Search Criteria: Research Area is "Neurobiology Research: Cortical Defects"
| Stock Number |
Strain Name Strain Description |
Standard Supply |
| 002810 | B6CBA-Tg(HDexon1)62Gpb/1J | Level 3 |
| This line is transgenic for the 5' end of the human HD gene carrying (CAG)115-(CAG)150 repeat expansions. The transgene is ubiquitously expressed. Transgenic mice exhibit a progressive neurological phenotype that mimics many of the features of HD, including choreiform-like movements, involuntary stereotypic movements, tremor, and epileptic seizures, as well as nonmovement disorder components, including unusual vocalization. They urinate frequently and exhibit loss of body weight and muscle bulk through the course of the disease. Neurologically they develop Neuronal Intranuclear Inclusions (NII) which contain both the huntingtin and ubiquitin proteins. Previously unknown, these NII have subsequently been identified in human HD patients. The age of onset of HD symptoms is reported to occur between nine and 11 weeks. Commonly known as the "R6/2" strain.
Transgenic mice develop hyperglycemia by 12 weeks of age with a corresponding decrease in insulin levels. Pancreatic beta cells devel
..... | ||
| 006494 | B6CBA-Tg(HDexon1)62Gpb/3J | Level 3 |
| This line is transgenic for the 5' end of the human HD gene carrying less than (CAG)150 repeat expansions. The transgene is ubiquitously expressed. Transgenic mice exhibit a progressive neurological phenotype that mimics many of the features of HD, including choreiform-like movements, involuntary stereotypic movements, tremor, and epileptic seizures, as well as nonmovement disorder components, including unusual vocalization. They urinate frequently and exhibit loss of body weight and muscle bulk through the course of the disease. Neurologically they develop Neuronal Intranuclear Inclusions (NII) which contain both the huntingtin and ubiquitin proteins. Previously unknown, these NII have subsequently been identified in human HD patients. The age of onset of HD symptoms is reported to occur between 9 and 11 weeks. Commonly known as the "R6/2" strain. Transgenic mice develop hyperglycemia by 12 weeks of age with a corresponding decrease in insulin levels. Pancreatic beta cells develop
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| 004337 | 129(Cg)-Foxg1tm1(cre)Skm/J | Repository- Live |
| This strain expresses Cre recombinase from the endogenous Foxg1 locus. Forkhead box G1 is required for telencephalon development and is expressed specifically in the telencephalon and discrete head structures. When crossed with a strain containing loxP site flanked sequence of interest, Cre-mediated recombination results in tissue-specific deletion of the target. Recombination occurs in the telencephalon, anterior optic vesicle (developing lens and retina), otic vesicle, facial and head ectoderm, olfactory epithelium, mid-hindbrain junction and pharyngeal pouches. Mice that are homozygous for the targeted mutation die perinatally. Heterozygous mutant mice are viable, fertile, normal in size and do not display any gross physical or behavioral abnormalities. This mutant mouse strain represents a model that may be useful in studies of telencephalic development. | ||
| 006084 | B6.129P2(Cg)-Foxg1tm1(cre)Skm/J | Repository- Live |
| This strain expresses Cre recombinase from the endogenous Foxg1 locus. Forkhead box G1 is required for telencephalon development and is expressed specifically in the telencephalon and discrete head structures. When crossed with a strain containing loxP site flanked sequence of interest, Cre-mediated recombination results in tissue-specific deletion of the target. Recombination occurs in the telencephalon, anterior optic vesicle (developing lens and retina), otic vesicle, facial and head ectoderm, olfactory epithelium, mid-hindbrain junction and pharyngeal pouches. Mice that are homozygous for the targeted mutation die perinatally. Heterozygous mutant mice are viable, fertile, normal in size. On the C57BL/6 background, forebrain volume in heterozygotes is substantially reduced especially in the cerebral cortex (40.7%), striatum (29.7%), and hippocampus (18.6%). In the adult, the thalamus is reduced in volume by 21.6%. This mutant mouse strain represents a model that ma
..... For more information please see the full descriiption on the strain data sheet | ||
| 004595 | B6.129P2-Htttm2Detl/J | Repository- Live |
| Mice homozygous for the targeted allele are viable and fertile. At 15-40 weeks of age mice carrying this allele on a segregating C57BL/6 and 129P2 background exhibit an abnormal gait, clasping behavior and diminished exploratory activity. Infrequent tonic-clonic like seizures may also be observed. Mice with a higher percentage of C57BL/6 in their genetic background develop behavioral and neurological phenotypes at a much later age (70-100 weeks). (Heng MY et al. 2007) Mutant mice may be noticeably smaller than wild-type littermates. Increased glial fibrillary acidic protein immunoreactivity is present in the striatum and ubiquititin- and huntingtin-positive neuronal intranuclear inclusions (NIIs) are detected throughout the dorsal striatum, nucleus accumbens and to a lesser extent other regions of the brain. Onset of symptoms occurs earlier for homozygotes than for heterozygotes.This mutant mouse strain represents a model that may be useful in studies related to Huntington's di
..... For more information please see the full descriiption on the strain data sheet | ||
| 005359 | B6.Cg-Tg(Camk2a-cre)T29-1Stl/J | Repository- Live |
| Mice homozygous for the transgenic insert are viable, fertile, normal in size and do not display any gross physical or behavioral abnormalities. These transgenic mice express the Cre recombinase under the control of the mouse calcium/calmodulin-dependent protein kinase II alpha promoter. Cre recombinase expression is detected in the forebrain, specifically to the CA1 pyramidal cell layer in the hippocampus. When crossed with a strain containing loxP site flanked sequence of interest, Cre-mediated recombination occurs in the pyramidal cell layer. | ||
| 006471 | B6.Cg-Tg(HDexon1)61Gpb/J | Repository- Live |
| Mice have been generated that are transgenic for the 5' end of the human HD gene carrying (CAG)115-(CAG)150 repeat expansions. In this founder line (61Gpb), as well as another similar line (62Gpb, see Stock No. 006494), the transgene is ubiquitously expressed. Transgenic mice exhibit a progressive neurological phenotype that mimics many of the features of HD, including choreiform-like movements, involuntary stereotypic movements, tremor, and epileptic seizures, as well as nonmovement disorder components, including unusual vocalization. They urinate frequently and exhibit loss of body weight and muscle bulk through the course of the disease. Neurologically they develop Neuronal Intranuclear Inclusions (NII) which contain both the huntingtin and ubiquitin proteins. These NII have also been identified in human HD patients. The age of onset of HD symptoms is reported to occur between 15 and 21 weeks for this 61Gpb line. These HDexon1
..... For more information please see the full descriiption on the strain data sheet | ||
| 002466 | B6;129P2-Prkcctm1Stl/J | Repository- Live |
| Mice homozygous for the Prkcctm1Stl targeted mutation are viable and develop normally. Homozygous mice show diminished long-term potentiation (LTP) in the hippocampus, but two other types of synaptic plasticities are normal, namely long-term depression and paired-pulse facilitation. Despite this diminished LTP capacity homozygotes can learn to do hippocampus-dependant tasks, such as the Morris water maze and context-dependent fear conditioning, with only slight deficits. | ||
| 003627 | B6C3-Tg(HD82Gln)81Dbo/J | Repository- Live |
| Mice expressing this transgene appear normal at birth through 1-2 months. Mice fail to gain weight, develop tremors, hypokinesis and lack coordination. They exhibit an abnormal gait and frequent hind limb clasping. Life expectancy is 5-6 months. Studies using huntingtin antibodies indicated numerous immunoreactive nuclear inclusions in multiple neuron populations. Neuritic damage is evident. | ||
| 000235 | B6C3Fe a/a-Relnrl/J | Repository- Live |
| Mice homozygous for the reeler (Relnrl) mutation exhibit an ataxic gait, dystonic posture and tremors starting around 2 weeks of age. These mutants are incapable of maintaining their hindquarters upright and often fall over during locomotor activity. Moreover, viability and fertility are greatly reduced, especially when the gene is carried on an inbred genetic background. Heterozygotes are visually indistinguishable from wildtype controls. Neuropathies characteristic of Relnrl/Relnrl mutants include a failure of neuronal layer formation in laminated brain regions during development. Neuronal positioning is abnormal within cerebellar, cerebral and hippocampal cortices. The behavioral phenotype is primarily attributed to the severe hypoplasia of the cerebellum, which lacks foliation. Here, there are reduced numbers of granule and Purkinje cells and these cells are aberrantly dispersed among the layers. In the Reln-deficient neo
..... For more information please see the full descriiption on the strain data sheet | ||
| 006579 | C57BL/6-Tg(Camk2a-Bdnf)A9Stl/J | Repository- Live |
| Hemizygous mice are viable and fertile, although the donating investigator reports that hemizygous mice have breeding problems likely resulting from a social anxiety-related phenotype. These "BDNF (line A9)" mice express the rat brain-derived neurotrophic factor (BDNF) primarily in forebrain regions, including the neocortex and hippocampus. Weak transgenic BDNF expression is detected also in cerebellum. Within the primary visual cortex, transgene expression is highest in the superficial layers. Hemizygous mice exhibit accelerated maturation of GABAergic innervation and inhibition, earlier termination of the critical period for ocular dominance plasticity, and accelerated development of visual acuity. These transgenic mice may be useful for studies involving BDNF overexpression and synaptic maturation and plasticity in the visual cortex. | ||
| 007892 | C57BL/6J-Relnrl-7J/J | Repository- Live |
| 007578 | CBy.Cg-Tg(HDexon1)61Gpb/J | Repository- Live |
| Mice have been generated that are transgenic for the 5' end of the human HD gene carrying approximately 100 CAG repeat expansions. In this founder line (61Gpb), the transgene is ubiquitously expressed. Transgenic mice exhibit a progressive neurological phenotype that mimics many of the features of HD, including choreiform-like movements, involuntary stereotypic movements, tremor, and epileptic seizures, as well as nonmovement disorder components, including unusual vocalization. They urinate frequently and exhibit loss of body weight and muscle bulk through the course of the disease. Neurologically they develop Neuronal Intranuclear Inclusions (NII) which contain both the huntingtin and ubiquitin proteins. These NII have also been identified in human HD patients. The age of onset of HD symptoms is reported to occur between 15 and 21 weeks for this 61Gpb line. On the BALB/cByJ genetic background, the CAG tract remains somatically stable throughout the life span of the mouse but may contr
..... For more information please see the full descriiption on the strain data sheet | ||
| 004938 | FVB-Tg(YAC128)53Hay/J | Repository- Live |
| These transgenic mice express the human huntingtin protein containing a 128 CAG repeat expansion. Human huntingtin mRNA and protein is detected. Hyperkinesis begins at 3 months of age with progressive motor impairment appearing at 6 months of age. This is followed by progressive neurodegeneration, starting at 9 months of age, and hypokinesis at 12 months. The motor dysfunction, Rotorod deficit, is correlated with neuronal loss. Mutants exhibit decreased brain weight and reduced striatal and cortical volumes. 18% shrinkage of striatal neurons is observed in 12 month old mutants. A significant decrease (15%) in the number of striatal neurons occurs by 12 months of age. Nuclear huntingtin aggregate inclusions of striatal neurons from 18 month old mutant mice are detected at the light microscopy level. This mutant mouse strain represents a model that may be useful in studies of Huntington's disease. | ||
| 006143 | FVB/N-Tg(Thy1-cre)1Vln/J | Repository- Live |
| Hemizygous mice are viable, fertile, normal in size, and do not display any gross physical or behavioral abnormalities. Cre activity is observed in nearly all neurons in cortex and hippocampus. When bred with any mouse containing a loxP-flanked sequence of interest, Cre-mediated recombination will result in postnatal, neuron-specific deletion of the flanked genome. These mice may be useful in studies of the nervous system, including Alzheimer's disease. | ||
| 007247 | FVB/N-Tg(YAC353G6)W7Hay/J | Repository- Live |
| These transgenic mice express the human huntingtin protein containing a 133 CAG repeat expansion and a mutation in exon 13 conferring resistance to caspase-6 cleavage to the gene product.
Expected caspase-6 cleaved fragments are not detected in brain lysates by Western blot analysis. Transgenic mice have brain weight and striatal volume similar to wildtype controls and do not exhibit neuronal loss at 12 months of age when compared to transgenic mice that express human huntingtin protein containing a 128 CAG repeat (FVB-Tg(YAC128)53Hay/J Stock No. 004938). These transgenic mice have activity levels and motor function similar to wildtype controls, and are resistant to neuron excitotoxicity. Immunohistochemical analysis of striatal brain sections reveals delayed nuclear localization of mutant huntingtin protein in these transgenic mice at nine months of age. Between nine and 12 months of age, an increase of nuclear huntingtin is observed. Homozygotes are viable, fertile, normal in
..... For more information please see the full descriiption on the strain data sheet | ||
| 003925 | MRL.129P2(B6)-B2mtm1Unc/Dcr-Dab1scm-2J/J | Repository- Live |
| See Stock No. 000486 for important information on the MRL/MpJ background. | ||
| 002043 | STOCK A/A-Dab1scm/J | Repository- Live |
| Mice homozygous for the scrambler spontaneous mutation (Dab1scm) are recognized by an unstable gait and whole-body tremor. The cerebella of 30-day-old scrambler homozygotes are hypoplastic and devoid of folia; however, neither seizures nor abnormal brain wave patterns have been observed. Scrambler is similar to the reeler mutation in phenotype and pathology and, like reeler, probably results from defective neuronal migration. Female homozygotes mate and breed. Homozygous scrambler mutants have an ataxic gait which in the male may be contributory factor in the failure to mate. Normal life span for both sexes. | ||
| 003454 | B6.129-Htttm3Mem/J | Repository-Cryopreserved |
| This strain carries 50 CAG repeat units in the first exon of the endogenous Htt gene. | ||
| 003597 | B6.129-Htttm4Mem/J | Repository-Cryopreserved |
| This strain carries 92 CAG repeat units in the first exon of the endogenous Htt gene. Huntington's-like pathology is seen in the striatum, including nuclear localization of the protein, N-terminal inclusions, and insoluble aggregate formation. Instability of the length of the CAG repeat between generations is seen. Expression of this phenotype is delayed relative to Htttm5 (Stock No. 003456). 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. This is the case for the strain above. 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. | ||
| 003598 | B6.129-Htttm5Mem/J | Repository-Cryopreserved |
| This strain carries 111 CAG repeat units in the first exon of the endogenous Htt gene. Huntington's-like pathology is seen in the striatum, including nuclear localization of the protein, N-terminal inclusions, and insoluble aggregate formation. Instability of the length of the CAG repeat between generations is seen. Expression of the phenotype occurs earlier than in Htttm4, (Stock No. 003455). 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. This is the case for the strain above. 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. | ||
| 002362 | B6.129P2-Camk2atm1Sva/J | Repository-Cryopreserved |
| Mice homozygous for the Camk2atm1Sva targeted mutation are viable but are reported not to breed. Homozygous mutant mice show no obvious anatomical defects in the nervous system. Postsynaptic mechanisms are intact, but long-term hippocampal potentiation (LTP), an electrophysiological manifestation of increased synapse strength, is deficient. These mutant mice show specific impairment in spatial learning, indicating that LTP is important to spatial though not necessarily to non-spatial memory. In a more recent study heterozygotes displayed normal offensive aggression. Heterozygotes exhibit a decreased fear response and an increase in defensive aggression. Homozygotes (in which both copies of the gene are absent) exhibit more pronounced behavior suggesting a gene dosage effect. | ||
| 003596 | B6.129S4-Cdk5tm1Kul/J | Repository-Cryopreserved |
| Cdk5 is an important molecule for brain development and neuronal differentiation. Cdk null mice exhibit unique lesions in the central nervous system associated with perinatal mortality. The brains of mutant mice lack cortical laminar structure and cerebellar foliation. The large neurons in the brain stem and in the spinal cord show chromatolytic changes with accumulation of neurofilament immunoreactivity. They also exhibit neuronal migration abnormalities, cerebellar defoliation, NF accumulation neuronal bodies, and degenerated motor neurons. 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. This is the case for the strain above. 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. | ||
| 004163 | B6.129S4-Cdk5r1tm1Lht/J | Repository-Cryopreserved |
| At birth, mice homozygous for this targeted allele are viable, fertile, normal in size and do not display any gross physical or behavioral abnormalities. Cdk5r protein product is not immunodetectable in homozygote whole-brain lysates. Histological analysis of homozygotes reveals severe defects in the patterning of the cerebral cortex and other areas of the brain. The normal lamination pattern of cortical neurons is disrupted; axonal trajectories and dendritic structures are altered. Homozygous mice are more susceptible to mortality from chemically induced-seizures. Sporadic adult lethality is also observed, presumably resulting from spontaneous seizures, a consequence of the disrupted cytoarchitecture observed in the cortex. This mutant mouse strain represents a model that may be useful in studies related to the mechanisms of cortical lamination, epilepsy, Alzheimer's and other neurodegenerative diseases. | ||
| 002959 | B6.129S4-Drd1atm1Jcd/J | Repository-Cryopreserved |
| Mice homozygous for the Drd1atm1Jcd targeted mutation exhibit growth retardation and show down-regulated expression of dynorphin and substance P. They also show behavioral anomolies in spatial learning, movement initiation, and responses to new stimuli. Administration of cocaine to homozygotes does not activate locomotion or up-regulate immediate early gene (IEG) expression; however, dopamine receptor-2-dependent IEG changes are intact. Acute cocaine administration increases substance P levels. Failure of locomotor activation is also seen with repeated amphetamine treatment. Dopamine receptor D1a deficient mice do retain cocaine-conditioned place preference. Please Note: Growth retardation, which may be due to abnormal or delayed tooth formation, is avoided if homozygotes are fed either hydrated or crushed grain from ~2-10 weeks of age. Homozygotes do appear thinner than wildtypes and have a very slight halting gait (unpublished observations, The Jackson Labora
..... For more information please see the full descriiption on the strain data sheet | ||
| 002688 | B6.129S4-Htttm1Mem/J | Repository-Cryopreserved |
| Mice homozygous for the Htttm1Mem targeted mutation die very early in embryogenesis (~day 8). | ||
| 003536 | B6;129-Cdk5tm1Kul/J | Repository-Cryopreserved |
| Cdk5 is an important molecule for brain development and neuronal differentiation. Cdk null mice exhibit unique lesions in the central nervous system associated with perinatal mortality. The brains of mutant mice lack cortical laminar structure and cerebellar foliation. The large neurons in the brain stem and in the spinal cord show chromatolytic changes with accumulation of neurofilament immunoreactivity. They also exhibit neuronal migration abnormalities, cerebellar defoliation, NF accumulation neuronal bodies, and degenerated motor neurons. | ||
| 003524 | B6;129S6-Lrp8tm1Her/J | Repository-Cryopreserved |
| Mutant mice have a targeted mutation of the apolipoprotein E receptor Lrp8 (also called Apoer2). Homozygotes are viable with no gross morphological abnormalities. Homozygous males have reduced fertility, while females are not affected. Using C-terminal specific antibodies, no endogenous protein is detected in the brains of homozygotes. Homozygous mice have a smaller and less foliated cerebellum with various hippocampus defects in granule cell positioning, cortical neuron migration, granule cell laminar organization, commissural fiber distribution, CA1 microtubule-associated protein 2 (MAP-2) distribution, and long term potentiation (LTP). Mutant mice show contextual fear conditioning deficits. These mice may be useful in studies of brain development, neuronal cytoarchitecture, Reelin signaling pathways, NMDA receptor activity, lipoprotein receptors, synaptic plasticity and learning, schizophrenia, and neurodegenerative disorders such as Alzheimer's disease. | ||
| 003120 | B6;129S7-L1camtm1Sor/J | Repository-Cryopreserved |
| The L1 gene is localized to the X chromosome. As a result, hemizygous males are affected and the mutation has to be propagated through females. Male mice hemizygous for the L1camtm1Sor targeted mutation have defects in the guidance of axons of the corticospinal tract. A substantial proportion of axons do not take their normal crossed course to the dorsal column at the pyramidal decussation. There is also a varying, but reduced number of corticospinal axons in the dorsal columns of the spinal cord. | ||
| 004360 | B6;SJL-Tg(HD)63Aron/J | Repository-Cryopreserved |
| These transgenic mice express the initial N-terminal third of the mutant human huntingtin gene (IT15) under the direction of the rat neuron-specific enolase promoter. Expected transgene expression was confirmed by Northern blot, RT-PCR and Western blot analysis. Mice heterozygous for the transgene have a phenotype mimicking much of the morphological and subcellular neuropathology that occurs in the striatum and cortex in human Huntington's disease. Behavioral abnormalities are varible in onset and intensity, beginning between three to six months of age. Transgenic mice exhibit increased levels of nuclear and cytoplasmic huntingtin and dysmorphic dendrites in the striatum and cortex. Electron microscopic analysis of nuclear inclusions of cortical and striatal neurons detects granular and filamentous structures that appear to be similar to structures seen in brain affected by Huntington's disease. Cortical stimulation and N-methyl-D-aspartate (NMDA) receptor activation produces abnormal
..... For more information please see the full descriiption on the strain data sheet | ||
| 001035 | B6C3Fe a/a-Napahyh/J | Repository-Cryopreserved |
| Although no overt phenotype is appearant in newborn hyh mice, they have dilated lateral ventricles. By 2 weeks of age, an outward phenotype of a domed head and a hop gait is apparent. Dissection and histological examination reveal "hydrocephalus of lateral and third ventricles and of the caudal aspects of the cerebreal aquiduct" increasing in severity with age (Bronson et al., 1990). Homozygotes have a decreased lifespan usually dying before 2 months of age. Some homozygotes will live for several months, but usually will not breed. | ||
| 002809 | B6CBA-Tg(HDexon1)61Gpb/1J | Repository-Cryopreserved |
| Mice have been generated that are transgenic for the 5' end of the human HD gene carrying (CAG)115-(CAG)150 repeat expansions. In both the 61Gpb and 62Gpb founder lines, the transgene is ubiquitously expressed. Transgenic mice exhibit a progressive neurological phenotype that mimics many of the features of HD, including choreiform-like movements, involuntary stereotypic movements, tremor, and epileptic seizures, as well as nonmovement disorder components, including unusual vocalization. They urinate frequently and exhibit loss of body weight and muscle bulk through the course of the disease. Neurologically they develop Neuronal Intranuclear Inclusions (NII) which contain both the huntingtin and ubiquitin proteins. These NII have also been identified in human HD patients. The age of onset of HD symptoms is reported to occur between 15 and 21 weeks for the 61Gpb line and between nine and 11 weeks for the 62Gpb line. | ||
| 007662 | C57BL/6-Arctm1Stl/J | Repository-Cryopreserved |
| Mice homozygous for this targeted mutation are viable and fertile and do not display any gross physical or behavioral abnormalities. A destabilized form of GFP (d2EGFP) is expressed under the control of the endogenous Arc promoter which is activated by neuronal stimulation in forebrain regions. The half-life of EGFP expression is shortened to approximately two hours which is comparable to the decay time of ARC protein. Homozygous mice have a reduced orientation specificity in the visual cortex. The loss of Arc mRNA expression in homozygous mice was verified by RT-PCR analysis of brain total RNA preparations. This strain may be useful in studies of cortical functions. | ||
| 004817 | C57BL/6J-Npc1nmf164/J | Repository-Cryopreserved |
| View strain phenotype and additional information on the Neuroscience Mutagenesis Facility web page for Npc1nmf164 entry. | ||
| 005744 | C57BL/6J-Relnrl-6J/J | Repository-Cryopreserved |
| View strain phenotype and additional information on the Neuroscience Mutagenesis Facility web page for Relnrl-6J entry. | ||
| 004823 | C57BL/6J-nmf205/J | Repository-Cryopreserved |
| View strain phenotype and additional information on the Neuroscience Mutagenesis Facility web page for nmf205 entry. | ||
| 003581 | CBy.129S4-Dab1tm1Cpr/J | Repository-Cryopreserved |
| Homozygous Dab1-null mice become tremulous and ataxic at approximately postnatal day 10. Multiple defects can be detected in brain tissue. Lamellar structures in the cortex and hippocampus appear disorganized and the cerebellum is small and disorganized. Although homozygotes null reportedly die at 4-5 weeks on a mixed B6,129 or 129/Sv background, mice on a BALB/cByJ are viable. | ||
| 003640 | FVB/NJ-Tg(YAC72)2511Hay/J | Repository-Cryopreserved |
| Mice homozygous for this transgene are viable and fertile. The human huntingtin transgenic protein is expressed widely in many tissues (identical to the endogenous huntingtin protein), but has highest levels of expression in the brain and testes. Electrophysiological abnormalities can be measured by six months. A behavioral phenotype is first detected at seven months when evidence of mild hyperkinetic movement disorder is noticeable. This disorder is characterized by progressive spontaneous hyperactivity during the dark phase of open field-testing. By 12 months of age selective degeneration of medium spiny neurons in the lateral striatum is observed. This degeneration is associated with the translocation of N-terminal huntingtin fragments to the nucleus. This strain represents a Huntington's Disease mouse model where a mutant full-length human huntingtin is expressed under control of its endogenous promoter. | ||
| 002322 | STOCK Drd1atm1Jcd/J | Repository-Cryopreserved |
| Mice homozygous for the Drd1atm1Jcd targeted mutation exhibit growth retardation and show down-regulated expression of dynorphin and substance P. They also show behavioral anomolies in spatial learning, movement initiation, and responses to new stimuli. Administration of cocaine to homozygotes does not activate locomotion or up-regulate immediate early gene (IEG) expression; however, dopamine receptor-2-dependent IEG changes are intact. Acute cocaine administration increases substance P levels. Failure of locomotor activation is also seen with repeated amphetamine treatment. Dopamine receptor D1a deficient mice do retain cocaine-conditioned place preference. Please Note: Growth retardation, which may be due to abnormal or delayed tooth formation, is avoided if homozygotes are fed either hydrated or crushed grain from ~2-10 weeks of age. Homozygotes do appear thinner than wildtypes and have a very slight halting gait (unpublished observations, The Jackson Labora
..... For more information please see the full descriiption on the strain data sheet | ||
| 003453 | STOCK Htttm2Mem/J | Repository-Cryopreserved |
| Mice with the Htttm2Mem targeted mutation display no overt phenotype. This strain carries 20 CAG repeat units in the first exon of the endogenous Hdh gene. This strain is a control for Stock No's. 003455 and 003456). | ||
| 003455 | STOCK Htttm4Mem/J | Repository-Cryopreserved |
| This strain carries 92 CAG repeat units in the first exon of the endogenous Htt gene. Huntington's-like pathology is seen in the striatum, including nuclear localization of the protein, N-terminal inclusions, and insoluble aggregate formation. Instability of the length of the CAG repeat between generations is seen. Expression of this phenotype is delayed relative to Htttm5 (Stock No. 003456). | ||
| 003456 | STOCK Htttm5Mem/J | Repository-Cryopreserved |
| This strain carries 111 CAG repeat units in the first exon of the endogenous Htt gene. Huntington's-like pathology is seen in the striatum, including nuclear localization of the protein, N-terminal inclusions, and insoluble aggregate formation. Instability of the length of the CAG repeat between generations is seen. Expression of the phenotype occurs earlier than in Htttm4, (Stock No. 003455). | ||
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