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Journal articles on the topic 'Mice – Nervous system'

Author: Grafiati

Published: 4 June 2021

Last updated: 7 February 2022

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1

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 α<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.  

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2

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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3

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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4

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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5

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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6

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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8

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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9

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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10

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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11

Kenison, Jessica E., Aditi Jhaveri, Zhaorong Li, Nikita Khadse, Emily Tjon, Sara Tezza, Dominika Nowakowska, et al. "Tolerogenic nanoparticles suppress central nervous system inflammation." Proceedings of the National Academy of Sciences 117, no. 50 (November 25, 2020): 32017–28. http://dx.doi.org/10.1073/pnas.2016451117.

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Therapeutic approaches for the induction of immune tolerance remain an unmet clinical need for the treatment of autoimmune diseases, including multiple sclerosis (MS). Based on its role in the control of the immune response, the ligand-activated transcription factor aryl hydrocarbon receptor (AhR) is a candidate target for novel immunotherapies. Here, we report the development of AhR-activating nanoliposomes (NLPs) to induce antigen-specific tolerance. NLPs loaded with the AhR agonist ITE and a T cell epitope from myelin oligodendrocyte glycoprotein (MOG)35–55 induced tolerogenic dendritic cells and suppressed the development of experimental autoimmune encephalomyelitis (EAE), a preclinical model of MS, in preventive and therapeutic setups. EAE suppression was associated with the expansion of MOG35–55-specific FoxP3+ regulatory T cells (Treg cells) and type 1 regulatory T cells (Tr1 cells), concomitant with a reduction in central nervous system-infiltrating effector T cells (Teff cells). Notably, NLPs induced bystander suppression in the EAE model established in C57BL/6 × SJL F1 mice. Moreover, NLPs ameliorated chronic progressive EAE in nonobese diabetic mice, a model which resembles some aspects of secondary progressive MS. In summary, these studies describe a platform for the therapeutic induction of antigen-specific tolerance in autoimmune diseases.

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12

Yang, Li, Jesse Slone, Zhuo Li, Xiaoting Lou, Yueh-Chiang Hu, Luis F. Queme, Michael P. Jankowski, and Taosheng Huang. "Systemic administration of AAV-Slc25a46 mitigates mitochondrial neuropathy in Slc25a46−/− mice." Human Molecular Genetics 29, no. 4 (January 16, 2020): 649–61. http://dx.doi.org/10.1093/hmg/ddz277.

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Abstract Mitochondrial disorders are the result of nuclear and mitochondrial DNA mutations that affect multiple organs, with the central and peripheral nervous system often affected. Currently, there is no cure for mitochondrial disorders. Currently, gene therapy offers a novel approach for treating monogenetic disorders, including nuclear genes associated with mitochondrial disorders. We utilized a mouse model carrying a knockout of the mitochondrial fusion–fission-related gene solute carrier family 25 member 46 (Slc25a46) and treated them with neurotrophic AAV–PHP.B vector carrying the mouse Slc25a46 coding sequence. Thereafter, we used immunofluorescence staining and western blot to test the transduction efficiency of this vector. Toluidine blue staining and electronic microscopy were utilized to assess the morphology of optic and sciatic nerves following treatment, and the morphology and respiratory chain activity of mitochondria within these tissues were determined as well. The adeno-associated virus (AAV) vector effectively transduced in the cerebrum, cerebellum, heart, liver and sciatic nerves. AAV–Slc25a46 treatment was able to rescue the premature death in the mutant mice (Slc25a46−/−). The treatment-improved electronic conductivity of the peripheral nerves increased mobility and restored mitochondrial complex activities. Most notably, mitochondrial morphology inside the tissues of both the central and peripheral nervous systems was normalized, and the neurodegeneration, chronic neuroinflammation and loss of Purkinje cell dendrites observed within the mutant mice were alleviated. Overall, our study shows that AAV–PHP.B’s neurotrophic properties are plausible for treating conditions where the central nervous system is affected, such as many mitochondrial diseases, and that AAV–Slc25a46 could be a novel approach for treating SLC25A46-related mitochondrial disorders.

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13

Gross, Volkmar, Jens Tank, Michael Obst, Ralph Plehm, Kendall J. Blumer, Andrè Diedrich, Jens Jordan, and Friedrich C. Luft. "Autonomic nervous system and blood pressure regulation in RGS2-deficient mice." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 288, no. 5 (May 2005): R1134—R1142. http://dx.doi.org/10.1152/ajpregu.00246.2004.

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Regulator of G protein signaling (RGS2) deletion in mice prolongs signaling by G protein-coupled vasoconstrictor receptors and increases blood pressure. However, the exact mechanism of the increase in blood pressure is unknown. To address this question we tested autonomic nervous system function and blood pressure regulation in RGS2-deficient mice (RGS2 −/−). We measured arterial blood pressure and heart rate (HR) with telemetry, computed time and frequency-domain measures for blood pressure and HR variability (HRV) as well as baroreflex sensitivity [BRS-low frequency (LF)], and assessed environmental stress sensitivity. Mean arterial blood pressure (MAP) was ∼10 mmHg higher in RGS2 −/− compared with RGS2 +/+ mice, while HR was not different between the groups, indicating a resetting of the baroreceptor reflex. Atropine increased MAP more in RGS2 −/− than in RGS2 +/+ mice while HR responses were not different. Urinary norepinephrine excretion was higher in RGS2 −/− than in RGS2 +/+ mice. The blood pressure decrease following prazosin was more pronounced in RGS2 −/− mice than in RGS2 +/+ mice. The LF and high-frequency (HF) power of HRV were reduced in RGS2 −/− compared with controls while BRS-LF and SBP-LF were not different. Atropine and atropine + metoprolol markedly reduced the HRV parameters in the time (RMSSD) and frequency domain (LF, HF, LF/HF) in both strains. Environmental stress sensitivity was increased in RGS2 −/− mice compared with controls. We conclude that the increase in blood pressure in RGS2 −/− mice is not solely explained by peripheral vascular mechanisms. A central nervous system mechanism might be implicated by an increased sympathetic tone. This state of affairs could lead to a baroreceptor-HR reflex resetting, while BRS remains unimpaired.

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Juricek, Ludmila, and Xavier Coumoul. "The Aryl Hydrocarbon Receptor and the Nervous System." International Journal of Molecular Sciences 19, no. 9 (August 24, 2018): 2504. http://dx.doi.org/10.3390/ijms19092504.

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The aryl hydrocarbon receptor (or AhR) is a cytoplasmic receptor of pollutants. It translocates into the nucleus upon binding to its ligands, and forms a heterodimer with ARNT (AhR nuclear translocator). The heterodimer is a transcription factor, which regulates the transcription of xenobiotic metabolizing enzymes. Expressed in many cells in vertebrates, it is mostly present in neuronal cell types in invertebrates, where it regulates dendritic morphology or feeding behavior. Surprisingly, few investigations have been conducted to unravel the function of the AhR in the central or peripheral nervous systems of vertebrates. In this review, we will present how the AhR regulates neural functions in both invertebrates and vertebrates as deduced mainly from the effects of xenobiotics. We will introduce some of the molecular mechanisms triggered by the well-known AhR ligand, 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD), which impact on neuronal proliferation, differentiation, and survival. Finally, we will point out the common features found in mice that are exposed to pollutants, and in AhR knockout mice.

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15

Yoshioka, T., L. Feigenbaum, and G. Jay. "Transgenic mouse model for central nervous system demyelination." Molecular and Cellular Biology 11, no. 11 (November 1991): 5479–86. http://dx.doi.org/10.1128/mcb.11.11.5479.

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A common feature of demyelinating diseases such as multiple sclerosis in humans and experimental autoimmune encephalomyelitis in rodents is the marked elevation in the expression of the major histocompatibility complex (MHC) antigens in the involved sites. By specific targeting of a syngeneic MHC class I gene to oligodendrocytes, we have generated transgenic mice which not only exhibit severe involuntary tremors and develop tonic seizures but also show extensive demyelination in both the brain and the spinal cord. The fact that demyelination in these mice occurs in the absence of immune infiltration dismisses an autoimmune involvement but suggests that the MHC class I antigens play a direct role in inducing disease. Our findings lend support to the possibility that demyelinating diseases are induced by infectious agents such as viruses which can either directly activate MHC gene expression in oligodendroglia or indirectly activate expression through the release by reactive T cells of gamma interferon in the brain.

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16

Yoshioka, T., L. Feigenbaum, and G. Jay. "Transgenic mouse model for central nervous system demyelination." Molecular and Cellular Biology 11, no. 11 (November 1991): 5479–86. http://dx.doi.org/10.1128/mcb.11.11.5479-5486.1991.

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A common feature of demyelinating diseases such as multiple sclerosis in humans and experimental autoimmune encephalomyelitis in rodents is the marked elevation in the expression of the major histocompatibility complex (MHC) antigens in the involved sites. By specific targeting of a syngeneic MHC class I gene to oligodendrocytes, we have generated transgenic mice which not only exhibit severe involuntary tremors and develop tonic seizures but also show extensive demyelination in both the brain and the spinal cord. The fact that demyelination in these mice occurs in the absence of immune infiltration dismisses an autoimmune involvement but suggests that the MHC class I antigens play a direct role in inducing disease. Our findings lend support to the possibility that demyelinating diseases are induced by infectious agents such as viruses which can either directly activate MHC gene expression in oligodendroglia or indirectly activate expression through the release by reactive T cells of gamma interferon in the brain.

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17

Hodgkinson, Victoria L., Sha Zhu, Yanfang Wang, Erik Ladomersky, Karen Nickelson, Gary A. Weisman, Jaekwon Lee, Jonathan D. Gitlin, and Michael J. Petris. "Autonomous requirements of the Menkes disease protein in the nervous system." American Journal of Physiology-Cell Physiology 309, no. 10 (November 15, 2015): C660—C668. http://dx.doi.org/10.1152/ajpcell.00130.2015.

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Menkes disease is a fatal neurodegenerative disorder arising from a systemic copper deficiency caused by loss-of-function mutations in a ubiquitously expressed copper transporter, ATP7A. Although this disorder reveals an essential role for copper in the developing human nervous system, the role of ATP7A in the pathogenesis of signs and symptoms in affected patients, including severe mental retardation, ataxia, and excitotoxic seizures, remains unknown. To directly examine the role of ATP7A within the central nervous system, we generated Atp7a Nes mice, in which the Atp7a gene was specifically deleted within neural and glial cell precursors without impairing systemic copper homeostasis, and compared these mice with the mottled brindle ( mo-br) mutant, a murine model of Menkes disease in which Atp7a is defective in all cells. Whereas mo-br mice displayed neurodegeneration, demyelination, and 100% mortality prior to weaning, the Atp7a Nes mice showed none of these phenotypes, exhibiting only mild sensorimotor deficits, increased anxiety, and susceptibility to NMDA-induced seizure. Our results indicate that the pathophysiology of severe neurological signs and symptoms in Menkes disease is the result of copper deficiency within the central nervous system secondary to impaired systemic copper homeostasis and does not arise from an intrinsic lack of ATP7A within the developing brain. Furthermore, the sensorimotor deficits, hypophagia, anxiety, and sensitivity to NMDA-induced seizure in the Atp7a Nes mice reveal unique autonomous requirements for ATP7A in the nervous system. Taken together, these data reveal essential roles for copper acquisition in the central nervous system in early development and suggest novel therapeutic approaches in affected patients.

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18

Luvisetto, Siro, Ornella Rossetto, Cesare Montecucco, and Flaminia Pavone. "Toxicity of botulinum neurotoxins in central nervous system of mice." Toxicon 41, no. 4 (March 2003): 475–81. http://dx.doi.org/10.1016/s0041-0101(02)00370-7.

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19

Pamphlett, Roger, and Stephen Kum-Jew. "Mercury vapor uptake into the nervous system of developing mice." Neurotoxicology and Teratology 23, no. 2 (March 2001): 191–96. http://dx.doi.org/10.1016/s0892-0362(00)00122-7.

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20

Harada, Akihiro. "Analyses of nervous system in knockout mice deficient in SNAREs." Neuroscience Research 71 (September 2011): e235-e236. http://dx.doi.org/10.1016/j.neures.2011.07.1028.

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21

Kim, Susan S., David P. Richman, Scott S. Zamvil, and Mark A. Agius. "Accelerated central nervous system autoimmunity in BAFF-receptor-deficient mice." Journal of the Neurological Sciences 306, no. 1-2 (July 2011): 9–15. http://dx.doi.org/10.1016/j.jns.2011.04.008.

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Ali, B. H., A. K. Bashir, N. R. Banna, and M. O. M. Tanira. "CENTRAL NERVOUS SYSTEM ACTIVITY OF RHAZYA STRICTA (DECNE) IN MICE." Clinical and Experimental Pharmacology and Physiology 22, no. 4 (April 1995): 248–53. http://dx.doi.org/10.1111/j.1440-1681.1995.tb01989.x.

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23

Woolf, Nigel. "MCMV tropism for the auditory nervous system in SCID mice." Journal of Clinical Virology 12, no. 2 (April 1999): 162. http://dx.doi.org/10.1016/s1386-6532(99)90522-x.

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Rosenfeld, M. G., E. B. Crenshaw, and S. A. Lira. "Transgenic Mice: Applications to the Study of the Nervous System." Annual Review of Neuroscience 11, no. 1 (March 1988): 353–72. http://dx.doi.org/10.1146/annurev.ne.11.030188.002033.

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25

Gingrich, Jeffrey R., and John Roder. "INDUCIBLE GENE EXPRESSION IN THE NERVOUS SYSTEM OF TRANSGENIC MICE." Annual Review of Neuroscience 21, no. 1 (March 1998): 377–405. http://dx.doi.org/10.1146/annurev.neuro.21.1.377.

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Fuke, Satoshi, Natsumi Minami, Hiroki Kokubo, Ayumu Yoshikawa, Hiroshi Yasumatsu, Noboru Sasagawa, Yumiko Saga, Toshifumi Tsukahara, and Shoichi Ishiura. "Hesr1knockout mice exhibit behavioral alterations through the dopaminergic nervous system." Journal of Neuroscience Research 84, no. 7 (November 15, 2006): 1555–63. http://dx.doi.org/10.1002/jnr.21062.

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Aaron, Rosemary H., Gertrude B. Elion, O. Michael Colvin, Michael Graham, Steven Keir, Darell D. Bigner, and Henry S. Friedman. "Busulfan therapy of central nervous system xenografts in athymic mice." Cancer Chemotherapy and Pharmacology 35, no. 2 (1994): 127–31. http://dx.doi.org/10.1007/bf00686634.

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Lee, K., J. Jung, D. Song, M. Kräuter, and Y. Kim. "Effects ofHumulus lupulusExtract on the Central Nervous System in Mice." Planta Medica 59, S 1 (December 1993): A691. http://dx.doi.org/10.1055/s-2006-959980.

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Al-Yousuf, M. H., B. H. Ali, A. K. Bashir, M. O. M. Tanira, and G. Blunden. "Central nervous system activity of Leucas inflata Benth. in mice." Phytomedicine 9, no. 6 (January 2002): 501–7. http://dx.doi.org/10.1078/09447110260573128.

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Aaron, Rosemary H., Gertrude B. Elion, Darell D. Bigner, H. S. Friedman, O. Michael Colvin, Michael Graham, and Steven Keir. "Busulfan therapy of central nervous system xenografts in athymic mice." Cancer Chemotherapy and Pharmacology 35, no. 2 (November 1, 1994): 127–31. http://dx.doi.org/10.1007/s002800050204.

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Tseng, Kuang-Wen, Mei-Lin Peng, Yang-Cheng Wen, Kang-Jen Liu, and Chung-Liang Chien. "Neuronal degeneration in autonomic nervous system of Dystonia musculorum mice." Journal of Biomedical Science 18, no. 1 (2011): 9. http://dx.doi.org/10.1186/1423-0127-18-9.

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Masliah, Eliezer, Margaret Mallory, Nianfeng Ge, Michael Alford, Isaac Veinbergs, and Allen D. Roses. "Neurodegeneration in the Central Nervous System of apoE-Deficient Mice." Experimental Neurology 136, no. 2 (December 1995): 107–22. http://dx.doi.org/10.1006/exnr.1995.1088.

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Pena Rossi, Claudia, Andrés McAllister, Myriam Tanguy, David Kägi, and Michel Brahic. "Theiler’s Virus Infection of Perforin-Deficient Mice." Journal of Virology 72, no. 5 (May 1, 1998): 4515–19. http://dx.doi.org/10.1128/jvi.72.5.4515-4519.1998.

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ABSTRACT Theiler’s virus, a murine picornavirus, infects the central nervous systems of C57BL/6 mice and is cleared after approximately 10 days by a process which requires CD8+ cytotoxic T cells. We used perforin-deficient C57BL/6 mice to test the role of this protein in viral clearance. Perforin-deficient mice died from viral encephalomyelitis between days 12 and 18 postinoculation. They had high levels of viral RNA in their central nervous systems until the time of death. In contrast, viral RNA had disappeared by day 11 postinoculation in wild-type C57BL/6 mice. Cytotoxic T cells can kill infected cells by two main mechanisms: the secretion of the pore-forming protein perforin or the interaction of the Fas ligand with the apoptosis-inducing Fas molecule on the target cell. Our results demonstrate that clearance of Theiler’s virus from the central nervous system in C57BL/6 mice is perforin dependent.

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Brum, Patricia C., Jon Kosek, Andrew Patterson, Daniel Bernstein, and Brian Kobilka. "Abnormal cardiac function associated with sympathetic nervous system hyperactivity in mice." American Journal of Physiology-Heart and Circulatory Physiology 283, no. 5 (November 1, 2002): H1838—H1845. http://dx.doi.org/10.1152/ajpheart.01063.2001.

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α2A-Adrenergic receptors (ARs) in the midbrain regulate sympathetic nervous system activity, and both α2A-ARs and α2C-ARs regulate catecholamine release from sympathetic nerve terminals in cardiac tissue. Disruption of both α2A- and α2C-ARs in mice leads to chronically elevated sympathetic tone and decreased cardiac function by 4 mo of age. These knockout mice have increased mortality, reduced exercise capacity, decreased peak oxygen uptake, and decreased cardiac contractility relative to wild-type controls. Moreover, we observed significant abnormalities in the ultrastructure of cardiac myocytes from α2A/α2C-AR knockout mice by electron microscopy. Our results demonstrate that chronic elevation of sympathetic tone can lead to abnormal cardiac function in the absence of prior myocardial injury or genetically induced alterations in myocardial structural or functional proteins. These mice provide a physiologically relevant animal model for investigating the role of the sympathetic nervous system in the development and progression of heart failure.

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Pouzoulet, Frederic, Keyvan Rezai, Zhimin Li, Qiu Yushi, Han W. Tun, Dalila Labiod, Sarah Bonnet-Boissinot, and Carole Soussain. "Preclinical Evaluation of Ibrutinib for Central Nervous System Lymphoma." Blood 128, no. 22 (December 2, 2016): 4170. http://dx.doi.org/10.1182/blood.v128.22.4170.4170.

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Abstract Introduction Primary CNS lymphoma (PCNSL) is a diffuse large B-cell lymphoma (DLBCL), predominantly of non-germinal center (non-GC) subtype. Currently available treatments remain disappointed with a non-optimal complete remission rate and a high relapse rate. As such, novel therapeutic agents are urgently needed. Constitutive activation of the NF-kB pathway via mutations in B cell receptor (BCR) (CD79B) and mutation of MYD 88 and TBL1XR1 pathways plays an important role in PCNSL. Ibrutinib, an inhibitor of BCR signaling, has been found to have significant therapeutic activity in relapsed or refractory non-CNS non-GC DLBCL that display similar NFKB mutational patterns. We have performed a CNS pharmacokinetic (PK) study of Ibrutinib and evaluated its therapeutic activity against CNS lymphoma (CNSL) in murine models. Methods CNS PK study in mice - The first study was done in a CNSL model created by intracerebral implantation of luciferase-transfected lymphoma cells (MC116) in nude mice in comparison to healthy nude mice without lymphoma cell implantation (N=5 per group). Once the tumor activity was confirmed by bioluminescence imaging in CNSL group, all the mice were treated with ibrutinib 12 or 30 mg/kg/day by oral gavage (OG) for 5 days. Blood and brain were collected 2 hours after the last dose. Ibrutinib was measured by ultra performance liquid chromatography with tandem mass spectrometry. Cerebro-spinal fluid (CSF) PK study in Sprague-Dawley (SD) rats - Ibrutinib 50 mg/kg single dose was given by OG (N=6). Microdialysates of CSF were collected from a ventricle of the brain and a carotid artery via microdialysis catheters every hour for 13 hours post-treatment. Drug concentrations were determined by capillary electrophoresis with laser detection. Preclinical therapeutic evaluation - A murine CNS lymphoma model was created by intracerebral injection of the OCI-Ly10 non-GC DLBCL cells, which were confirmed to have CD79 A and MYD 88 mutations and show high sensitivity to Ibrutinib in vitro. Animals were sacrificed if they showed severe clinical signs or symptoms or >20% weight loss. Ibrutinib 30 mg/kg was administered by OG daily starting at day 7 post-implantation and until the last sacrifice in the control group treated with vehicle. Therapeutic efficacy was determined by Kaplan-Meier survival analysis using date of sacrifice as endpoint. Results CNS PK study in mice - 1) Ibrutinib levels in plasma, normal brain tissue and brain-tumor were analyzed. Ibrutinib was not detected in healthy control mice treated with vehicle. In healthy mice treated with ibrutinib (12 mg/kg and 30 mg/kg), Ibrutinib mean plasmatic levels were 9.31 (±3.56) ng/mL and 42.2 (±20.9) ng/mL respectively. At 12 mg/kg dose level, ibrutinib was detectable but not quantifiable in brain tissue. After treatment with 30 mg/kg,iIbrutinib mean levels were 0.0077 (±0.0053) and 0.0071 (±0.00483) ng/g tissue in right and left cerebral hemispheres respectively. In CNSL mice treated with ibrutinib (12 mg/kg and 30 mg/kg), Ibrutinib mean plasmatic levels were 12.03 (±9.04) ng/mL and 42.64 (±42.04) ng/mL respectively, brain ibrutinib levels were 0.008 (±0.005) and 0.007 (±0.003) ng/g tissue for tumor-bearing right hemisphere and non-tumor bearing left hemisphere respectively for 30 mg/kg, while brain ibrutinib level was detectable but not quantifiable at 12mg/kg. CSF PK study in SD rats - CSF penetration of ibrutinib was determined to be ~5.2 % as calculated by area under the curve (AUC) ratio of CSF and blood samples. Cmax in CSF is ~0.35 uM, which is significantly higher than published EC50 concentrations for DLBCL cell lines. Preclinical therapeutic evaluation -Ibrutinib showed an excellent therapeutic activity with significant prolongation of survival (p=0.0137) (fig 1). At a median follow-up of 112 days, the median survival in treated CNSL group is 56 days compared to 33 days in the control group. At the end of the follow-up 33% of animals in treated CNSL group are still alive without treatment. Conclusion Ibrutinib achieves high concentrations in brain and CSF in murine CNS PK models with promising single-agent preclinical therapeutic activity against CNS lymphoma in a murine model. Further studies to develop combination regimen are ongoing. Figure Figure. Disclosures Soussain: Roche: Research Funding; Celgene: Research Funding; Pharmacyclics: Research Funding.

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Chang, David F., Samuel M. Zuber, Elizabeth A. Gilliam, Laura-Marie A. Nucho, Gabriel Levin, Fengnan Wang, Anthony I. Squillaro, Sha Huang, Jason R. Spence, and Tracy C. Grikscheit. "Induced pluripotent stem cell-derived enteric neural crest cells repopulate human aganglionic tissue-engineered intestine to form key components of the enteric nervous system." Journal of Tissue Engineering 11 (January 2020): 204173142090570. http://dx.doi.org/10.1177/2041731420905701.

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Models for enteric neuropathies, in which intestinal nerves are absent or injured, are required to evaluate possible cell therapies. However, existing options, including transgenic mice, are variable and fragile. Here immunocompromised mice were implanted with human pluripotent stem cell–derived tissue-engineered small intestine 10 weeks prior to a second survival surgery in which enteric nervous system precursor cells, or saline controls, were injected into the human intestinal organoid–derived tissue-engineered small intestine and analyzed 4 weeks later. Human intestinal organoid–derived tissue-engineered small intestine implants injected with saline as controls illustrated formation of intestinal epithelium and mesenchyme without an enteric nervous system. Second surgical introduction of human pluripotent stem cell–generated enteric nervous system precursors into developing human intestinal organoid–derived tissue-engineered small intestine implants resulted in proliferative migratory neuronal and glial cells, including multiple neuronal subtypes, and demonstrated function in contractility assays.

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Salomon, Benoît, Lesley Rhee, Helene Bour-Jordan, Honor Hsin, Anthony Montag, Betty Soliven, Jennifer Arcella, Ann M. Girvin, Stephen D. Miller, and Jeffrey A. Bluestone. "Development of Spontaneous Autoimmune Peripheral Polyneuropathy in B7-2–Deficient Nod Mice." Journal of Experimental Medicine 194, no. 5 (September 3, 2001): 677–84. http://dx.doi.org/10.1084/jem.194.5.677.

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An increasing number of studies have documented the central role of T cell costimulation in autoimmunity. Here we show that the autoimmune diabetes-prone nonobese diabetic (NOD) mouse strain, deficient in B7-2 costimulation, is protected from diabetes but develops a spontaneous autoimmune peripheral polyneuropathy. All the female and one third of the male mice exhibited limb paralysis with histologic and electrophysiologic evidence of severe demyelination in the peripheral nerves beginning at 20 wk of age. No central nervous system lesions were apparent. The peripheral nerve tissue was infiltrated with dendritic cells, CD4+, and CD8+ T cells. Finally, CD4+ T cells isolated from affected animals induced the disease in NOD.SCID mice. Thus, the B7-2–deficient NOD mouse constitutes the first model of a spontaneous autoimmune disease of the peripheral nervous system, which has many similarities to the human disease, chronic inflammatory demyelinating polyneuropathy (CIDP). This model demonstrates that NOD mice have “cryptic” autoimmune defects that can polarize toward the nervous tissue after the selective disruption of CD28/B7-2 costimulatory pathway.

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Scotland, Paula, Daixing Zhou, Helene Benveniste, and Vann Bennett. "Nervous System Defects of AnkyrinB (−/−) Mice Suggest Functional Overlap between the Cell Adhesion Molecule L1 and 440-kD AnkyrinB in Premyelinated Axons." Journal of Cell Biology 143, no. 5 (November 30, 1998): 1305–15. http://dx.doi.org/10.1083/jcb.143.5.1305.

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The L1 CAM family of cell adhesion molecules and the ankyrin family of spectrin-binding proteins are candidates to collaborate in transcellular complexes used in diverse contexts in nervous systems of vertebrates and invertebrates. This report presents evidence for functional coupling between L1 and 440-kD ankyrinB in premyelinated axons in the mouse nervous system. L1 and 440-kD ankyrinB are colocalized in premyelinated axon tracts in the developing nervous system and are both down-regulated after myelination. AnkyrinB (−/−) mice exhibit a phenotype similar to, but more severe, than L1 (−/−) mice and share features of human patients with L1 mutations. AnkyrinB (−/−) mice exhibit hypoplasia of the corpus callosum and pyramidal tracts, dilated ventricles, and extensive degeneration of the optic nerve, and they die by postnatal day 21. AnkyrinB (−/−) mice have reduced L1 in premyelinated axons of long fiber tracts, including the corpus callosum, fimbria, and internal capsule in the brain, and pyramidal tracts and lateral columns of the spinal cord. L1 was evident in the optic nerve at postnatal day 1 but disappeared by postnatal day 7 in mutant mice while NCAM was unchanged. Optic nerve axons of ankyrinB (−/−) mice become dilated with diameters up to eightfold greater than normal, and they degenerated by day 20. These findings provide the first evidence for a role of ankyrinB in the nervous system and support an interaction between 440-kD ankyrinB and L1 that is essential for maintenance of premyelinated axons in vivo.

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Pekny, Milos, Clas B. Johansson, Camilla Eliasson, Josefina Stakeberg, Åsa Wallén, Thomas Perlmann, Urban Lendahl, Christer Betsholtz, Claes-Henric Berthold, and Jonas Frisén. "Abnormal Reaction to Central Nervous System Injury in Mice Lacking Glial Fibrillary Acidic Protein and Vimentin." Journal of Cell Biology 145, no. 3 (May 3, 1999): 503–14. http://dx.doi.org/10.1083/jcb.145.3.503.

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In response to injury of the central nervous system, astrocytes become reactive and express high levels of the intermediate filament (IF) proteins glial fibrillary acidic protein (GFAP), vimentin, and nestin. We have shown that astrocytes in mice deficient for both GFAP and vimentin (GFAP−/−vim−/−) cannot form IFs even when nestin is expressed and are thus devoid of IFs in their reactive state. Here, we have studied the reaction to injury in the central nervous system in GFAP−/−, vimentin−/−, or GFAP−/−vim−/− mice. Glial scar formation appeared normal after spinal cord or brain lesions in GFAP−/− or vimentin−/− mice, but was impaired in GFAP−/−vim−/− mice that developed less dense scars frequently accompanied by bleeding. These results show that GFAP and vimentin are required for proper glial scar formation in the injured central nervous system and that some degree of functional overlap exists between these IF proteins.

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Yao, Hisayuki, Trevor Price, Lindsey Olivere, Matthew Warner, Stacey Tannheimer, and Dorothy A. Sipkins. "PI3Kδ Inhibition Suppresses Central Nervous System Involvement of Acute Lymphoblastic Leukemia." Blood 128, no. 22 (December 2, 2016): 282. http://dx.doi.org/10.1182/blood.v128.22.282.282.

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Abstract The majority of children and adults who experience relapse of acute lymphoblastic leukemia (ALL) will die from the disease. The presence of leukemic blasts within the cerebrospinal fluid (CSF) is an important predictor of disease recurrence in both the bone marrow (BM) and central nervous system (CNS), a frequent site of disease involvement. In the absence of intrathecal chemotherapy or craniospinal irradiation, 30%‒50% of patients will in fact develop CNS disease. All patients therefore receive CNS prophylaxis. High-risk patients require intensive CNS-directed treatment that causes toxic side effects and can impact cognitive development in children. Patients who develop recurrence in the CNS have limited treatment options and an extremely poor prognosis. The enzyme PI3K plays an important role in many biological effects including cell proliferation, migration, and apoptosis. The d isoform of PI3K is specifically expressed in immune cells. The PI3Kd inhibitor idelalisib is approved for use in combination with rituximab for the treatment of chronic lymphocytic leukemia (CLL). However, little is known about the efficacy of PI3Kd inhibition in ALL. Here, the PI3Kd inhibitor GS-649443, a potent and specific in vivo tool compound, was evaluated in a xenograft mouse model. The in vivo effects of GS-649443 were investigated in a Nalm-6 pre-B ALL SCID model. At approximately 40 days postengraftment, untreated mice all developed symptoms of CNS involvement and displayed hind limb paralysis. Hind limb paralysis is the clinical endpoint for sacrifice, occurring prior to death from progressive BM disease. Mice were treated with GS-649443 by oral gavage beginning on postengraftment day 1 and continuing until the development of clinical symptoms requiring sacrifice (hind limb paralysis, weight loss >20%, respiratory or other distress). Only 17% of GS-649443‒treated mice developed hind limb paralysis at their clinical endpoint, while 100% of vehicle-treated mice showed hind limb paralysis. In addition, mice treated with GS-649443 or vehicle control were paired. When either mouse in a treatment pair reached a clinical endpoint, both were sacrificed so disease burden in individual organs could be compared at matched time points. There was no difference in tumor burden or leukemic cell apoptotic rate in the BM of treated vs vehicle control groups. In contrast, there was a significant decrease in the number of leukemic blasts harvested from the CSF of treated mice (Fig. 1). Consistent with the inhibition of CNS disease progression, GS-649443 significantly prolonged the survival of treated mice (Fig. 2). While compromised blood-brain barrier in leukemic mice may allow therapeutic targeting of CNS disease, it is unknown whether GS-649443 enters the CNS in healthy rodents. Given the well-described effects of idelalisib on CLL cell migration, we hypothesized that PI3Kd blockade impacts disease in this ALL model by impairing leukemia migration into the CNS. To investigate the in vitro effect of GS-649443 on ALL cell migration, transwell migration assays with SDF-1 as chemoattractant were performed. Both GS-649443 and idelalisib suppressed migration of Nalm-6 and primary human ALL cells toward SDF-1. Lastly, the effects of GS-649443 in combination with conventional chemotherapy were examined. GS-649443 alone did not cause significant cytotoxicity of Nalm-6 in vitro, however, treatment with GS-649443 after cytarabine significantly increased apoptosis. Leukemic mice (20 days post-engraftment) were then treated with cytarabine (days 1‒5) in combination with GS-649443 or cytarabine alone (days 1‒7) for 1 cycle. In contrast to the single-agent study, significant decreases in the number of leukemic blasts harvested from both the BM and CSF of treated mice were observed, suggesting that PI3Kd inhibition sensitized ALL cells to cytarabine chemotherapy (Fig. 3). This decrease in residual disease after combination therapy led to significantly prolonged survival in GS-649443‒treated mice (Fig. 4). Taken together, this study provides evidence that PI3Kd inhibition prevents ALL progression in the CNS. In addition, GS-649443 and conventional chemotherapy appear to synergize to decrease residual BM disease. The potential for PI3Kd inhibition to improve chemotherapy response and impede development of CNS disease in ALL warrants further investigation in a translational clinical study. Disclosures Yao: Gilead Sciences, Inc.: Research Funding. Price:Gilead Sciences, Inc.: Research Funding. Olivere:Gilead Sciences, Inc.: Research Funding. Warner:Gilead Sciences, Inc.: Research Funding. Tannheimer:Gilead Sciences: Employment. Sipkins:Gilead Sciences, Inc.: Research Funding.

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Amano, Izuki, Ayane Ninomiya, Megan Ritter, Kristen R. Vella, Anthony Neil Hollenberg, and Noriyuki Koibuchi. "Nuclear Receptor Corepressors NCoR1 and SMRT Plays Unique Roles in Central Nervous System." Journal of the Endocrine Society 5, Supplement_1 (May 1, 2021): A976. http://dx.doi.org/10.1210/jendso/bvab048.1995.

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Abstract The nuclear corepressor 1 (NCoR1) and the silencing mediator of retinoid and thyroid hormone receptors (SMRT) are critical coregulators of the thyroid hormone receptor (TR), mediating transcriptional repression via histone deacetylation. Thyroid hormone (TH) plays an essential role in many physiological processes via the TR. How the corepressors regulate TR signaling is not fully understood, especially in central nervous system (CNS). To determine the role of NCoR1 and SMRT in the CNS, we used mice with conditional NCoR1 (NCoR1lox/lox) and SMRT (SMRTlox/lox) alleles in combination with mice that express Cre recombinase in a neuronal specific fashion (Snap25-Cre). Global deletion of NCoR1 or SMRT during embryogenesis results in lethality. We also showed that NCoR1/SMRT double knock-out mice die within two weeks after induction of Cre activity in adult mice. Now, we found that neuronal specific NCoR1 or SMRT KO mice survive without obvious impairment of neuronal development. However, NCoR1/SMRT double knock-out mice die within postnatal 1-2 weeks and have impaired body growth. Thus, both NCoR1 and SMRT have important roles in maintaining normal neuronal function. Recently, cased of mutations in NCoR1 and SMRT in humans have been reported. These cases report phenotypes including Autism Spectrum Disorder (ASD) and intellectual disability. The cerebellum has been thought to contribute to motor control and learning. Surprisingly, it has also been shown to be a key brain structure involved in social cognition and its dysfunction may play a role in ASD. The Purkinje cell is the main neuron in the cerebellum. Thus, we generated cerebellar Purkinje cell specific NCoR1/SMRT knock-out mice using L7/Pcp2-Cre mice. In contrast to neuronal specific KO mice, both NCoR1 or SMRT single or double knock-out mice survive until adulthood. SMRT Purkinje cell knock-out mice showed abnormalities in 3ch social interaction test indicating impaired social functioning, similar to some ASD symptoms. Electrophysiological testing showed current injection evoked more action potentials in SMRT KO mice. These results suggest Purkinje cell dysfunction caused by SMRT deletion may result in social disability. Our data demonstrate for the first time that NCoR1 and SMRT have separate functions in different areas of the brain but also have some redundant function when knocked out together in all neurons.

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Christine Zink, M., Victoria Laast, Kristi Helke, Angela Brice, Sheila Barber, Janice Clements, and Joseph Mankowski. "From Mice to Macaques – Animal Models of HIV Nervous System Disease." Current HIV Research 4, no. 3 (July 1, 2006): 293–305. http://dx.doi.org/10.2174/157016206777709410.

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Kupper, H., H. Gerlach, H. Wessel, D. Kleemann, and S. Schmerling. "Involvement of the central nervous system in malignant lymphomas of mice." Experimental pathology 31, no. 3 (January 1987): 185–89. http://dx.doi.org/10.1016/s0232-1513(87)80108-1.

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Huang, Ying, Lei Zhang, Ning-Ning Song, Ze-Lan Hu, Jia-Yin Chen, and Yu-Qiang Ding. "Distribution of Satb1 in the central nervous system of adult mice." Neuroscience Research 71, no. 1 (September 2011): 12–21. http://dx.doi.org/10.1016/j.neures.2011.05.015.

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Abeliovich, A., D. Gerber, O. Tanaka, M. Katsuki, A. Graybiel, and S. Tonegawa. "On somatic recombination in the central nervous system of transgenic mice." Science 257, no. 5068 (July 17, 1992): 404–10. http://dx.doi.org/10.1126/science.1631561.

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Kim, Young-Jin, Hun Hee Kang, Joong Ho Ahn, and Jong Woo Chung. "Hypoxic changes in the central nervous system of noise-exposed mice." Acta Oto-Laryngologica 127, sup558 (January 2007): 73–77. http://dx.doi.org/10.1080/03655230701624905.

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Okugawa, Hitoshi, Reiko Ueda, Katsuhiko Matsumoto, Kazuko Kawanishi, and Atsushi Kato. "Effects of Agarwood Extracts on the Central Nervous System in Mice." Planta Medica 59, no. 01 (February 1993): 32–36. http://dx.doi.org/10.1055/s-2006-959599.

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Farr, Olivia M., Eleni Pilitsi, and Christos S. Mantzoros. "Of mice and men: incretin actions in the central nervous system." Metabolism 98 (September 2019): 121–35. http://dx.doi.org/10.1016/j.metabol.2019.05.013.

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Silva, Maria Izabel Gomes, Manuel Rufino de Aquino Neto, Paulo Florentino Teixeira Neto, Brinell Arcanjo Moura, Jeferson Falcão do Amaral, Damião Pergentino de Sousa, Silvânia Maria Mendes Vasconcelos, and Francisca Cléa Florenço de Sousa. "Central nervous system activity of acute administration of isopulegol in mice." Pharmacology Biochemistry and Behavior 88, no. 2 (December 2007): 141–47. http://dx.doi.org/10.1016/j.pbb.2007.07.015.

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Davern, Pamela J., Thu-Phuc Nguyen-Huu, Luisa La Greca, Amany Abdelkader, and Geoffrey A. Head. "Role of the Sympathetic Nervous System in Schlager Genetically Hypertensive Mice." Hypertension 54, no. 4 (October 2009): 852–59. http://dx.doi.org/10.1161/hypertensionaha.109.136069.

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