Table 1.
Phenotype | Chromosome | LODa | Locationb | Candidate gene(s) | Evidencec | Reference |
---|---|---|---|---|---|---|
Acute/tonic pain | ||||||
Capsaicin | 2 | 5.9 | 30 | (185) | ||
7 | 4.8 | 10 | (185) | |||
7 | 5.8 | 50 | (185) | |||
8 | 4.4 | 30 | (185) | |||
Formalin | 10 | 4.3 | 70 | (186) | ||
Hargreaves | 7 | 6.3 | 50 | Calca (54 cM) | Pharm., siRNA, gene expr. | (113) |
Hot-plate | 4 | 3.8 (♂ only) | 71 | Oprd1 (65 cM) | Pharm. | (187) |
Tail withdrawal | 4 | 3.6 (♂ only) | 56 | Oprd1 (65 cM) | Position | (123) |
7 | 12.6 | 33 | Trpv1 (44 cM) | Position | (123) | |
11 | 7.8 | 46 | (123) | |||
Chronic pain | ||||||
Autotomy | 15 | 3.9 | 44 | (188) | ||
15 | 3.0 | 44 | (189) | |||
15 | 3.3 (♀ only) | 32 | (190) | |||
2 (rat) | 3.6 | 20 | (191) | |||
Analgesia | ||||||
Clonidine | 1 | 4.7 | 100 | Kcnj9 (94 cM) | Mutant, gene expr. | (123) |
Morphine | 1 | 4.7 (♀ only) | 10 | Oprk1 (6 cM) | Position | (122) |
1 | 3.2 | 91 | (123) | |||
9 | 5.2 (♀ only) | 20 | (122) | |||
9 | 4.5 | 42 | Htr1b (46 cM) | Pharm. | (192) | |
10 | 7.5 | 9 | Oprm1 (8 cM) | Receptor binding | (121) | |
Stress-induced | 8 | 6.1 (♀ only) | 56 | Mc1r (68 cm) | Position | (193) |
U50,488 | 8 | 2.7 (♀ only) | 67 | Mc1r (68 cM) | Pharm., mutant | (129) |
WIN55,212–2 | 1 | 4.4 | 100 | Kcnj9 (94 cM) | Mutant, gene expr. | (123) |
7 | 4.8 | 40 | Trpv1 (44 cM) | Position | (123) | |
Opioid hyperalgesia | ||||||
Chronic morphine | 5 | p = 0.000083* | 1 | Abcb1b (1 cM) | Pharm., mutant | (119) |
18 | p = 0.00037* | 34 | Adrb2 (34 cM) | Pharm., mutant | (194) |
LOD: logarithm of the odds.
Location of peak LOD score in centiMorgans (cM), a unit of genetic distance. Note that confidence intervals in QTL mapping projects are generally very large.
Gene expr.: strain-dependent expression of the candidate gene; Mutant: null mutation of the candidate gene shown to affect phenotype; Pharm.: strain-dependent effects of pharmacological manipulation of the candidate gene product; Position: inference based on genomic position of candidate gene; Receptor binding: demonstrated correlation of phenotype to strain-dependent density of candidate gene product; siRNA: rescue of strain difference using siRNA knockdown of candidate gene mRNA.
Study used haplotype mapping; p-values represent uncorrected correlation between phenotypic and haplotype block distributions of a set of inbred mouse strains.