Search Criteria: Research Area is "Neurobiology Research: Parkinson's Disease"
| Stock Number |
Strain Name Phenotype |
Standard Supply |
| 002609 | B6.129P2-Nos2tm1Lau/J | Level 3 |
| Mice homozygous for the Nos2tm1Lau targeted mutation resemble wildtype mice in appearance and histology. Homozygotes are viable and fertile. Unlike Nos1 and Nos3, Nos2 is synthesized de novo in response to a variety of inflammatory stimuli. Induction of Nos2 results in the production of large amounts of nitric oxide (NO) over prolonged periods of time. Excessive NO production has been shown to be beneficial through its antitumor and antimicrobial activities. It is also thought to cause tissue damage and contribute to pathology in a variety of inflammatory conditions including rheumatoid arthritis, inflammatory bowel disease, cardiac allograft rejection, hepatoxicity, myocardial ischemia-reperfusion and septic shock. NO has been demonstrated to play a role in the regulation of blood pressure and hemodynamics. In an LPS-induced model of septic shock, Nos2tm1Lau homozygotes had virtually no serum NO response, but were
..... For more information please see the full phenotype on the strain data sheet | ||
| 003243 | B6;129S-Tnfrsf1atm1Imx Tnfrsf1btm1Imx/J | Level 4 |
| Mice homozygous for both the Tnfrsf1atm1Imx and Tnfrsf1btm1Imx targeted mutations (p55 and p75 deficient) are viable and fertile. Double homozygous mutant mice fail to bind TNF. Thymus, spleen, and other lymphoid tissue are normal, indicating that TNF is not required for normal development of these organs. | ||
| 007587 | 129S-Park2tm1Rpa/J | Repository- Live |
| Mice carrying this mutation are viable, fertile, and display no apparent defects or abnormalities. Mutations in the human homolog of this gene are associated with autosomal juvenile parkinsonism, a heritable form of Parkinson's disease. | ||
| 002779 | 129S-Parp1tm1Zqw/J | Repository- Live |
| Mice that are homozygous null for the targeted gene are viable, fertile, normal in size and do not display any gross physical or behavioral abnormalities. Although a shortened transcript is generated, no enzymatic activity is detected in tissues. Proliferation of homozygous-null fibroblasts and thymocytes is impaired following gamma-radiation in comparison to cells derived from wild-type mice. Older mice are susceptible to spontaneous development of skin disease. A significant portion of older mice ( ~30%) can be expected to exhibit epidermal hyperplasia. Null mice are also less susceptible to damage induced by the neurotoxin MPTP. | ||
| 004684 | B6(129P2) Nos2tm1Lau-chtl/J | Repository- Live |
| This mutant has an overall lighter coat, tail and ears than a black +/+ control. Both males and females breed and it is maintained as a homozygous stock. | ||
| 004608 | B6(Cg)-Htra2mnd2/J | Repository- Live |
| Mice homozygous for the recessive Htra2mnd2 mutation have a basal ganglia disorder initially described as an early onset motor neuron disease. This is first outwardly evident by 21 to 24 days of age as an unsteady gait with extended hind limbs, repetitive movements and episodes of sudden arrests. This progresses to include severe muscle atrophy, hunched posture, increased imbalance, chorea, dystonia, and progressive akinesis. A failure to gain weight becomes evident shortly after the onset of the other symptoms and by 35 days of age wildtype littermates are twice as heavy as the mutants. Body fat is not detectable at necropsy. Both the spleen and the thymus drop from normal weights at 23 days of age to 10% of normal at 30 days of age and the thymic corticomedullary junction is lost. Death usually occurs within two weeks of disease onset, by 40 days of age. The growth retardation is not the primary cause since disease is not delayed by intragastric feeding.
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| 004744 | B6.129P2-Esr1tm1Ksk/J | Repository- Live |
| At birth, mice homozygous for the targeted allele are viable and normal in size and appearence. Female mice exhibit ovaries that lack corpora lutea and hypoplastic uteri that are unresponsive to estrogen. In males, below normal testis weight is associated with a diminished sperm count (10% of normal). Homozygous females are infertile. The fertility of homozygous males is greatly reduced, but not abolished. | ||
| 006582 | B6.129S4-Park2tm1Shn/J | Repository- Live |
| Homozygous mice are viable and fertile, and exhibit grossly normal brain morphology. Western blot analysis using antibody specific to C-terminal sequences indicates the absence of full length gene product. RT-PCR shows that exon 2 splices to exon 4, skipping exon 3 entirely, resulting in a frame shift and a premature stop codon in exon 5. While EGFP transcripts are present, little parkin-EGFP fusion protein is detectable by Western analysis. Homozygous mice have increased extracellular dopamine concentration in the striatum. Further, medium-sized striatal spiny neurons require greater currents to induce synaptic responses, suggesting a reduction in synaptic excitability in the absence of the endogenous gene. Homozygotes also exhibit deficits in behavioral paradigms sensitive to dysfunction of the nigrostriatal pathway. The numbers of dopaminergic neurons in the substantia nigra, however, are normal up to the age of 24 months, in contrast to the substantial loss of nigral neurons charac
..... For more information please see the full phenotype on the strain data sheet | ||
| 004936 | B6.129S6(Cg)-Spp1tm1Blh/J | Repository- Live |
| Mice that are homozygous for the targeted mutation are viable, fertile, normal in size and do not display any gross physical or behavioral abnormalities. No gene product (mRNA) is detected by RT-PCR analysis of embryonic fibroblasts and kidney. Immunohistochemical analysis of kidney and bone tissue also fails to detect gene product (protein). Homozygotes exhibit disorganized ultrastructural wound matrix remodeling and defective macrophage infiltration and accumulation at sites of injury and infection. Experimentally induced hyperoxaluria results in renal tubule deposition of calcium oxalate crystals. Accelerated ectopic calcification mineralization in soft tissues occurs after subcutaneous implantation of glutaraldehyde-fixed aortic valve tissue. Mutant macrophage response to mycobacteria infection and pulmonary granulomatous response and inflammation are impaired. According to a recent publication (Hsieh et al 2006 Cancer Res 2006 66:7119-27), mutant mice treated with a skin chemical
..... For more information please see the full phenotype on the strain data sheet | ||
| 005491 | B6.Cg-Mapttm1(EGFP)Klt Tg(MAPT)8cPdav/J | Repository- Live |
| Mice that are homozygous for the targeted allele and hemizygous for the transgene are viable and fertile. Although no endogenous mouse MAPT is detected, all six isoforms (including both 3R and 4R forms) of human MAPT are expressed. Hyperphosphorylated MAPT is detected in cell bodies and dendrites by 3 months of age. Paired helical filaments of aggregated insoluble MAPT can be isolated from brain tissue as early as 2 months of age. These mutant mice may be useful in studies examining the relationship between human MAPT and Alzheimer's disease pathogenesis In an attempt to offer alleles on well-characterized or multiple genetic backgrounds, alleles are frequently moved to a genetic background different from that on which an allele was first characterized. It should be noted that the phenotype could vary from that originally described. We will modify the strain description if necessary as published results become available. | ||
| 006577 | B6.Cg-Park7tm1Shn/J | Repository- Live |
| Homozygous mice are viable and fertile. Western blot analysis using antibody specific to C-terminal sequences indicates the absence of full length gene product. Homozygous mice exhibit hypokinesia and nigrostriatal dopaminergic deficits: evoked dopamine overflow in the striatum is reduced (primarily as a result of increased dopamine uptake), nigral neurons (dopaminergic neurons) have abnormal action potential characteristics, and long term depression is absent in medium spiny neurons. Also, D2-receptor mRNA abundance and radioligand binding is normal. Dopaminergic neurons from substantia nigra pars compacta (SNpc) of homozygous mice exhibit significantly higher sensitivity to energy metabolism impairment and nigral dopaminergic neurons are particularly sensitive to Na+/K+ ATPase impairment. These mutant mice may be useful in studies of Parkinson's disease, dopaminergic physiology, nigrostriatal function, locomotor inactivity, and other neurobiological research.
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| 007004 | B6.Cg-Tg(Camk2a-tTA)1Mmay/DboJ | Repository- Live |
| Transgenic mice expressing the tetracycline-controlled transactivator protein (tTA) under regulatory control of the forebrain-specific calcium-calmodulin-dependent kinase II (Camk2a) promoter are viable and fertile. When hemizygotes are mated to a second strain carrying a gene of interest under the regulatory control of a tetracycline-responsive promoter element (TRE; tetO), expression of the target gene can be blocked by administration of the tetracycline analog, doxycycline (dox). These mice are a "Tet-Off" tool that allow the inducible expression of genes in forebrain neurons, and may be useful in studying brain disorders such as Alzheimer's disease (when used in conjunction with Stock No. 005706, Stock No. 007049, Stock No. 007051, Stock No. 007052), Parkinson's
..... For more information please see the full phenotype on the strain data sheet | ||
| 007894 | B6.Cg-Tg(Rgs4-EGFP)4Lvt/J | Repository- Live |
| Hemizygous RGS4 BAC transgenic mice are viable and fertile. As the RGS4 BAC transgene has an IRES2-eGFP construct inserted into the 3' UTR of the regulator of G-protein signaling 4 (Rgs4) locus, transgenic RGS4 transcripts and EGFP protein expression is observed in a pattern consistent with endogenous Rgs4. While the transgene is designed to co-express EGFP and RGS4, over-expression of RGS4 is not reported to result in unfaithful reporting of endogenous RGS4 expression. Under the control of the RGS4 promoter/enhancer elements, transgene expression reports dynamic developmental, regional, and cellular specific expression in developing and mature cerebral cortex neurons across all cortical domains, as well as developing and mature subcortical regions (telencephalon, diencephalon, and brainstem). While immunostaining against the transgenic product ("RGS4-GFP") allows detailed cellular resolution of neuronal cell bodies and processes, the subcellular localization of EGFP cann
..... For more information please see the full phenotype on the strain data sheet | ||
| 008135 | B6.Cg-Tg(THY1-SNCA*A53T)M53Sud/J | Repository- Live |
| Hemizygous transgenic mice are viable and fertile and develop a Parkinson-like phenotype upon aging. Hind limb paralysis due to loss of motor neurons and a resting tremor are initially seen at about six months of age. No Lewy body-like pathology is noted. Cell death in the spinal cord (extensive) and brain are observed. | ||
| 006390 | B6;129-Sncatm1Sud Sncbtm1.1Sud/J | Repository- Live |
| Mice homozygous for this targeted mutation are viable and fertile and do not display any gross physical or behavioral abnormalities. No protein product from these targeted genes is detected in brain tissue. Overall brain morphology and structure appears normal. No significant changes in the ultrastructure, short- or long-term synaptic plasticity, or in the pool size or replenishment of recycling synaptic vesicles is detected. Dopamine levels in the double targeted mice are decreased by approximately 20%, but dopamine uptake and release from isolated nerve terminals is normal. Serotonin levels are unchanged. This mutant mouse strain represents a model that may be useful in studies of synaptic function and neurodegenerative disease. | ||
| 002596 | B6;129P2-Nos2tm1Lau/J | Repository- Live |
| Mice homozygous for the Nos2tm1Lau targeted mutation resemble wildtype mice in appearance and histology. Homozygotes are viable and fertile. Unlike Nos1 and Nos3, Nos2 is synthesized de novo in response to a variety of inflammatory stimuli. Induction of Nos2 results in the production of large amounts of nitric oxide (NO) over prolonged periods of time. Excessive NO production has been shown to be beneficial through its antitumor and antimicrobial activities. It is also thought to cause tissue damage and contribute to pathology in a variety of inflammatory conditions including rheumatoid arthritis, inflammatory bowel disease, cardiac allograft rejection, hepatoxicity, myocardial ischemia-reperfusion and septic shock. NO has been demonstrated to play a role in the regulation of blood pressure and hemodynamics. In an LPS-induced model of septic shock, Nos2tm1Lau homozygotes had virtually no serum NO response, but were
..... For more information please see the full phenotype on the strain data sheet | ||
| 003692 | B6;129X1-Sncatm1Rosl/J | Repository- Live |
| Homozygous null mice are viable, fertile, normal in size and do not display any gross abnormalities. No gene product (mRNA or protein) is detected in brain tissue. A wildtype complement of dopamine neurons, fibers and synaptic terminals is present and the overall brain architecture appears to be intact. They suffer from a reduction in total striatal dopamine and exhibit an attenuated locomotor response when given amphetamine. Normal dopamine release is observed upon stimulation of the nigrostriatal terminal with a single electrical pulse. When multiple stimuli are applied however, null mice exhibit an accelerated recovery of dopamine release. A similar acceleration is seen in wildtype mice in the presence of increased extracellular calcium. The phenotype observed in homozygous Snca-null mice suggests that Snca is an activity-dependent negative regulator of dopamine neurotransmission. | ||
| 004479 | B6;C3-Tg(Prnp-SNCA*A53T)83Vle/J | Repository- Live |
| Mice homozygous for the transgenic insert are viable and normal in size. These transgenic mice express human A53T variant alpha-synuclein (full-length, 140 amino acid isoform) under the direction of the mouse prion protein promoter. At 8 months of age, some homozygous mice develop a progressively severe motor phenotype. By 16 months of age, all homozygous mice display the phenotype. Lax grooming, weight loss and diminished mobility precede movement impairment, partial limb paralysis, trembling and inability to stand. Immunohistochemistry analysis of mutants between 8 to 12 months of age reveals widely distributed alpha-synuclein inclusions, with dense accumulation in the spinal cord, brainstem, cerebellum and thalamus. The appearance of alpha-synuclein aggregate inclusions parallels the onset of the motor impairment phenotype. Axons and myelin sheaths exhibit progressive ultrastructural degeneration. Immunoelectron microscopy and biochemical analysis show the inclusions in neurons are
..... For more information please see the full phenotype on the strain data sheet | ||
| 006302 | B6;SJL-Slc6a3tm1.1(cre)Bkmn/J | Repository- Live |
| Mice homozygous for this dopamine transporter IRES-cre (DATIREScre or DAT-cre) mutant allele are viable and fertile. Cre recombinase activity is observed as early as embryonic day 15, and co-localizes with endogenous gene expression in adult dopaminergic cell groups (substantia nigra (SN) and ventral tegmental area (VTA), as well as in the retrorubral field). Lower Cre recombinase activity is detected in adult olfactory bulb glomeruli, mimicking the known lower Slc6a3 (or DAT) expression in this tissue. Although the pattern and intensity of DAT immunostaining in the SN, VTA and striatum do not differ between wildtype and mutant mice, striatum DAT protein levels are moderately reduced (17%) in heterozygotes and significantly reduced (47%) in homozygotes. This decrease in DAT protein levels in homozygous mutant striatum is associated with significantly increased neuropeptide PDyn (but not D1, D2, or PPE) mRNA levels compared to wildtype. Increases in these mRNA l
..... For more information please see the full phenotype on the strain data sheet | ||
| 000231 | B6C3Fe a/a-Csf1op/J | Repository- Live |
| Mice homozygous for the osteopetrosis spontaneous mutation (Csf1op) are viable and exhibit osteopetrosis. The osteoclasts are the primary cell type affected in homozygous mutant mice. This results in a generalized macrophage deficiency, monocytopenia, and defective bone remodeling. Homozygous mutant mice also have abnormal calcium regulation, impaired dental growth and female mice fail to lactate. Total leukocyte counts are reduced and marrow cells are decreased to one-tenth of normal control mice. Homozygous mutant mice have a deficient microglia and macrophage response, and therefore may be useful tools to study the role of glia in neurological disease if mated to transgenic models of neurodegenerative disease. | ||
| 006618 | C57BL/6-Tg(tetO-COX8A/EYFP)1Ksn/J | Repository- Live |
| Hemizygotes are viable and fertile. These transgenic mice express a mitochondrial-specific EYFP fusion protein under the control of a tetracycline-responsive promoter element (TRE;tetO). When hemizygotes are bred with another transgenic mouse expressing either reverse tetracycline-controlled transactivator protein (rtTA) or tetracycline-controlled transactivator protein (tTA) under the regulation of tissue-specific promoter, tissue-specific expression of EYFP in mitochondria of the bitransgenic offspring can be regulated with the tetracycline analog, doxycycline. When bred to a strain expressing rtTA or tTA in forebrain neurons (see Stock No. 003010 for example), this mutant mouse strain may be useful in studies of neuronal mitochondrial dysfunction. | ||
| 007677 | CB6-Tg(Gad1-EGFP)G42Zjh/J | Repository- Live |
| Mice hemizygous for this GAD67-GFP transgene are viable and fertile. GAD67-GFP (line G42) mice selectively express enhanced green fluorescent protein (EGFP) in the calcium-binding protein parvalbumin (Pv)-expressing subclass of basket interneurons (soma, dendrites, and axons) and also in putative presynaptic boutons. While transgene expression (EGFP expression) is published as early as postnatal day 0 (P0) with high expression levels throughout postnatal development, the donating investigator additionally reports transgene expression as early as embryonic day 14 (E14). EGFP expression is not reported in other interneuron classes positive for somatostatin (SOM), cholecystokinin (CCK), calretinin (CR), and VIP. These GAD67-GFP (line G42) mice may be useful for fluorescent labeling of the Pv-expressing subset of GABAergic neurons, allowing reliable and efficient characterization of perisomatic innervation in vivo. Of note, this GAD67-GFP strain is one of many fluorescent GABAerg
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| 004808 | STOCK Mapttm1(EGFP)Klt Tg(MAPT)8cPdav/J | Repository- Live |
| Mice that are homozygous for the targeted allele and hemizygous for the transgene are viable and fertile. Although no endogenous mouse MAPT is detected, all six isoforms (including both 3R and 4R forms) of human MAPT are expressed. Hyperphosphorylated MAPT is detected in cell bodies and dendrites by 3 months of age. Paired helical filaments of aggregated insoluble MAPT can be isolated from brain tissue as early as 2 months of age. These mutant mice may be useful in studies examining the relationship between human MAPT and Alzheimer's disease pathogenesis. | ||
| 006340 | STOCK Tg(Gad1-EGFP)98Agmo/J | Repository- Live |
| Mice hemizygous for the transgenic insert are viable, fertile, normal in size and do not display any gross physical or behavioral abnormalities. These transgenic mice express Enhanced Green Fluorescent Protein (EGFP) under the direction of the mouse Gad1 (glutamic acid decarboxylase 1 or GAD67) promoter. In the neocortex, EGFP expression is detected predominantly in layers 5B and 6, and to a lesser extent in layers 2/3. Low levels of fluorescence are detected in small cells with glial morphology. EGFP expression is also observed in area CA1 of the hippocampus, mainly in large interneurons in the oriens-alveus layers. In the neocortex of founder line 98 transgenic mice, fluorescence is observed in infragranular, calbindin immunoreactive interneurons with axonal arborizations in layer 1. In animals younger than two weeks of age, an increased number of EGFP labeled neurons is observed in the supragranular layers, and EGFP expression is also observed in some cells with pyramidal m
..... For more information please see the full phenotype on the strain data sheet | ||
| 005987 | 129-Achetm1Loc/J | Repository-Cryopreserved |
| Homozygous mice have 25% fetal mortality. Those born have retarded growth, fine motor tremors, unusual posture and gait, no righting reflex, malformed pinna, and sealed eyelids. These mice die emaciated and dehydrated by 3 weeks of age. Enriched diets for the nursing female and pups allow homozygous mice to survive to adulthood. Males exhibit no breeding behavior. Homozygous females can become pregnant when bred to heterozygous or wildtype males, but both female and pups do not survive. Acetylcholinesterase (AChE) activity is completely abrogated in serum and tissue from homozygous mice, and approximately half in heterozygotes. Many symptoms of organophosphate poisoning are observed in homozygous mice, including pulsating paws, body tremor, abnormal gait, pinpoint pupils, muscle weakness, and early death following seizure. When restrained, a white mucus forms on the eyes and seizures may occur. Mice also have several developmental delays, low body mass, decreased pain response, sexual
..... For more information please see the full phenotype on the strain data sheet | ||
| 008133 | B6.129-Sncbtm1Sud/J | Repository-Cryopreserved |
| These mice possess loxP sites on either side of exon 2 of the targeted gene. Mice that are homozygous for this allele are viable, normal in size and do not display any gross physical or behavioral abnormalities, but breed very poorly. Protein levels are normal. When bred to a strain expressing Cre recombinase, this mutant mouse strain may be useful in studies of presynaptic proteins and synaptic vesicles. | ||
| 004322 | B6.129S1-Mapk10tm1Flv/J | Repository-Cryopreserved |
| Mice that are homozygous for the targeted mutation are viable, normal in size and do not display any gross physical or behavioral abnormalities. No gene product, mRNA or protein, is detected in brain tissue. Histological and immunohistological examination of the brains of homozygous mutant mice reveal normal development and cellular organization. Mutant mice are resistant to seizures and neuronal apoptosis caused by administration of excitotoxic glutamate-receptor agonist kainic acid. With higher doses of kainic acid, mutant mice display severe tonic-clonic convulsions, but survive the treatment while wildtype mice have 60% mortality. This mutant mouse strain represents a model that may be useful in studies related to neurotoxicity of excitatory amino acids and induced models of Parkinson's disease and stroke. | ||
| 003190 | B6.129S2-Drd2tm1Low/J | Repository-Cryopreserved |
| Mice with a disrupted D2 dopamine receptor gene display chronic hyperprolactinemia and develop anterior lobe lactotrophhyperplasia without evidence of adenomatous transformation. Homozygous mutant mice have no hyperplasia of the intermediate lobe melanotrophs. Aged female D2 receptor homozygous mice develop uterine adenomyosis in response to prolonged prolactin exposure. They also exhibit a locomotor deficit manifested as a 50% reduction in activity and decreased initiation of movement. Female homozygous mice develop prolactinomas of the anterior pituitary gland. Homozygous mice exhibit decreased sensitivity to the rewarding and locomotor effects of ethanol. Drd2tm1Low mice may provide a model for Parkinson's disease. | ||
| 005934 | B6.129S4-Ucp2tm1Lowl/J | Repository-Cryopreserved |
| Homozygous mice are viable and fertile and do not express full length mRNA in heart, kidney, spleen, white adipose tissue, and pancreatic islets. In splenic mitochondria, endogenous protein was undetectable. When grown under high glucose conditions, cultured pancreatic islet cells from homozygous mice have increased insulin secretion and ATP levels compared to wildtype. Homozygous mice have 18% lower blood glucose levels. Whether fasting or fed, homozygotes have approximately 3-fold greater serum insulin due to increased insulin secretion. Similarly, glucose-stimulated insulin secretion is significantly increased. High fat diet-fed mice or palmitate-treated islets maintain pancreatic glucose responsiveness in vivo and in vitro compared to wildtype. Mitochondria isolated from the dopaminergic mesencephalic nigral cells of homozygous mice have increased reactive oxygen species but lesser mitochondria number and increased sensitivity to MPTP, mimicking Parkinson’s dise
..... For more information please see the full phenotype on the strain data sheet | ||
| 000567 | B6.Cg-T2J +/+ Qkqk/J | Repository-Cryopreserved |
| Mice homozygous for the quaking spontaneous mutation (Qkqk) have marked rapid tremor which disappears when they are at rest but increases during locomotion. The tremor in homozygous mutant mice begins at about 10 days and is fully developed by 3 weeks. Mature mice may have seizures in which a motionless posture is maintained for many seconds. Females are viable and fertile, males are sterile due to defective spermatic differentiation. The entire CNS of quaking mutant mice is severely deficient in myelin and there is a less severe myelin deficiency in the PNS. In this strain the brachyury 2 Jackson mutation (T2J) is maintained in repulsion with the quaking mutation. | ||
| 003139 | B6.Cg-Tg(DBHn-lacZ)8Rpk/J | Repository-Cryopreserved |
| Transgenic mice carry a beta-galactosidase reporter gene driven by dopamine beta hydroxylase promotor. LacZ expression is seen in neurons of the locus ceruleus and other classic noradrenergic brain stem nuclei, sympathetic ganglion neurons, and adrenal chromaffin cells. LacZ expression is also observed in neurons of the enteric system, the retina, some sensory and all cranial parasympathetic ganglia, and some diencephalic and telencephalic brain nuclei. | ||
| 000544 | B6.D2-Cacna1atg/J | Repository-Cryopreserved |
| Mice homozygous for the tottering spontaneous mutation (Cacna1atg) are characterized by a wobbly gait beginning at around 3 to 4 weeks of age and affecting, particularly, the hindquarters and by intermittent, spontaneous seizures. The seizures are of two kinds: i) Sudden arrests of movement (behavioral absence seizures) begin at about 3 weeks and are accompanied by abnormal bursts of bilaterally synchronous spike waves in ECG; they last about 0.3 to 10 seconds, occur hundreds of times per day, and continue throughout life; ii) Stereotyped partial motor seizures begin at about 4 weeks and are accompanied by abnormal ECG activity; they last 20 to 30 minutes, occur once or twice a day, and persist throughout life. Homozygous mutant mice of both sexes are fertile, but breeding performance is poor. Leaner/tottering heterozygotes (Cacna1atg-la/Cacna1atg) show ataxia, stiffness, and retarded motor activity at 15 to 17 days of age. Within a few
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| 000506 | B6C3Fe a/a-Qkqk/J | Repository-Cryopreserved |
| Mice homozygous for the quaking spontaneous mutation (Qk) have marked rapid tremor which disappears when they are at rest but increases during locomotion. The tremor in homozygous mutant mice begins at about 10 days and is fully developed by 3 weeks. Mature mice may have seizures in which a motionless posture is maintained for many seconds. Females are viable and fertile, males are sterile due to defective spermatic differentiation. The entire CNS of quaking mutant mice is severely deficient in myelin and there is a less severe myelin deficiency in the PNS. | ||
| 003741 | B6D2-Tg(Prnp-MAPT)43Vle/J | Repository-Cryopreserved |
| These transgenic mice express the human fetal tau MAPT isoform under the direction of the mouse prion protein promoter. Hyperphosphorylated, insoluble MAPT protein is widely expressed in neurons of the CNS at levels approximately ten-fold higher than the endogenous mouse counterpart. Mice homozygous for the transgenic insert die at about three months of age. In the hemizygous mice intraneural inclusions that stain positive with T14, a monoclonal antibody specific for MAPT, are observed in brain and spinal cord tissue at 1 month of age. The number of inclusions increases until 6-9 months of age. Transmission electron microscopy studies of these inclusions reveals tightly packed aggregates of randomly arranged 10-20 nm straight filaments. Mice suffer progressive, age-dependant neuronal damage, motor weakness and gliosis. These mice recapitulate key features of tauopathies and provide a model for studying the underlying mechanism of related diseases such as FTDP-17, Alzheimer's and
..... For more information please see the full phenotype on the strain data sheet | ||
| 008389 | C57BL/6-Tg(THY1-SNCA)1Sud/J | Repository-Cryopreserved |
| This transgenic strain carries a human THY1 promoter driving expression of the human synuclein, alpha (SNCA) gene. Levels of expression show a 5-fold increase in the brain and a 10-fold increase in the spinal cord. Hemizygotes are viable and fertile and unlike some similar mutant transgenic lines, do not display any Parkinson-like phenotype upon aging. | ||
| 005706 | C57BL/6-Tg(tetO-CDK5R1/GFP)337Lht/J | Repository-Cryopreserved |
| Hemizygous transgenic mice are viable, fertile, normal in size and do not display any behavioral abnormalities. Mice homozygous for this transgene may not be viable. When these transgenic mice are bred with mice expressing the tetracycline-controlled transactivator protein (tTA) under the regulation of a tissue-specific promoter, expression of the CDK5R1/GFP fusion protein in the appropriate tissue of the bitransgenic offspring can be regulated by doxycycline administration. These mice may be useful in studies of Alzheimer's disease and other neurodegenerative tauopathies, amyotrophic lateral sclerosis (ALS), Niemann Pick Type C (NPC) disease, and Parkinson's disease.
Note: this transgenic strain was designed to breed with Tg(Camk2a-tTA) transgenic mice, (Stock No. 003010), a transgenic strain that expresses tTA in forebrain neurons. The resulting bitransgenic offspring exhibit the hallmark phenotype of Alzheimer's disease;
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| 000942 | STOCK Pitx3ak/2J | Repository-Cryopreserved |
| Mice homozygous for the Pitx3ak mutation exhibit microphthalmia (small eyes) and aphakia (no lens) related to arrested lens development. The mesencephalic dopamine system is malformed and as a result homozygotes fail to develop dopaminergic neurons of the substantia nigra (Smidt et al., 2004). Homozygotes display sensorimotor deficits specific to the nigrostriatal pathway such as the challenge beam and pole test and the test for spontaneous exploratory activitiy in a cylinder. These deficits can be reversed by L-DOPA administration (Hwang et al., 2005). This mutant mouse strain may be useful in studies of Parkinson's disease. | ||
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