The mice from the strain C57Bl6J OLA HSD from Harlan Laboratories are mutated on the alphasynuclein gene. We have spent lot of time understanding why, after injection of LPS into the nigra, the dopaminergic cells did not degenerate as expected.
It could be explained by this mutation, but we did not check with another strain as the C56BL6J RccHSD. If anyone has already tried to make dopaminergic neurons degenerate using mice C56BL6J RccHSD, it would be really helpful to let us know.
Sincerely ,
Marie.
These mice cost my lab hundreds of thousands of dollars when it was first discovered that they had the alpha-synuclein mutation. We bred it out of our transgenics. Several groups have studies synuclein knockouts using mice generated with traditional methods. One group even knocked out alpha, beta, and gamma synuclein (the mice survive). Unless you are specifically studying alpha-synuclein I would stay away from these mice.
I would argue that based on our experience that your observations are completely due to the lack of synuclein. The Emson lab made mice with low vesicular monoamine transporter on this background. We put them on a regular background. Our mice displayed age-dependent progressive nigrostriatal degeneration of the dopamine neurons, Emson's did not. We had a review in TINS that explained this.
Article Altered vesicular dopamine storage in Parkinson's disease: A...
Dear Marie,
Sorry - but this is not an answer to your question, but question for you -- do you know of any mutated mice strains that over express alpha-synuclein so that you can observe fibrils (Lew pathology) not only in the brain BUT ALSO in peripheral tissues, including the gastrointestinal tract and perhaps the skin?
Best wishes,
Per
Dear Per, no, sorry, we do not work on alphasynuclein model, but only on LPS-induced dopaminergic cells death for the moment.
Best,
Marie.
These mice cost my lab hundreds of thousands of dollars when it was first discovered that they had the alpha-synuclein mutation. We bred it out of our transgenics. Several groups have studies synuclein knockouts using mice generated with traditional methods. One group even knocked out alpha, beta, and gamma synuclein (the mice survive). Unless you are specifically studying alpha-synuclein I would stay away from these mice.
I would argue that based on our experience that your observations are completely due to the lack of synuclein. The Emson lab made mice with low vesicular monoamine transporter on this background. We put them on a regular background. Our mice displayed age-dependent progressive nigrostriatal degeneration of the dopamine neurons, Emson's did not. We had a review in TINS that explained this.
Article Altered vesicular dopamine storage in Parkinson's disease: A...
Dear Gary, thank you very much for this usefull reply.
You said "regular background" : Would you thinck that C56BL6J RccHSD could be considered as a regular background ?
Best,
Marie
While regular is a loaded term, I would say that Harlan's non-synuclein mutant C57BL6 strains would be considered normal. But we do see variation to MPTP toxicity among vendors. We have historically used Charles River mice and have used the same mice to backcross all of our mice to avoid the variability.
- Badges
- Science topic
- Similar topics
- Medicine
- Disease
- Disease Models
- Animal Models
- Rodent Models
- Mouse Models