Mapping Data

Experiment

• Experiment
  TEXT-Congenic
• Chromosome
  18
• Reference
  J:132288 McLin JP, et al., Genes on distal chromosome 18 determine vulnerability to excitotoxic neurodegeneration following status epilepticus, but not striatal neurodegeneration induced by quinolinic acid. Neurobiol Dis. 2008 Mar;29(3):391-9
• ID
  MGI:3775637

Genes

Gene	Assay Type
Sicd4	resistance/susceptibility
D18Mit144	PCR
D18Mit33	PCR

Notes

• Experiment
  A previously identified kainic acid-induced seizure susceptibility locus on mouse Chromosome 18 (Sicd1, 57 cM) was further investigated using congenic lines. Congenic line BDChr18D (distal) consists of DBA/2J-derived donor DNA from D18Mit33 (44 cM; 69.8 Mb) to D18Mit144 (57 cM; 86 Mb) on a C57BL/6J genetic background. Congenic line BDChr18PM (proximal/medial) consists of DBA/2J-derived donor DNA from SNP marker rs3672215 (45 cM; 72.5 Mb) to rs6335278 (47 cM; 73.08 Mb). Donor strain DBA/2J is susceptible to neurodegeneration following kainic acid-induced seizures whereas background strain C57BL/6J displays minimal neuronal damage in most brain regions after kainic acid-induced seizures.
  
  8.26.2015 Curators Note: Because Scid1 was originally mapped in J:119634 in 2004 using a (FVB/NJ x C57BL/6J)F1 x FVB/NJ backcross, which differs from the cross used here, we consider the current study a separate mapping experiment and have named the QTL identified here Sicd4 (distal QTL) and Sicd5 (proximal/medial QTL).
  
  When animals were challenged with kainic acid and phenotyped for neurodegeneration following 5 seizures, the distal congenic BDChr18D displayed widespread neurodegeneration similar to but not as severe as parental strain DBA/2J. The proximal congenic BDChr18PM displayed limited neurodegeneration and resembled the phenotype observed in background strain C57BL/6J.
  
  When different sections of the hippocampus were examined for cell death distal congenic BDChr18D displayed significant neurodegeneration in the hilus of the dentate gyrus similar to that seen in donor strain DBA/2J, while neurodegeneration in CA3 was minimal and resembled the level seen in C57BL/6J. Interestingly, proximal congenic BDChr18PM displayed significant neurodegeneration in CA3 similar to that observed in DBA/2J. Neurodegeneration in the hilus of the dentate gyrus was minimal in BDChr18PM congenics and resembled the level seen in resistant background strain C57BL/6J.
  
  Authors hypothesize the incompletely penetrant phenotypes observedin thecongenic lines may be attributed to other loci (possibly on chrs 4 and 15) influencing kainic acid-induced neurodegeneration. In addition, Sicd1 was originally mapped using a different susceptible strain (FVB/N) that wascrossedto resistant strain C57BL/6J.