3.6 Neuropathic pain: Absence of MOPs in primary sensory neurons
results in enhanced, bilateral, mechanical hypersensitivity after nerve
injury
We investigated whether the absence of peripheral MOPs affects the
development of SNIt-induced mechanical allodynia. Before
nerve injury, PWFs of left and right hind paws were similar and did not
differ significantly between genotypes. At 2 days after nerve injury,
ipsilateral PWF in response to high force mechanical stimuli had
increased significantly in WT mice from 38 ± 3.27% to 74 ± 5.62% and
in Oprm1 cKO mice from 32 ± 4.16% to 66 ± 5.62% (Figure
7) . This nerve-injury induced increase in PWF was also observed in
response to low force mechanical stimuli and persisted for up to 17 days
post-injury. In the Oprm1 cKO group, withdrawal frequencies in
the contralateral paw also increased significantly from pre-injury
baseline values. This effect peaked 5 days post-injury, with PWF in
response to high force mechanical stimuli increasing significantly from
29 ± 2.77% at baseline to 56 ± 3.06%. Notably, on day 5, allodynia to
high force mechanical stimuli contralateral to nerve injury inOprm1 cKO mice was as severe as that in the ipsilateral paw of WT
mice. The WT group did not exhibit an injury-induced increase in
contralateral PWF to mechanical stimuli. Tests with Oprm1 cKO
sham-operated mice confirmed that the peripheral MOP-mediated bilateral
mechanical allodynia was induced by nerve injury (Supplemental
Figure 2A ).
Deletion of MOPs in primary sensory neurons did not impair gross motor
function after nerve injury. Post-SNIt rotarod activity
did not differ between genotypes, and, when compared to their naïve
counterparts, neither genotype showed significant differences in the
open field test after nerve injury (Supplemental Figure 2B, C) .
No significant differences were observed in the body weight of
nerve-injured animals (not shown), and no sex-dependent differences were
noted in their behavioral and motor activity (not shown).