The origins and uses of mouse outbred stocks

Chia, Ruth; Achilli, Francesca; Festing, Michael F. W.; Fisher, Elizabeth

doi:10.1038/ng1665

Cited by 323 publications

(304 citation statements)

References 49 publications

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“…The "2B/-"mice are maintained on a hybrid C57BL/6xCD1 background (83). The CD1 mouse strain is known to differ from other mouse strains on physiological and genetic measures (72)(73)(74)(75). Given similar myocyte culture conditions between our study and those of Hayhurst et al (65) and Boyer et al (36), we believe that the differences in results are most likely due to the different mouse models used, including their genetically different controls.…”

Section: Fayzullina Andmentioning

confidence: 62%

DNA Damage Response and DNA Repair in Skeletal Myocytes From a Mouse Model of Spinal Muscular Atrophy

Fayzullina

Martin

2016

J Neuropathol Exp Neurol

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We studied DNA damage response (DDR) and DNA repair capacities of skeletal muscle cells from a mouse model of infantile spinal muscular atrophy (SMA) caused by loss-of-function mutation of survival of motor neuron (Smn). Primary myocyte cultures derived from skeletal muscle satellite cells of neonatal control and mutant SMN mice had similar myotube length, myonuclei, satellite cell marker Pax7 and differentiated myotube marker myosin, and acetylcholine receptor clustering. DNA damage was induced in differentiated skeletal myotubes by c-irradiation, etoposide, and methyl methanesulfonate (MMS). Unexposed control and SMA myotubes had stable genome integrity. After c-irradiation and etoposide, myotubes repaired most DNA damage equally. Control and mutant myotubes exposed to MMS exhibited equivalent DNA damage without repair. Control and SMA myotube nuclei contained DDR proteins phosphop53 and phospho-H2AX foci that, with DNA damage, dispersed and then re-formed similarly after recovery. We conclude that mouse primary satellite cell-derived myotubes effectively respond to and repair DNA strand-breaks, while DNA alkylation repair is underrepresented. Morphological differentiation, genome stability, genome sensor, and DNA strand-break repair potential are preserved in mouse SMA myocytes; thus, reduced SMN does not interfere with myocyte differentiation, genome integrity, and DNA repair, and faulty DNA repair is unlikely pathogenic in SMA.

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Section: Fayzullina Andmentioning

confidence: 62%

DNA Damage Response and DNA Repair in Skeletal Myocytes From a Mouse Model of Spinal Muscular Atrophy

Fayzullina

Martin

2016

J Neuropathol Exp Neurol

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“…The major difference between this previous and the present study was the vendor (Harlan vs. Charles River) from which the outbred NMRI mice were obtained. Outbred mouse strains such as NMRI are widely used in many fields of research, including pharmacology 11. Such mice are randomly outbred; hence, allelic variations can occur across separate colonies so that outbred mice from different vendors may have little in common with each other besides their names and similarities in pelage 36.…”

Section: Discussionmentioning

confidence: 99%

“…Outbred male NMRI (Naval Medical Research Institute) mice, which originated from a colony of Swiss mice and which are used as a general‐purpose stock in many fields of research including pharmacology,11 were obtained from Charles River (Sulzfeld, Germany) and inbred female FVB/N mice from Taconic (Ejby, Denmark) at an age of 4–7 weeks (body weight 20–22 g). FVB/N mice also originated from an outbred colony of Swiss mice (N:GP; NIH general‐purpose mouse) established at the NIH in 1935 12.…”

Section: Methodsmentioning

confidence: 99%

The effects of carbamazepine in the intrahippocampal kainate model of temporal lobe epilepsy depend on seizure definition and mouse strain

Twele¹,

Töllner²,

Bankstahl³

et al. 2016

Epilepsia Open

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SummaryObjectiveMesial temporal lobe epilepsy (TLE) with hippocampal sclerosis is a predominant form of acquired epilepsy, characterized by recurrent simple and complex partial seizures that are often resistant to treatment. Mice developing spontaneous recurrent nonconvulsive and convulsive seizures after intrahippocampal injection of the excitotoxic glutamate agonist kainate are thought to represent a valuable model of mesial TLE. Epileptic electroencephalogram (EEG) activity recorded in this model from the kainate focus in the ipsilateral hippocampus is resistant to antiseizure drugs such as carbamazepine (CBZ). We compared the efficacy of CBZ in this model in two different mouse strains (FVB/N and NMRI). Furthermore, we evaluated whether changes in the definition of electrographic seizures affect the antiseizure efficacy of CBZ.MethodsAs in previous studies, two types of epileptic EEG activity were defined: high‐voltage sharp waves (HVSWs) and hippocampal paroxysmal discharges (HPDs). The characteristics of these paroxysmal EEG events in epileptic mice were compared with EEG criteria for nonconvulsive seizures in patients. For HVSWs, different spike frequencies, interevent intervals, and amplitudes were used as inclusion and exclusion criteria. In addition to CBZ, some experiments were performed with diazepam (DZP) and phenobarbital (PB).ResultsFemale epileptic FVB/N mice predominantly exhibited frequent HVSWs, but only infrequent HPDs or secondarily generalized convulsive seizures. Slight changes in HVSW definition determined whether they were resistant or responsive to CBZ. Male NMRI mice exhibited both HVSWs and HPDs. HVSWs were more resistant than HPDs to suppression by CBZ. Both types of epileptic EEG activity were rapidly suppressed by DZP and PB.SignificanceThe data demonstrate that focal electrographic seizures in the intrahippocampal kainate mouse model are less resistant than previously thought. Both mouse strain and the criteria chosen for definition of EEG seizures determine whether such seizures are drug‐resistant or ‐responsive.

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“…We performed the study in two different mouse strains, the inbred C57BL/6 and the outbred CD1, obtaining overlapping results. However, taking into account the pitfalls of using outbred mouse strains (29), and the retinal degeneration observed in CD1 mice, which might affect the results of some behavioral tests (30), we have herein reported only results achieved with the inbred stock C57BL/6; behavioral responses to CNF1 of CD1 mice are reported in supporting information (SI) Figs. 6 and 7.…”

mentioning

confidence: 99%

Enhancement of learning and memory after activation of cerebral Rho GTPases

Diana

Valentini

Travaglione

et al. 2007

Proc. Natl. Acad. Sci. U.S.A.

118

115

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The mechanism whereby the morphology and connectivity of the dendritic tree is regulated depends on an actin dynamics that, in turn, is controlled by Rho GTPases, a family of small GTP-binding proteins encompassing Rho, Rac, and Cdc42 subfamilies. Cytotoxic necrotizing factor 1 (CNF1), a protein toxin from Escherichia coli, constitutively activates Rho GTPases, thus leading to remodeling of the actin cytoskeleton in intact cells. Here, we show that the modulation of cerebral RhoA and Rac1 activity induced by CNF1 in mice leads to (i) rearrangement of cerebral actin cytoskeleton, (ii) enhanced neurotransmission and synaptic plasticity, and (iii) improved learning and memory in various behavioral tasks. The effects persist for weeks and are not observed in mice treated with a recombinant CNF1, in which the enzymatic activity was abolished by substituting serine to cysteine at position 866. The results suggest that learning ability can be improved through pharmacological manipulation of neural connectivity.cytotoxic necrotizing factor 1 ͉ brain ͉ bacterial toxins ͉ dendritic spines ͉ drug therapy

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The origins and uses of mouse outbred stocks

Cited by 323 publications

References 49 publications

DNA Damage Response and DNA Repair in Skeletal Myocytes From a Mouse Model of Spinal Muscular Atrophy

DNA Damage Response and DNA Repair in Skeletal Myocytes From a Mouse Model of Spinal Muscular Atrophy

The effects of carbamazepine in the intrahippocampal kainate model of temporal lobe epilepsy depend on seizure definition and mouse strain

Enhancement of learning and memory after activation of cerebral Rho GTPases

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