Search Criteria: Research Area is "Neurobiology Research: Neurodevelopmental Defects (Autism)"
| Stock Number |
Strain Name Strain Description |
Standard Supply |
| 002282 | BTBR T+ tf/J | Level 4 |
| BTBR mice exhibit a 100% absence of the corpus callosum and a severly reduced hippocampal commissure (Wahlsten D, 2003 Brain Res). This strain exhibits several symptoms of autism including: reduced social interactions, impaired play, low exploratory behavior, unusual vocalizations and high anxiety as compared to other inbred strains (McFarlane HG, 2008, Gen, Brain Behav; Moy SS, 2007, Behav Br Res, Scattoni ML, 2008, PLos). | ||
| 002711 | B6;129-Gabrb3tm1Geh/J | Repository- Live |
| The gamma-Aminobutyric acid type A receptors mediate the majority of rapid inhibitory synaptic transmission in the CNS. The beta3 subunit is an essential component of these receptors in many brain regions, especially during development, and is implicated in several pathophysiologic processes. The majority of mice homozygous for the Gabrb3tm1Geh mutation (or beta3-/-) die at birth with ~60% displaying cleft palate and the remaining ~35% die for unidentified reasons. Homozygous females that survive are fertile but do not care for their pups. Survivors have frequent myoclonus and occasional epileptic seizures, are hypersensitive to external stimuli and handling, have a lack of coordination and display altered responses to certain anesthesias. In addition, the observed behavioral deficits (especially regarding social behaviors) indicate that mutant mice may be a useful model of autism spectrum disorders. Of note, several strains bearing gamma-aminobutyric acid (GABA-A)
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| 008394 | B6;129-Nlgn3tm2.1Sud/J | Repository-Cryopreserved |
| This targeted mutation strain carries a deletion of exons 2 and 3 of the gene. These mice show no alteration in their inhibitory synaptic transmission characteristics. No protein product is detected by Western blot analysis of homozygous brain extracts. Homozygotes are viable, normal in size and do not display any gross physical abnormalities. This mutant mouse strain may be useful in studies of synapse formation and/or function. | ||
| 002657 | B6;129S2-En2tm1Alj/J | Repository-Cryopreserved |
| Mice homozygous for the En2tm1Alj targeted mutation are viable but show defects in adult cerebellar foliation patterning. Development is also delayed in areas of the brain with abnormal formation of specific fissures. The posterior region of the cerebellum is most severely affected. Both homozygotes and heterozygotes show an impairment in motor learning compared to wildtype littermates with the homozygotes improving the least in the rotating rod motor learning paradigm. | ||
| 006160 | B6;129X1-Avpr1btm1Wsy/J | Repository-Cryopreserved |
| Mice homozygous for this targeted mutation are viable, fertile, normal in size, exhibit apparently normal sexual behavior, and do not display any gross physical abnormalities. Homozygous mice exhibit less social agression, altered chemoinvestigatory behavior, and impaired social recognition. These mice may be useful in studies of agressive behavior, social motivation, and appropriate behavioral responses, and may be potential models of autism and agression accompanying dementia and traumatic brain injury. | ||
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