Search Criteria: Research Area is "Neurobiology Research: Channel and Transporter Defects (sodium/potassium)"
| Stock Number |
Strain Name Strain Description |
Standard Supply |
| 003232 | B6.129S7-Chrna7tm1Bay/J | Repository- Live |
| Mice homozygous for the Chrna7tm1Bay mutation are viable and fertile. Neuropathological and histochemical assessment of the brain reveals no abnormalities. High-affinity nicotine binding sites are present but there is an absence of high-affinity 125alpha-BGT sites. Homozygotes lack rapidly desensitizing, methyllycaconitine-sensitive, nicotinic currents that are present in hippocampal neurons. | ||
| 003143 | B6.129-Gria2tm1Rod/J | Repository-Cryopreserved |
| Mice homozygous for the Gria2tm1Rod targeted mutation (GluR2-deficient) were originally reported to be about one half the size of their normal littermates by two to three weeks of age, leading to some preweaning mortality. Growth retardation and mortality can be diminished by reducing litter size and eliminating some competition for the mother's milk. By eight weeks of age, homozygotes appear similar in size and weight to their unaffected littermates. Neurons from Gria2-deficient mice exhibit a 9-fold increase in Ca2+ permeability and enhanced long-term potentiation (LTP). Antagonists of AMPA and NMDA receptors block all the enhanced LTP seen in homozygous null mice. Changes in pain thresholds, sensitivity to anaesthetics, focal cerebral ischemia, apoptosis of neuronal subpopulations and learning impairments are also observed. It has been the experience of The Jackson Laboratory that no homozygous animals have been recovered from heterozygous s
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| 005797 | B6.129P2-Chrna2tm1Dgen/J | Repository-Cryopreserved |
| This targeted mutant was created and characterized by Deltagen, Inc. View phenotypic data developed by Deltagen. | ||
| 004164 | B6.129S7-Chrna3tm1Bay/J | Repository-Cryopreserved |
| On the C57BL/6J background, most mice homozygous for the targeted allele die during postnatal week 1-2 (On a 129 background, most survived to postnatal week 4-6). These older, surviving mice fail to open their eyes. Upon inspection, the eye is found to be smaller than that seen in wildtype mice with the pupil being widely dilated and unresponsive to light. The urinary bladders of these mice are severely distended with urine and in the case of older animals, urinary stones. Nicotine fails to elicit a contractile response in bladder tissue derived from homozygotes. Heterozygotes are phenotypically normal. | ||
| 005696 | CBACaJ;129S-Chrna9tm1Bedv/J | Repository-Cryopreserved |
| Mice homozygous for the targeted mutation are viable and fertile and have normal balance, movement, cochlear duct morphology, and gross development and position of the olivo-cochlear (OC) bundle. However, most outer hair cells are innervated by one large OC efferent fiber terminal instead of multiple smaller terminals as in wildtype. OC terminal plexus in close apposition to the inner hair somata are absent in homozygotes. Null mice fail to show electrophysiological cochlear responses during efferent fiber activation. This mutant may be suitable for use in studies related to auditory-related studies of the inner ear, including the cochlea, organ of Corti, and hair cells as well as acetylcholine receptor/neurotransmitter or olfactory research. | ||
| 002913 | STOCK Gria2tm1Rod/J | Repository-Cryopreserved |
| Mice homozygous for the Gria2tm1Rod targeted mutation (GluR2) were originally reported to be about one half the size of their normal littermates by two to three weeks leading to some preweaning mortality. Growth retardation and mortality can be diminished by reducing litter size and eliminating some competition for the mother's milk. Homozygotes do appear similar in size and weight by eight weeks of age. Neurons lacking Gria2 exhibit a 9-fold increase in Ca2+ permeability and enhanced long-term potentiation (LTP). Antagonists of AMPA and NMDA receptors block all the enhanced LTP seen in homozygous null mice. Unpublished data show changes in pain thresholds, sensitivity to anaesthetics, focal cerebral ischemia, apoptosis of neuronal subpopulations and learning impairments.
It has been the experience of The Jackson Laboratory that no homozygous animals can be recovered from heterozygous sibling matings. | ||
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