SHORT REPORT Open Access
Mechanical sensitization of cutaneous sensory
fibers in the spared nerve injury mouse model
Amanda K Smith, Crystal L O’Hara and Cheryl L Stucky*
Background: The spared nerve injury (SNI) model of neuropathic pain produces robust and reproducible
behavioral mechanical hypersensitivity. Although this rodent model of neuropathic pain has been well established
and widely used, peripheral mechanisms underlying this phenotype remain incompletely understood. Here we
investigated the role of cutaneous sensory fibers in the maintenance of mechanical hyperalgesia in mice post-SNI.
Findings: SNI produced robust, long-lasting behavioral mechanical hypersensitivity compared to sham and naïve
controls beginning by post-operative day (POD) 1 and continuing through at least POD 180. We performed teased
fiber recordings on single cutaneous fibers from the spared sural nerve using ex vivo skin-nerve preparations.
Recordings were made between POD 16–42 after SNI or sham surgery. Aδ-mechanoreceptors (AM) and C fibers,
many of which are nociceptors, from SNI mice fired significantly more action potentials in response to suprathreshold
mechanical stimulation than did fibers from either sham or naïve control mice. However, there was no increase in
Conclusions: To our knowledge, this is the first study evaluating the contribution of primary afferent fibers in the
SNI model. These data suggest that enhanced suprathreshold firing in AM and C fibers may play a role in the
marked, persistent mechanical hypersensitivity observed in this model. These results may provide insight into
mechanisms underlying neuropathic pain in humans.
Keywords: Neuropathic, Nociceptor, Sensory neuron, C fiber, A fiber, Hyperalgesia, Mechanotransduction
Peripheral neuropathic pain results from complete or
partial lesion to peripheral nerves [1,2]. Occurring in many
neurological disorders, neuropathic pain affects 6-8% of
the population and is characterized by spontaneous and
stimulus-evoked pain . The mechanisms driving nerve
injury-induced hyperalgesia are not well understood making
treatments sub-optimal [1-4]. Several rodent models of
neuropathic pain have been developed including, chronic
constriction injury (CCI) , partial sciatic nerve injury ,
and spinal nerve ligation (SNL) . These models often in-
volve variability within cohorts [1,4] and present a challenge
in determining the role of injured versus non-injured, intact
sensory afferents in neuropathic pain because they involve
a high degree of co-mingling of intact and injured axons
distal to the lesion .
We used the spared nerve injury (SNI) model of neuro-
pathic pain which produces a pronounced, long-lasting
and reproducible behavioral phenotype characterized by
intense mechanical allodynia and hyperalgesia that mimics
many features of clinical neuropathic pain [1,3,9]. SNI
comprises complete transection of two of the three sciatic
nerve branches (tibial and common peroneal), leaving the
sural nerve intact . Furthermore, SNI involves minimal
co-mingling of intact and injured axons distal to the lesion
, thereby allowing investigators to specifically target
non-directly-injured nerve fibers. Although SNI is well
established, the peripheral mechanisms contributing to the
pain phenotype are not clear. While teased fiber recordings
have been used to investigate peripheral sensitization in
SNL in monkey and rat [10,11], and in CCI in rat [12,13],
to our knowledge, these experiments have not been per-
formed in the SNI model. Thus, the goal of this study was
to determine whether intact cutaneous afferent fibers from
the spared sural nerve are sensitized to mechanical stimuli
* Correspondence: firstname.lastname@example.org
Department of Cell Biology, Neurobiology, and Anatomy, Medical College of
Wisconsin, 8701 Watertown Plank Road, Milwaukee, WI, USA
© 2013 Smith et al.; licensee BioMed Central Ltd. This is an open access article distributed under the terms of the Creative
Commons Attribution License (http://creativecommons.org/licenses/by/2.0), which permits unrestricted use, distribution, and
reproduction in any medium, provided the original work is properly cited.
Smith et al. Molecular Pain 2013, 9:61
and thereby, may contribute to the maintenance of mech-
anical hypersensitivity after SNI.
SNI mice exhibit long-lasting behavioral mechanical
As previously reported, SNI mice exhibited pronounced
hypersensitivity to mechanical stimuli compared to sham
and naïve animals beginning by post-operative day (POD) 1
and continuing for at least 6 months post-surgery (Figure 1).
The dynamic component of the Light Touch Behavioral
Assay  was used as a control to ensure adequate
denervation of the tibial territory post-SNI injury. SNI
mice showed significant tibial desensitization, measured
by percent response to a puffed cotton swab applied to
the tibial territory of the glabrous skin, from POD 1–42
(Figure 1A, p < 0.005), which was expected because of
transection of the tibial nerve and subsequent denervation
of the skin territory. However, by POD 49, sensation in the
tibial area began to return (Figure 1A). In sural nerve-
targeted behavioral testing, SNI mice showed a significant
decrease in paw withdrawal threshold by POD 1 through
POD 180 (Figure 1B, p<0.005) and exhibited a signifi-
cantly higher percent response to the suprathreshold 3.31
mN monofilament from POD 1–49 (Figure 1C, p<0.005).
Locomotor activity of the mice did not differ between
groups (data not shown). Complete transection of the
tibial and common peroneal nerves was validated post-
mortem. Overall, these results parallel those found in rat
 and previously shown in mouse [3,9].
Aδ and C fibers from SNI mice exhibit enhanced
Sensory afferent sensitization is known to contribute
to mechanical hypersensitivity observed in diabetic and
chemotherapy-induced neuropathies [15,16], and has been
shown to contribute to hypersensitivity observed in other
models of nerve injury [10-12]. To assess the contribution
of cutaneous sensory afferents to SNI-induced mechanical
hypersensitivity, we performed ex vivo teased fiber record-
ings on the spared sural nerve. Fibers from SNI animals
exhibited enhanced suprathreshold firing compared to
controls. Specifically, Aδ-mechanoreceptor (AM) fibers
fired an average of 22% more action potentials across
all forces compared to sham or naïve mice, and C fibers
exhibited 24% more action potentials across all forces
compared to sham and 28% more than naïve mice (AM:
Figure 2A, p < 0.01; C: Figure 2C, p < 0.05). Post hoc
comparison showed no differences at individual forces for
either AM or C fibers (Figure 2). There were no differences
in mechanical thresholds or conduction velocity of any
fiber subtype across treatment groups (Table 1). There
was no difference in the percentage of Aβ, Aδ, and C
fibers encountered in preparations from the different
surgical groups (Figure 3A, p>0.05). There was also no
Figure 1 SNI mice exhibit prominent behavioral
hypersensitivity. A) In response to dynamic stroke of a puffed
cotton swab, SNI mice show significant desensitization of the tibial
territory beginning POD 1 and continuing through POD 42
compared to sham or naïve animals (***p<0.005). At POD 49 SNI
mice begin to regain sensation in the tibial territory, in that SNI mice
still showed some sensitization compared to naïve animals (*p<0.05)
but not sham animals (p>0.05). Treatments were compared across
time using a repeated measure 2-way ANOVA with Tukey’s post hoc
comparisons. B) SNI mice show a significant decrease in the 50%
mechanical withdrawal threshold beginning POD 1 and continuing
through POD 49 compared to sham or naïve mice (***p<0.005).
Furthermore, SNI mice continue to show a significant decrease in
mechanical withdrawal threshold at POD 90 compared to sham
(***p<0.005) and at POD 180 compared to sham (*p<0.05). Treatments
were compared across time using a 2-way ANOVA with Bonferroni
post hoc tests. SNI and sham treatments were compared at POD 90
and POD 180 using Mann–Whitney U tests. C) In response to
repeated stimulus with a 3.31 mN monofilament, SNI mice exhibit
prominent hypersensitivity beginning POD 1 and continuing
through at least POD 49 compared to sham or naïve animals
(***p<0.005). Treatments were compared across time using a 2
way-ANOVA with Bonferroni post hoc tests. Error bars for all three
graphs indicate S.E.M.
Smith et al. Molecular Pain 2013, 9:61
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difference in the proportion of slowly adapting (AM) and
rapidly adapting (D-hair) Aδ fibers (Figure 3B, p > 0.05).
There was an overall difference in the distribution of
Aβ fibers among SNI, sham and naïve mice (Figure 3C,
p < 0.05). There was a decrease in the distribution of
slowly adapting (SA) A-beta fibers from SNI animals
compared to sham (Figure 3C, p< 0.5), although no dif-
ference was observed between SNI and naive animals
(Figure 3C, p> 0.5). We also measured spontaneous ac-
tivity because spontaneous activity in primary afferent fi-
bers accompanies other nerve injury animal models
including SNL and CCI [10-13,17-19]. There was no dif-
ference in the percentage of AM or C fibers that exhib-
ited spontaneous activity in SNI versus sham or naïve
groups (Figure 4, p > 0.05). Furthermore, preliminary
analysis of Aβ fibers from SNI preparations also does
Figure 2 Aδ-Mechanoreceptor and C fibers in SNI mice exhibit enhanced mechanical firing. Using ex vivo skin nerve recordings, 10 sec mechanical
stimuli ranging 5-200mN were applied to the receptive field of each fiber using a 0.8 mm probe. All recordings were performed on the sural nerve and its
innervating territory. A) Aδ-Mechanoreceptor (AM) fibers fired an average 22% more action potentials per second across all forces compared to sham or to
naïve animals (**p<0.01). B) Examples of AM fiber action potentials evoked by sustained mechanical stimuli in naïve, sham and SNI treatment groups. C) C
fibers fired an average 24% more action potentials per second across all forces compared to sham and 28% more compared to naïve animals (*p<0.05). D)
Examples of C fiber action potentials evoked by sustained mechanical stimuli in naïve, sham and SNI treatment groups. Number of action potentials fired
per second was compared across all forces and treatment groups using a 2-way ANOVA with Bonferroni post hoc comparisons. Error bars indicate S.E.M.
Table 1 Summary of fiber properties in Naive, Sham and SNI mice
Fiber type Genotypen Median von
frey threshold (mN)
Naive24 6.826.82 13.884.30 0.41
Aδ-MechanoreceptorSham 25 6.82 5.41 11.705.330.62
SNI206.82 4.00 11.703.950.71
Naive5 0.66 0.661.15 4.80 0.86
D-hairSham7 0.660.27 0.664.93 0.80
SNI7 0.27 0.23 1.635.570.54
Naive11 6.826.82 11.700.66 0.10
C Sham 17 11.70 5.41 14.600.68 0.06
SNI136.82 4.0011.700.65 0.08
Naive7 1.630.664.0011.60 1.05
Sham 10 0.66 0.66 1.6313.991.38
SNI171.63 0.661.63 12.850.58
Naive8 1.631.63 3.4113.471.46
Sham 131.63.632.81 14.491.33
SNI111.630.66 4.00 14.761.15
Smith et al. Molecular Pain 2013, 9:61
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not suggest increased spontaneous firing, as has been
observed in SNL or CCI (data not shown). There was also
no difference in the frequency of spontaneous action
potential firing in SNI versus controls for any fiber type
(data not shown). In dividing groups into early and late
stages post SNI, there was no significant difference in
the spontaneous activity of fibers recorded at POD 16–
21 compared to those at POD 37–42 for Aβ, Aδ, or C fi-
bers (data not shown).
To our knowledge, this is the first study to assess
sensitization of primary afferent fibers in SNI. Our results
suggest that enhanced suprathreshold firing in AM and C
fibers may contribute to the robust behavioral mechanical
hypersensitivity that occurs in the SNI model of neuro-
pathic pain. Sensitized nociceptors might contribute to
SNI-induced behavioral hypersensitivity either directly
through increased suprathreshold firing in response to
external stimuli, or indirectly by driving central sensiti-
zation [10,11]. Previous nerve injury studies that used
the SNL and CCI models of nerve injury suggest that
Wallerian Degeneration of injured nerves drives sensiti-
zation of adjacent intact afferent fibers [10-12]. However,
unlike CCI and SNL, Wallerian Degeneration is not a
major factor in the SNI model of neuropathic pain as SNI
involves minimal co-mingling of intact and injured affer-
ent fibers . Therefore, a different mechanism(s) likely
drives the afferent mechanical sensitization observed
in this model. One potential mechanism is paracrine
signaling between injured and intact cell bodies within
the dorsal root ganglia (DRG), a level where co-mingling
Figure 3 Distribution of cutaneous fiber types in SNI mice. Since SNI mice fired significantly more action potentials per second across all
forces, we compared the percent distribution of each fiber type across treatment groups. A) There was not a significant difference in percent
fiber distribution in SNI mice compared to sham or naïve animals (p>0.05). B) SNI mice have a similar distribution of AM and DH fibers as sham
and naïve animals (p>0.05). C) There was an overall difference in the distribution of Aβ fibers among SNI, sham and naïve mice (*p<0.05). There
was a decrease in the proportion of slowly adapting (SA) Abeta fibers in SNI mice compared to sham (*p<0.5), although no difference was
observed between SNI and naive animals (p>0.5). Distribution data was analyzed using a Chi-square analysis and Fisher’s exact post hoc tests.
Figure 4 Spontaneous activity is similar in AM and C fibers from naïve, sham, and SNI mice. SNI mice did not differ from sham or naïve
mice in that the percent of non-evoked spontaneous discharges was similar across treatment groups in either AM or C fibers (p>0.05). Data was
analyzed using Chi-square analysis.
Smith et al. Molecular Pain 2013, 9:61
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occurs. A previous study has shown an increase in macro-
phage infiltration, expression of inflammatory mediators
such as IL-6 and TNF-α, and expression of neurotrophins
BDNF and NGF in the DRG after sciatic nerve injury ,
and these may be key factors driving afferent sensitization
in the SNI model . Alternatively or in addition, at the
peripheral terminals, collateral sprouting of intact sensory
afferent terminals into the denervated skin territory of the
transected nerves has been shown in other neuropathic
pain models [21,22], and may also occur and contribute to
sensitization in SNI.
It has been shown that degeneration of injured fibers
induces spontaneous activity in nearby uninjured primary
afferent fibers . Furthermore, previous studies have
shown that increased spontaneous activity in A and C fibers
can contribute to sensitization after nerve injury in other
models of neuropathic pain [10-13,17-19]. However, we
did not observe more spontaneous activity in either A or
C fibers post-SNI. One explanation for the absence of
spontaneous activity may be that ectopic discharge rates
change over time after injury. Previous studies on injured
primary afferent fibers show that there is a higher frequency
of spontaneous activity early after nerve injury (POD 1–3)
and less activity in late stages (POD 11–14) [17,18].
Furthermore, studies on uninjured afferents, which show
spontaneous activity, have been performed primarily at
early stages after nerve injury [13,23]. Thus, our recordings
at later stages (POD 16–42) after injury may have occurred
after SNI-induced spontaneous activity subsided. Another
likely explanation is that spontaneous activity may not be
present in the SNI model due to minimal co-mingling of
injured and adjacent fibers. Previous reports of spontan-
eous activity after nerve injury have been recorded from
nerve injury models that involve considerable Wallerian
Degeneration and extensive co-mingling of intact and
injured axons [10-12]. Sensitizing compounds associated
with Wallerian Degeneration, such as TNF-α, have been
shown to sensitize primary afferent fibers . However,
in the absence of co-mingling of intact and injured axons
distal to the site of lesion, and the minimal degeneration
of injured fibers proximal to the lesion, these compounds
may not affect the intact peripheral afferent fibers in the
These results may provide insight into the mechanisms
underlying neuropathic pain in humans with traumatic
peripheral nerve injury. Our results show an increase in
suprathreshold firing in Aδ-mechanoreceptor (AM) and
C fibers, suggesting that enhanced primary afferent drive
may contribute to nerve injury-induced hypersensitivity,
and peripheral afferent fibers may be targets for pharma-
cological treatment of neuropathic pain.
Materials and methods
Male C57BL/6 mice (Jackson Labs), 8 weeks at time of
injury, were used for all behavioral and teased fiber skin
nerve experiments. Animals were housed individually
after surgery and handled equally during all experiments.
All experimental protocols were approved by the Medical
College of Wisconsin’s Institutional Animal Care and Use
SNI surgery was performed as previously described .
Briefly, under ketamine-induced anesthesia, animals under-
went surgery to ligate and transect the left tibial and com-
mon peroneal nerves, and 2-4 mm of nerve distal to the
ligation was removed to prevent regeneration. Care was
taken to avoid damage to the sural nerve. Sham animals
underwent anesthesia and skin and muscle incisions
identical to the SNI animals, without ligation or axotomy
of the tibial and peroneal nerves. Naïve animals received
no surgical treatment or anesthetic. Although we attempted
to blind the experimenter to surgery type, it was possible
to distinguish which animals had undergone SNI, sham or
Behavioral sensitivity to dynamic light touch was assessed
on the tibial skin territory of the left paw as previously
reported . Mechanical threshold and sensitivity to
suprathreshold mechanical force were assessed on the
sural territory of the left hind paw as previously reported
. The animals were tested twice before surgery and on
post-operative-days (POD) 1, 2, 4, 7, 14, 21, 28, 35, 42, 49,
90, and 180.
Teased fiber skin-nerve recordings
Teased fiber recordings were used to determine the mech-
anical response properties of cutaneous primary afferent
fibers in skin nerve preparations from SNI, sham and
naïve mice as previously described . Briefly, the sural
nerve and innervated skin of the left hindlimb were
dissected and placed corium side up in a recording bath
superfused with oxygenated synthetic interstitial fluid at
32±0.5°C. The nerve was desheathed and fascicles were
teased apart until single, functionally distinct fibers, could
be distinguished. Fibers were characterized by mechanical
threshold and conduction velocity. Units with conduction
velocities over 10 m/s were classified as Aβ, and Aδ for
units with conduction velocities between 1.2 m/s and
10 m/s. C fibers were classified as units that had con-
duction velocities less than 1.2 m/s. Units were further
sub-classified as slowly adapting (SA) or rapidly adapting
(RA) based on the rate of adaptation to mechanical force.
Following characterization, fibers were recorded for 2 min
Smith et al. Molecular Pain 2013, 9:61
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to assess spontaneous activity. Next a feedback-controlled
mechanical stimulator was used to deliver increasing
sustained mechanical forces (5-200 mN) for 10 sec each
with 1 min recovery period between stimuli. Action
potentials were recorded and analyzed using Lab Chart
Data Acquisition Software (AD Instruments, Colorado
All data sets were compared between SNI, sham, and
naïve groups. Behavioral Data: Percent response to light
touch was analyzed across time using repeated measures
two-way ANOVA with Tukey’s post hoc test. Mechanical
withdrawal thresholds and the percent response to a 3.31
mN monofilament were compared across time (Baseline 1
through POD 49) using a 2-way ANOVA with Bonferroni
post hoc analysis. Withdrawal thresholds for SNI and sham
were compared POD 90 and POD 180 with Mann Whitney
U tests. Skin-Nerve Data: Each fiber type was analyzed
for: 1) number of action potentials fired across mechanical
forces using a two-way ANOVA with Bonferroni post hoc
comparisons, 2) conduction velocity using a one-way
ANOVA with Tukey’s multiple comparisons, 3) von Frey
thresholds using Kruskal-Wallis with Dunn’s multiple
comparisons, and 4) percent spontaneous fibers using
Chi-square analysis. Column statistics of each fiber type
were analyzed to compare the sum of the average number
of action potentials fired across all forces. Percent
distribution of the fiber types was compared using
Chi-square analysis and Fisher’s exact post hoc tests.
Data analysis was completed using Prism 6 Software
(GraphPad, La Jolla, CA).
SNI: Spared nerve injury; CCI: Chronic constriction injury; SNL: Spinal nerve
ligation; POD: Post, operative day; AM: Aδ-Mechanoreceptor; DRG: Dorsal
The authors declare that they have no competing interests.
All authors read and approved the final manuscript. AS and CO conducted
the experiments and analyzed the data. AS and CS designed the study and
wrote the manuscript.
This work was completed with support from the National Institute of Health
grants NS040538 and NS070711 to C.L.S.
Received: 29 July 2013 Accepted: 22 November 2013
Published: 29 November 2013
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Cite this article as: Smith et al.: Mechanical sensitization of cutaneous
sensory fibers in the spared nerve injury mouse model. Molecular Pain
Smith et al. Molecular Pain 2013, 9:61
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