2016): S32. http://dx.doi.org/10.1016/j.freeradbiomed.2016.04.064.

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12

Macchiarini, Francesca, Markus G. Manz, A. Karolina Palucka, and Leonard D. Shultz. "Humanized mice." Journal of Experimental Medicine 202, no. 10 (November 21, 2005): 1307–11. http://dx.doi.org/10.1084/jem.20051547.

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Animal models have been instrumental in increasing the understanding of human physiology, particularly immunity. However, these animal models have been limited by practical considerations and genetic diversity. The creation of humanized mice that carry partial or complete human physiological systems may help overcome these obstacles. The National Institute of Allergy and Infectious Diseases convened a workshop on humanized mouse models for immunity in Bethesda, MD, on June 13–14, 2005, during which researchers discussed the benefits and limitations of existing animal models and offered insights into the development of future humanized mouse models.

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13

Tamashiro, Kellie L. K., Teruhiko Wakayama, Yukiko Yamazaki, Hidenori Akutsu, Stephen C. Woods, Sylvia Kondo, Ryuzo Yanagimachi, and Randall R. Sakai. "Phenotype of Cloned Mice: Development, Behavior, and Physiology." Experimental Biology and Medicine 228, no. 10 (November 2003): 1193–200. http://dx.doi.org/10.1177/153537020322801015.

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14

Myers, Daniel L., Kelley J. Harmon, Volkhard Lindner, and Lucy Liaw. "Alterations of Arterial Physiology in Osteopontin-Null Mice." Arteriosclerosis, Thrombosis, and Vascular Biology 23, no. 6 (June 2003): 1021–28. http://dx.doi.org/10.1161/01.atv.0000073312.34450.16.

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15

Lei, Yuan, Xuejin Zhang, Maomao Song, Jihong Wu, and Xinghuai Sun. "Aqueous Humor Outflow Physiology in NOS3 Knockout Mice." Investigative Opthalmology & Visual Science 56, no. 8 (July 28, 2015): 4891. http://dx.doi.org/10.1167/iovs.15-16564.

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16

Lindström, Per. "The Physiology of Obese-Hyperglycemic Mice [ob/obMice]." Scientific World JOURNAL 7 (2007): 666–85. http://dx.doi.org/10.1100/tsw.2007.117.

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This review summarizes key aspects of what has been learned about the physiology of leptin deficiency as it can be observed in obese-hyperglycemicob/obmice. These mice lack functional leptin. They are grossly overweight and hyperphagic, particularly at young ages, and develop severe insulin resistance. They have been used as a model for obesity and as a rich source of pancreatic islets with high insulin release capacity. The leptin deficiency manifests also with regard to immune function, the cardiovascular system including angiogenesis, supportive tissue function, malignancies, and reproductive function.ob/obMice are well suited for studies on the interaction between leptin and insulin, and for studies on initial aspects of metabolic disturbances leading to type-2diabetes.

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Mobley, C. Brooks, Ivan J. Vechetti, Taylor R. Valentino, and John J. McCarthy. "CORP: Using transgenic mice to study skeletal muscle physiology." Journal of Applied Physiology 128, no. 5 (May 1, 2020): 1227–39. http://dx.doi.org/10.1152/japplphysiol.00021.2020.

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The development of tissue-specific inducible transgenic mice has provided a powerful tool to study gene function and cell biology in almost any tissue of interest at any given time within the animal’s life. The purpose of this review is to describe how to use two different inducible transgenic systems, the Cre-loxP system and the Tet-ON/OFF system, that can be used to study skeletal muscle physiology. Myofiber- and satellite cell-specific Cre-loxP transgenic mice are described as is how these mice can be used to knockout a gene of interest or to deplete satellite cells in adult skeletal muscle, respectively. A myofiber-specific Tet-ON system is described as is how such mice can be used to overexpress a gene of interest or to label myonuclei. How to effectively breed and genotype the transgenic mice are also described in detail. The hope is this review will provide the basic information necessary to facilitate the incorporation of tissue-specific inducible transgenic mice into a skeletal muscle research program.

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18

Meir, Tomer, Ronen Levi, Liesbet Lieben, Steven Libutti, Geert Carmeliet, Roger Bouillon, Justin Silver, and Tally Naveh-Many. "Deletion of the vitamin D receptor specifically in the parathyroid demonstrates a limited role for the receptor in parathyroid physiology." American Journal of Physiology-Renal Physiology 297, no. 5 (November 2009): F1192—F1198. http://dx.doi.org/10.1152/ajprenal.00360.2009.

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1,25(OH)2D3 decreases parathyroid hormone (PTH) gene transcription through the vitamin D receptor (VDR). Total body VDR−/− mice have high PTH levels, hypocalcemia, hypophosphatemia, and bone malformations. To investigate PTH regulation by the VDR specifically in the parathyroid, we generated parathyroid-specific VDR knockout mice ( PT-VDR−/−). In both strains, there was a decrease in parathyroid calcium receptor (CaR) levels. The number of proliferating parathyroid cells was increased in the VDR−/− mice but not in the PT-VDR−/− mice. Serum PTH levels were moderately but significantly increased in the PT-VDR−/− mice with normal serum calcium levels. The sensitivity of the parathyroid glands of the PT-VDR−/− mice to calcium was intact as measured by serum PTH levels after changes in serum calcium. This indicates that the reduced CaR in the PT-VDR−/− mice enables a physiologic response to serum calcium. Serum C-terminal collagen crosslinks, a marker of bone resorption, were increased in the PT-VDR−/− mice with no change in the bone formation marker, serum osteocalcin, consistent with a resorptive effect due to the increased serum PTH levels in the PT-VDR−/− mice. Therefore, deletion of the VDR specifically in the parathyroid decreases parathyroid CaR expression and only moderately increases basal PTH levels, suggesting that the VDR has a limited role in parathyroid physiology.

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19

Chang, Jason Y. H., W. Daniel Stamer, Jacques Bertrand, A. Thomas Read, Catherine M. Marando, C. Ross Ethier, and Darryl R. Overby. "Role of nitric oxide in murine conventional outflow physiology." American Journal of Physiology-Cell Physiology 309, no. 4 (August 15, 2015): C205—C214. http://dx.doi.org/10.1152/ajpcell.00347.2014.

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Elevated intraocular pressure (IOP) is the main risk factor for glaucoma. Exogenous nitric oxide (NO) decreases IOP by increasing outflow facility, but whether endogenous NO production contributes to the physiological regulation of outflow facility is unclear. Outflow facility was measured by pressure-controlled perfusion in ex vivo eyes from C57BL/6 wild-type (WT) or transgenic mice expressing human endothelial NO synthase (eNOS) fused to green fluorescent protein (GFP) superimposed on the endogenously expressed murine eNOS (eNOS-GFPtg). In WT mice, exogenous NO delivered by 100 μM S-nitroso- N-acetylpenicillamine (SNAP) increased outflow facility by 62 ± 28% (SD) relative to control eyes perfused with the inactive SNAP analog N-acetyl-d-penicillamine (NAP; n = 5, P = 0.016). In contrast, in eyes from eNOS-GFPtg mice, SNAP had no effect on outflow facility relative to NAP (−9 ± 4%, P = 0.40). In WT mice, the nonselective NOS inhibitor NG-nitro-l-arginine methyl ester (l-NAME, 10 μM) decreased outflow facility by 36 ± 13% ( n = 5 each, P = 0.012), but 100 μM l-NAME had no detectable effect on outflow facility (−16 ± 5%, P = 0.22). An eNOS-selective inhibitor (cavtratin, 50 μM) decreased outflow facility by 19 ± 12% in WT ( P = 0.011) and 39 ± 25% in eNOS-GFPtg ( P = 0.014) mice. In the conventional outflow pathway of eNOS-GFPtg mice, eNOS-GFP expression was localized to endothelial cells lining Schlemm's canal and the downstream vessels, with no apparent expression in the trabecular meshwork. These results suggest that endogenous NO production by eNOS within endothelial cells of Schlemm's canal or downstream vessels contributes to the physiological regulation of aqueous humor outflow facility in mice, representing a viable strategy to more successfully lower IOP in glaucoma.

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20

Premont, Richard T., and Jonathan S. Stamler. "Essential Role of Hemoglobin βCys93 in Cardiovascular Physiology." Physiology 35, no. 4 (July 1, 2020): 234–43. http://dx.doi.org/10.1152/physiol.00040.2019.

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The supply of oxygen to tissues is controlled by microcirculatory blood flow. One of the more surprising discoveries in cardiovascular physiology is the critical dependence of microcirculatory blood flow on a single conserved cysteine within the β-subunit (βCys93) of hemoglobin (Hb). βCys93 is the primary site of Hb S-nitrosylation [i.e., S-nitrosothiol (SNO) formation to produce S-nitrosohemoglobin (SNO-Hb)]. Notably, S-nitrosylation of βCys93 by NO is favored in the oxygenated conformation of Hb, and deoxygenated Hb releases SNO from βCys93. Since SNOs are vasodilatory, this mechanism provides a physiological basis for how tissue hypoxia increases microcirculatory blood flow (hypoxic autoregulation of blood flow). Mice expressing βCys93A mutant Hb (C93A) have been applied to understand the role of βCys93, and RBCs more generally, in cardiovascular physiology. Notably, C93A mice are unable to effect hypoxic autoregulation of blood flow and exhibit widespread tissue hypoxia. Moreover, reactive hyperemia (augmentation of blood flow following transient ischemia) is markedly impaired. C93A mice display multiple compensations to preserve RBC vasodilation and overcome tissue hypoxia, including shifting SNOs to other thiols on adult and fetal Hbs and elsewhere in RBCs, and growing new blood vessels. However, compensatory vasodilation in C93A mice is uncoupled from hypoxic control, both peripherally (e.g., predisposing to ischemic injury) and centrally (e.g., impairing hypoxic drive to breathe). Altogether, physiological studies utilizing C93A mice are confirming the allosterically controlled role of SNO-Hb in microvascular blood flow, uncovering essential roles for RBC-mediated vasodilation in cardiovascular physiology and revealing new roles for RBCs in cardiovascular disease.

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21

Dauchy, Robert T., David E. Blask, Aaron E. Hoffman, Shulin Xiang, John P. Hanifin, Benjamin Warfield, George C. Brainard, et al. "Influence of Daytime LED Light Exposure on Circadian Regulatory Dynamics of Metabolism and Physiology in Mice." Comparative Medicine 69, no. 5 (October 1, 2019): 350–73. http://dx.doi.org/10.30802/aalas-cm-19-000001.

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Light is a potent biologic force that profoundly influences circadian, neuroendocrine, and neurobehavioral regulation in animals. Previously we examined the effects of light-phase exposure of rats to white light-emitting diodes (LED), which emit more light in the blue-appearing portion of the visible spectrum (465 to 485 nm) than do broad-spectrum cool white fluorescent (CWF) light, on the nighttime melatonin amplitude and circadian regulation of metabolism and physiology. In the current studies, we tested the hypothesis that exposure to blue-enriched LED light at day (bLAD), compared with CWF, promotes the circadian regulation of neuroendocrine, metabolic, and physiologic parameters that are associated with optimizing homeostatic regulation of health and wellbeing in 3 mouse strains commonly used in biomedical research (C3H [melatonin-producing], C57BL/6, and BALB/c [melatonin-non-producing]). Compared with male and female mice housed for 12 wk under 12:12-h light:dark (LD) cycles in CWF light, C3H mice in bLAD evinced 6-fold higher peak plasma melatonin levels at the middark phase; in addition, high melatonin levels were prolonged 2 to 3 h into the light phase. C57BL/6 and BALB/c strains did not produce nighttime pineal melatonin. Body growth rates; dietary and water intakes; circadian rhythms of arterial blood corticosterone, insulin, leptin, glucose, and lactic acid; pO2 and pCO2; fatty acids; and metabolic indicators (cAMP, DNA, tissue DNA 3H-thymidine incorporation, fat content) in major organ systems were significantly lower and activation of major metabolic signaling pathways (mTOR, GSK3β, and SIRT1) in skeletal muscle and liver were higher only in C3H mice in bLAD compared with CWF. These data show that exposure of C3H mice to bLAD compared with CWF has a marked positive effect on the circadian regulation of neuroendocrine, metabolic, and physiologic parameters associated with the promotion of animal health and wellbeing that may influence scientific outcomes. The absence of enhancement in amelatonic strains suggests hyperproduction of nighttime melatonin may be a key component of the physiology.

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22

Charlton, Harry. "Neural transplantation in hypogonadal (hpg) mice – physiology and neurobiology." Reproduction 127, no. 1 (January 2004): 3–12. http://dx.doi.org/10.1530/rep.1.00066.

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The hypogonadal (hpg) mouse mutant has a deletion in the region encoding the hypothalamic gonadotrophic hormone-releasing hormone decapeptide. As a consequence pituitary gonadotrophic hormone synthesis and release is severely curtailed and there is little or no post-natal gonadal development. Grafts of late fetal/early neonatal brain tissue containing the decapeptide-producing neurones into the third ventricle of hpg mice result, in a majority of animals, in a near normalisation of pituitary function with full spermatogenesis in male mice and full follicular and uterine development in females. The vast majority of positive responding females with vaginal opening and uterus growth show no evidence of spontaneous oestrous cycles, ovulation or corpora lutea. These female mice mate with normal males with many of them demonstrating reflex ovulation. In both male and female mutants with successful grafts there is an absence of gonadal steroid negative feedback upon the synthesis and secretion of pituitary gonadotrophic hormones. The releasing factor axon terminals from grafts within the third ventricle identified by immunohistochemical methods are targeted specifically to the median eminence. There is evidence for host innervation of grafts, but how specific this is for the control of gonadotrophic hormone-releasing hormone cell bodies remains to be elucidated.

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Dlugosz, Elizabeth M., Breanna N. Harris, Wendy Saltzman, and Mark A. Chappell. "Glucocorticoids, Aerobic Physiology, and Locomotor Behavior in California Mice." Physiological and Biochemical Zoology 85, no. 6 (November 2012): 671–83. http://dx.doi.org/10.1086/667809.

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24

Daniel, Hannelore, Amin Moghaddas Gholami, David Berry, Charles Desmarchelier, Hannes Hahne, Gunnar Loh, Stanislas Mondot, et al. "High-fat diet alters gut microbiota physiology in mice." ISME Journal 8, no. 2 (September 12, 2013): 295–308. http://dx.doi.org/10.1038/ismej.2013.155.

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25

Leibel, R. L. "Molecular physiology of weight regulation in mice and humans." International Journal of Obesity 32, S7 (December 2008): S98—S108. http://dx.doi.org/10.1038/ijo.2008.245.

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26

Zielinska, Agnieszka E., Elizabeth A. Walker, Paul M. Stewart, and Gareth G. Lavery. "Biochemistry and physiology of hexose-6-phosphate knockout mice." Molecular and Cellular Endocrinology 336, no. 1-2 (April 2011): 213–18. http://dx.doi.org/10.1016/j.mce.2010.12.004.

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27

Muglia, Louis J., Lauren Jacobson, Stacie C. Weninger, Katia P. Karalis, Kyeong-Hoon Jeong, and Joseph A. Majzoub. "The physiology of corticotropin-releasing hormone deficiency in mice." Peptides 22, no. 5 (May 2001): 725–31. http://dx.doi.org/10.1016/s0196-9781(01)00385-0.

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Hanson, Jesse E., Adrienne L. Orr, and Daniel V. Madison. "Altered Hippocampal Synaptic Physiology in Aged Parkin-Deficient Mice." NeuroMolecular Medicine 12, no. 3 (March 16, 2010): 270–76. http://dx.doi.org/10.1007/s12017-010-8113-y.

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Tyan, J. L., M. I. Sotelo, C. M. Markunas, J. G. Morrow, and A. Eban-Rothschild. "0211 Sleep-Preparatory Behaviors Modulate Sleep Physiology in Mice." Sleep 43, Supplement_1 (April 2020): A82. http://dx.doi.org/10.1093/sleep/zsaa056.209.

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Abstract Introduction Prior to sleep, animals perform various sleep-preparatory behaviors, yet little is known about their contribution to sleep physiology. Sleep hygiene, which involves proper sleep preparation, is an effective treatment for insomnia in humans. The high prevalence of sleep disorders and drawbacks of available pharmacological interventions necessitate a better understanding of the ecological and evolutionary contexts of sleep. Nest-building is a sleep-preparatory behavior performed by many species. In this study, we aimed to determine whether the presence of a nest modulates sleep. Specifically, we investigated the effects of a nest on sleep/wake architecture and activity in wake-promoting neurons in mice. Methods To examine the role of nesting in sleep/wake architecture, we recorded EEG/EMG activity over 24 hrs (n=14, 7 males and 7 females) in the presence/absence of a nest. To determine whether the lack of a nest activates wake-promoting neurons, we utilized TRAP (targeted recombination in active populations) technology to label neurons activated by nest removal (n=4 mice per experimental group). Results Mice without nests exhibited increased latencies to NREM and REM sleep and spent less time asleep during the inactive/light phase. Mice without nests also exhibited shorter episodes of NREM and REM sleep and more transitions between arousal states. Additionally, our preliminary results suggest that nest removal significantly increases population activity in multiple brain regions, including several cortical and thalamic regions. Conclusion Our findings support the hypothesis that the presence of a nest facilitates and consolidates sleep. The causal role of specific neuronal populations in sleep fragmentation in the absence of a nest remains to be elucidated. Taken together, our findings provide the first evidence for a role of sleep-preparatory behaviors in the facilitation and consolidation of sleep and could shape the development of novel treatments for sleep disorders. Support This work is supported by the Sloan Alfred P. Foundation, the Brain and Behavior Research Foundation, and the Eisenberg Translational Research Award.

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Kitamura, Tadahiro, C. Ronald Kahn, and Domenico Accili. "Insulin Receptor Knockout Mice." Annual Review of Physiology 65, no. 1 (March 2003): 313–32. http://dx.doi.org/10.1146/annurev.physiol.65.092101.142540.

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Cheatham, M. A., K. H. Huynh, J. Gao, J. Zuo, and P. Dallos. "Cochlear function inPrestinknockout mice." Journal of Physiology 560, no. 3 (October 29, 2004): 821–30. http://dx.doi.org/10.1113/jphysiol.2004.069559.

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Dohm, M. R., C. S. Richardson, and T. Garland. "Exercise physiology of wild and random-bred laboratory house mice and their reciprocal hybrids." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 267, no. 4 (October 1, 1994): R1098—R1108. http://dx.doi.org/10.1152/ajpregu.1994.267.4.r1098.

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We conducted a "common garden" experiment to compare aspects of exercise physiology and voluntary wheel-running behavior in wild and random-bred (i.e., non-inbred) laboratory house mice and their reciprocal crosses. Analysis of covariance indicated that, after effects of body mass and other appropriate covariates (e.g., age at testing) were accounted for, wild (range 2.46-3.30 m/s, n = 12) and hybrid (range 1.69-3.30 m/s, n = 24) mice exhibited forced maximal sprint running speeds that averaged approximately 50% higher than those of random-bred laboratory mice (range 1.11-2.12 m/s, n = 19). Wild and hybrid mice also had significantly higher (+22%) mass-corrected maximal rates of oxygen consumption (VO2max) during forced exercise and greater (+12%) relative ventricle masses than lab mice. Wild and hybrid mice also showed statistically higher swimming endurance times relative to body mass than lab mice, although these differences were insignificant when body mass was not used as a covariate. No significant differences were found for relative gastrocnemius muscle mass, liver mass, hematocrit, or blood hemoglobin content. During a 7-day test on voluntary activity wheels, both wild and hybrid mice ran significantly more total revolutions (+101%), ran at higher average velocities when they were active (+69%), and exhibited higher maximum revolutions in any single 1-min period (+41% on the 7th day of testing), but the total number of active 1-min intervals did not differ significantly among groups. In general, the behavioral and/or whole organisms performance traits showed greater differences than the lower-level traits; thus, during the domestication of house mice, behavior may have evolved more rapidly than physiology.

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Semenza, Gregg L. "O2-regulated gene expression: transcriptional control of cardiorespiratory physiology by HIF-1." Journal of Applied Physiology 96, no. 3 (March 2004): 1173–77. http://dx.doi.org/10.1152/japplphysiol.00770.2003.

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The cardiovascular and respiratory systems play key roles in O2 homeostasis. Physiological responses to hypoxia involve changes in gene expression that are mediated by the transcriptional activator hypoxia-inducible factor (HIF)-1. Analysis of mice heterozygous for a knockout allele at the locus encoding the O2-regulated HIF-1α or HIF-2α subunit has revealed that these proteins are required for multiple physiological responses to chronic hypoxia, including erythrocytosis and pulmonary vascular remodeling. In mice with partial HIF-2α deficiency, hypoxia-induced expression of endothelin-1 and norepinephrine is dramatically impaired, and the mice fail to develop pulmonary hypertension after 4 wk of exposure to 10% O2. In mice with partial HIF-1α deficiency, the ability of the carotid body to sense and/or respond to acute or chronic hypoxia is lost. In wild-type mice, brief episodes of intermittent hypoxia are sufficient to induce production of erythropoietin (EPO), which protects the heart against apoptosis after ischemia-reperfusion, whereas in mice with partial HIF-1α deficiency, intermittent hypoxia does not induce EPO production or cardiac protection. Parenteral administration of EPO to rodents is sufficient to induce dramatic protection against ischemia-reperfusion injury in the heart. Thus HIF-1 mediates critical physiological responses to hypoxia, and the elucidation of these homeostatic mechanisms may lead to novel therapies for the most common causes of mortality in the US population.

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Stewart, Nathan D., Gabriela F. Mastromonaco, and Gary Burness. "No island-effect on glucocorticoid levels for a rodent from a near-shore archipelago." PeerJ 8 (February 18, 2020): e8590. http://dx.doi.org/10.7717/peerj.8590.

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Island rodents are often larger and live at higher population densities than their mainland counterparts, characteristics that have been referred to as “island syndrome”. Island syndrome has been well studied, but few studies have tested for island-mainland differences in stress physiology. We evaluated island syndrome within the context of stress physiology of white-footed mice (Peromyscus leucopus) captured from 11 islands and five mainland sites in Thousand Islands National Park, Ontario, Canada. Stress physiology was evaluated by quantifying corticosterone (a stress biomarker), the primary glucocorticoid in mice, from hair and its related metabolites from fecal samples. White-footed mice captured in this near-shore archipelago did not display characteristics of island syndrome, nor differences in levels of hair corticosterone or fecal corticosterone metabolites compared with mainland mice. We suggest that island white-footed mice experience similar degrees of stress in the Thousand Islands compared with the mainland. Although we did not find evidence of island syndrome or differences in glucocorticoid levels, we identified relationships between internal (sex, body mass) and external (season) factors and our hormonal indices of stress in white-footed mice.

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Oliverio, Michael I., and Thomas M. Coffman. "Angiotensin II Receptor Physiology Using Gene Targeting." Physiology 15, no. 4 (August 2000): 171–75. http://dx.doi.org/10.1152/physiologyonline.2000.15.4.171.

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The study of mice with targeted disruptions of angiotensin receptor genes has provided new insights into the roles of the individual receptor subtypes, i.e., AT1A, AT1B, and AT2, in growth, development, and the regulation of blood pressure.

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Jay Bean, N., Antonio A. Nunez, and Charles J. Wysocki. "70-kHz vocalizations by male mice do not inhibit aggression in lactating mice." Behavioral and Neural Biology 46, no. 1 (July 1986): 46–53. http://dx.doi.org/10.1016/s0163-1047(86)90883-6.

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Wershil, Barry K. "IX. Mast cell-deficient mice and intestinal biology." American Journal of Physiology-Gastrointestinal and Liver Physiology 278, no. 3 (March 1, 2000): G343—G348. http://dx.doi.org/10.1152/ajpgi.2000.278.3.g343.

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Mutant mice that express abnormalities in mast cell development represent a powerful tool for the investigation of multiple aspects of mast cell biology. In addition, the identification of the genes affected by these mutations has not only increased our knowledge about the mast cell but has opened new areas of investigation as to the role of these gene products in gastrointestinal pathology, immunology, and physiology.

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Hamada, Akiko, Kiyotoshi Inenaga, Shuichi Nakamura, Masamichi Terashita, and Hiroshi Yamashita. "Disorder of salivary secretion in inbred polydipsic mouse." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 278, no. 4 (April 1, 2000): R817—R823. http://dx.doi.org/10.1152/ajpregu.2000.278.4.r817.

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To find mechanisms of an extreme polydipsia in an inbred strain of mice, STR/N, this study was undertaken using Institute of Cancer Research (ICR) mice as a control. During food deprivation, daily water intake of both strains decreased. The decrement in the STR/N mice was larger than that in the ICR mice. During dehydration, daily food intake of the STR/N mice was smaller than that of the ICR mice. These data indicate that prandial drinking was more severely affected for the STR/N mice. Under anesthesia, the stimulated salivary secretion by pilocarpine of the STR/N mice was significantly smaller than that of the ICR mice. The submandibular gland of the STR/N mice was lighter and harder than that of the ICR mice. After desalivation from the major three salivary glands, the ICR mice drank as much as the STR/N mice. Young STR/N mice with undeveloped polydipsia did not show different salivary secretion stimulated by pilocarpine from the young ICR mice. These findings indicate a dysfunction with age in the salivary glands of the STR/N mice, and they suggest that the decreased saliva induces thirst and triggers extraordinary drinking in the polydipsic mice.

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Wanke, R., E. Wolf, G. Brem, and W. Hermanns. "Physiology and pathology of growth - studies in GH transgenic mice." Journal of Animal Breeding and Genetics 113, no. 1-6 (January 12, 1996): 445–56. http://dx.doi.org/10.1111/j.1439-0388.1996.tb00635.x.

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Chen, Duan, and Chun-Mei Zhao. "Genetically engineered mice: a new paradigm to study gastric physiology." Current Opinion in Gastroenterology 23, no. 6 (November 2007): 602–6. http://dx.doi.org/10.1097/mog.0b013e3282f01dbd.

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Speerschneider, T., and M. B. Thomsen. "Physiology and analysis of the electrocardiographic T wave in mice." Acta Physiologica 209, no. 4 (October 24, 2013): 262–71. http://dx.doi.org/10.1111/apha.12172.

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42

Narumiya, Shuh. "Physiology and pathophysiology of prostanoids; lessons from receptor-knockout mice." Japanese Journal of Pharmacology 82 (2000): 3. http://dx.doi.org/10.1016/s0021-5198(19)47499-4.

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Butler, Avigdor, Xingxuan He, Ronald E. Gordon, Hai-Shan Wu, Shimon Gatt, and Edward H. Schuchman. "Reproductive Pathology and Sperm Physiology in Acid Sphingomyelinase-Deficient Mice." American Journal of Pathology 161, no. 3 (September 2002): 1061–75. http://dx.doi.org/10.1016/s0002-9440(10)64267-8.

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Sutherland, M. A., G. P. Shome, L. E. Hulbert, N. Krebs, M. Wachtel, and J. J. McGlone. "Acute stress affects the physiology and behavior of allergic mice." Physiology & Behavior 98, no. 3 (September 2009): 281–87. http://dx.doi.org/10.1016/j.physbeh.2009.06.003.

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Hamilton, Katherine J., Yukitomo Arao, and Kenneth S. Korach. "Estrogen hormone physiology: Reproductive findings from estrogen receptor mutant mice." Reproductive Biology 14, no. 1 (March 2014): 3–8. http://dx.doi.org/10.1016/j.repbio.2013.12.002.

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Okatani, Yuji, Akihiko Wakatsuki, Russel J. Reiter, and Yasuyo Miyahara. "Acutely administered melatonin restores hepatic mitochondrial physiology in old mice." International Journal of Biochemistry & Cell Biology 35, no. 3 (March 2003): 367–75. http://dx.doi.org/10.1016/s1357-2725(02)00260-1.

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Thorens, B. "Physiology of GLP-1 - Lessons from Glucoincretin Receptor Knockout Mice." Hormone and Metabolic Research 36, no. 11/12 (November 2004): 766–70. http://dx.doi.org/10.1055/s-2004-826161.

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Yamada, Y., and Y. Seino. "Physiology of GIP - A Lesson from GIP Receptor Knockout Mice." Hormone and Metabolic Research 36, no. 11/12 (November 2004): 771–74. http://dx.doi.org/10.1055/s-2004-826162.

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Salgado, Giorgiana, Yi Zhen Ng, Li Fang Koh, Christabelle S. M. Goh, and John E. Common. "Human reconstructed skin xenografts on mice to model skin physiology." Differentiation 98 (November 2017): 14–24. http://dx.doi.org/10.1016/j.diff.2017.09.004.

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Ko, Miau-Hwa, Wen-Pin Chen, Shoei-Yin Lin-Shiau, and Sung-Tsang Hsieh. "Age-Dependent Acrylamide Neurotoxicity in Mice: Morphology, Physiology, and Function." Experimental Neurology 158, no. 1 (July 1999): 37–46. http://dx.doi.org/10.1006/exnr.1999.7102.

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