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• W1572547065 abstract "Non-Technical Summary Regeneration of muscle nerves damaged by crush reconnects the peripheral limb of neural circuits that pass through the spinal cord, but the mechanisms underlying functional recovery remain uncertain. We examined the actions of natural muscle stretch that initiates muscle contraction, i.e. the stretch reflex, through a spinal circuit that aids in adjusting body movement and posture in response to destabilizing forces in the external environment. Stretch applied to muscles reinnervated by crushed nerves produced reflexive contraction that was more forceful than normal, despite yielding less than normal synaptic excitation to spinal motoneurons. Incomplete recovery of synaptic function by stretch-activated sensory neurons means that the enhanced stretch reflex contraction necessarily involves additional neural adaptations, possibly increased motoneuron excitability. These findings give further support to the importance of the central nervous system in restoring the ability of the regenerated neuromuscular system to respond to external disturbances of movement and posture. Abstract Sensorimotor functions are restored by peripheral nerve regeneration with greater success following injuries that crush rather than sever the nerve. Better recovery following nerve crush is commonly attributed to superior reconnection of regenerating axons with their original peripheral targets. The present study was designed to estimate the fraction of stretch reflex recovery attributable to functional recovery of regenerated spindle afferents. Recovery of the spindle afferent population was estimated from excitatory postsynaptic potentials evoked by muscle stretch (strEPSPs) in motoneurons. These events were measured in cats that were anaesthetized, so that recovery of spindle afferent function, including both muscle stretch encoding and monosynaptic transmission, could be separated from other factors that act centrally to influence muscle stretch-evoked excitation of motoneurons. Recovery of strEPSPs to 70% of normal specified the extent of overall functional recovery by the population spindle afferents that regained responsiveness to muscle stretch. In separate studies, we examined recovery of the stretch reflex in decerebrate cats, and found that it recovered to supranormal levels after nerve crush. The substantial disparity in recovery between strEPSPs and stretch reflex led us to conclude that factors in addition to recovery of spindle afferents make a large contribution in restoring the stretch reflex following nerve crush. Persistent deficits in sensory feedback contribute in limiting recovery of normal motor function following regeneration of a severed peripheral nerve (Brink & Mackel, 1987; Lundborg, 2000, 2004; Jaquet et al. 2001; Rosen & Lundborg, 2001; Duff, 2005). Despite good recovery of force generation (for review see Gordon et al. 2004), reinnervated muscle does not regain its stretch reflex (Cope et al. 1994; Huyghues-Despointes et al. 2003; Haftel et al. 2005; Maas et al. 2007). Even under favourable conditions in which the nerve to a single muscle is cut and allowed to regenerate over short distance with minimal delay to reinnervate its original muscle, the affected limb exhibits abnormal joint coordination more than 1 year after nerve transection (Abelew et al. 2000; Maas et al. 2007; Chang et al. 2009). Losses in joint coordination and the stretch reflex reflect losses in the effectiveness of proprioceptive feedback that are not fully understood and that are the subject of the present report. Recovery of the muscle stretch reflex clearly requires that regenerated spindle afferents regain their responsiveness to muscle stretch. After nerve section, the afferent signal for muscle stretch recovers, but only partially (Gregory et al. 1982; Banks & Barker, 1989; Lewin & McMahon, 1991; see for review Scott, 1996 and Zalena 1994), because some proprioceptors either fail to reconnect with receptors or are misrouted to the wrong receptor type (Collins et al. 1986; Munson et al. 1988; Banks & Barker, 1989). While it is possible for some spindle afferents to express mechanosensitivity without reconnecting to receptors (Johnson & Munson, 1991; Proske et al. 1995), the prevalence and long-term stability of this condition is unknown. If the degree of reconnection between sensory afferents and their cognate receptors determines the extent of functional recovery, then the stretch reflex should recover much better from nerve crush. Nerve crush, or axonotmesis, severs axons, but unlike nerve transection may not interrupt the endoneurial tubes that can physically guide regenerating axons back to their original targets (e.g. Sumner, 1990; Fournier & Strittmatter, 2002; Nguyen et al. 2002). Superior reconnection with spindle receptors probably explains better recovery of spindle afferent responsiveness to muscle stretch after nerve crush (Brown & Butler, 1976; Hyde & Scott, 1983; Barker et al. 1985, 1988) compared to cut (see above), and probably also to better recovery of the stretch reflex. Recovery of the stretch reflex may also depend on neural changes induced in the central nervous system by peripheral nerve injury (e.g. Valero-Cabre & Navarro, 2002; Haftel et al. 2005; Navarro, 2009; for review see Navarro, 2009). Postsynaptic integration of stretch-evoked synaptic input by polysynaptic pathways, e.g. presynaptic inhibition, and by properties intrinsic to motoneurons, e.g. voltage-sensitive conductances, can substantially amplify or suppress the stretch reflex (Heckman et al. 2005; Jankowska & Edgley, 2010). An effect of injury on these mechanisms has the capacity to influence stretch reflex recovery, and there is evidence that peripheral nerve injury alters the strength of segmental spinal circuits (see Navarro, 2009). Central mechanisms are recognized, therefore, for their potential importance to stretch reflex recovery, but their significance relative to peripheral mechanisms remains unknown. The question remains whether the recovery of afferent peripheral responsiveness, although necessary, is sufficient to provide the full explanation for stretch reflex recovery from nerve crush, i.e. is stretch reflex recovery fixed by the fraction of afferents that regain stretch responsiveness; to what extent is recovery boosted by additional mechanisms? The present study was designed to estimate the portion of stretch reflex recovery attributable to the fraction of spindle afferents that regain stretch responsiveness following nerve crush. The aggregate action of all spindle afferents responding to muscle stretch was measured from the strEPSPs they produced in motoneurons in normal cats versus cats studied approximately 1 year after nerve injury. Confounding contributions from other factors, e.g. transmission in polysynaptic pathways and ionic currents intrinsic to motoneurons (see above and Discussion), were reduced by measuring strEPSPs in cats that were anaesthetized. In separate studies, the full set of factors required to produce the stretch reflex were allowed expression by removing anaesthesia in acutely decerebrated cats. Comparison of the findings from these studies showed that afferent function reflected in strEPSPs recovered to only 70% of normal and fell far short of accounting for recovery of the stretch reflex in decerebrate cats that exceeded normal levels. These findings suggest that mechanisms in addition to recovery of spindle afferent function contribute significantly to reflex recovery, and our findings aid in constraining possible candidates which are considered in the Discussion. Studies were performed on nine cats as approved by the Laboratory Animal Care and Use Committees at Emory University and Wright State University. All were mixed-breed, adult females (weighing 2.5–3.5 kg). Six received nerve treatment in survival surgery, three served as untreated controls, and all were studied in terminal experiments after which they were killed by barbiturate overdose (150 mg kg−1). In six cats, the nerve supplying the medial gastrocnemius (MG) muscle in the left leg was crushed and allowed to regenerate in order to examine the capacity for select measures of sensorimotor function to recover. Nerve injury was produced using sterile surgical procedures in a dedicated surgical suite with the cat under deep anaesthesia induced and maintained by isoflurane inhalation (1.5–2.5% in 100% O2). Oxygen saturation, pulse rate, respiration rate and body temperature were monitored throughout the procedure, which was typically completed within ca. 1.5 h. The MG nerve in the popliteal fossa was exposed by skin incision (ca. 5 cm) and gently separated from surrounding tissues within 1 cm of its entry into the MG muscle. The MG nerve was crushed between the prongs of no. 5 microsurgical forceps with firm pressure applied for ca. 10 s, leaving the nerve intact but visibly compressed at the injury site. Following MG nerve crush, the incision was closed by suture and analgesics were administered before discontinuing anaesthesia. Cats were continuously monitored, kept warm until regaining sternal posture, and then returned to their housing and monitored for signs of discomfort or infection. All cats quickly recovered normal behaviour and activity in their open room housing. Within a few weeks, movements of the treated and untreated hind limbs were indistinguishable in casual visual inspection. Each cat received scheduled veterinary examination and daily care without any experimental study until their use in terminal experiments performed approximately 1 year post-operatively. All nine cats were studied in one of the two kinds of terminal experiments described below. Several features were common to both experiments. Cats were deeply anaesthetized (absent withdrawal and corneal reflexes) and fitted with monitors of vital signs, including blood pressure obtained through a left carotid cannula (mean 60–120 mmHg), rectal temperature (35–38°C), pulse rate (100–160 beats min−1) and blood O2 saturation (90–100% measured by a light-emitting clip placed on a front paw), and expired CO2 (3–4%) sampled from a tracheal cannula. Fluids (10 ml h−1 lactated Ringer solution and/or barbiturate anaesthetic as necessary) were delivered by cannula through the left external jugular vein. Delivery of anaesthetic, Ringer solution, radiant heat and/or artificial respiration used in some cases were adjusted to maintain vital signs within the physiological ranges indicated above. Anaesthesia level and vital signs were maintained from the beginning of terminal experiments through surgery and data collection up to 20 h later when cats were killed. In all experiments, the study focused on responses (either synaptic or muscle reflex) to controlled stretch applied to the MG muscle. With one or both hind limbs dissected to expose triceps surae muscles and nerves (see below), cats were secured in a rigid frame and the hind limb was clamped on the distal femur and tibia holding the knee and ankle joints at approximately 135 deg and 90 deg, respectively. The MG was detached from its insertion on the calcaneus and attached by rigid linkage to a force transducer in series with a length-servo motor. During data collection (described below), static muscle length was held near resting muscle length (Lo) measured by markers positioned in the limb and on the MG muscle before its detachment. The amount of passive force at Lo was approximately 100 g for all cats. Ramp–hold–release stretches of the MG muscle were used to study both synaptic and reflex responses (see below). Muscle length was ramped from Lo to 2–3 mm at constant velocity (30–40 mm s−1) over 100 ms, held for 300 ms, and then released back to Lo at constant velocity over 100 ms. These stretch parameters are within the normal physiological range of hind limb muscle length changes observed in walking cats (Goslow et al. 1973; Walmsley et al. 1978; Maas et al. 2007), and are similar to those used in earlier studies of physiological responses to natural muscle stretch (Westbury, 1972; Nichols, 1989). Stretches were repeated at 4 s intervals so as to minimize history-dependent effects (Nichols, 1989). To investigate the limits of recovery from nerve injury, all cats with nerve crush were studied more than 1 year post-operatively, as previous studies report nearly complete restoration of electrically evoked contraction of reinnervated cat muscles at this recovery time (Gordon & Stein, 1982; Foehring et al. 1986). Evidence of successful and selective self-reinnervation of the MG muscle was obtained in terminal experiments for all six cats following MG nerve crush. First, the reinnervated MG was observed to contract forcefully and exclusively to electrical stimulation of the MG nerve at a site rostral to surgical nerve injury. Second, the masses of MG muscles reinnervated after nerve crush were within 1% wet weight of their contralateral control MG muscles in all six cats, and an earlier report shows that cat MG muscles which recover weight following nerve crush also recover tetanic force (Rafuse & Gordon, 1996). Seven cats (4 with nerve crush, 3 untreated controls) were prepared for intracellular recording from MG motoneurons as follows. Deep anaesthesia was maintained by barbiturate (Nembutal, 40 mg kg−1 i.v.) in order to reduce excitation of motoneurons through either polysynaptic pathways or intrinsic currents and, thereby, to focus study on monosynaptic excitation from stretch-activated primary afferents onto motoneurons. In one of three control cats, anaesthesia was maintained by inhalation of isoflurane (1.5–2.5%) carried in equal parts of compressed room air and compressed O2 combined through an air mixer. Data collected from this cat were not significantly different from those collected in the two barbiturate-anaesthetized controls (see Results). Intracellular recording from MG motoneurons supplying the left hind limb proceeded as detailed in our earlier reports (Prather et al. 2001). Briefly, removal of the laminae of vertebrae L4–S1 exposed the dorsal spinal cord, permitting access to MG motoneurons by glass micropipettes (5–10 MΩ, 2 m potassium acetate) and to MG afferents recorded extracellularly by bipolar electrodes placed on dorsal roots L7 and S1. Motoneurons were positively identified as innervating the MG muscle when antidromic action potentials were generated by bipolar electrical stimulation of the MG nerve and were studied in detail when the intracellular action potentials exceeded 60 mV in amplitude. MG motoneurons were characterized by injecting depolarizing current pulses, which generated action potentials used to determine rheobase current (50 ms pulse duration, at threshold current strengths which produced action potentials in some, but not all, trials) and afterhyperpolarization (AHP) half-decay time (1 ms pulse duration, suprathreshold current strength typically 5× rheobase current), measured as the time taken for motoneuron potential to decay from the peak to half-amplitude of the AHP. The remaining recording time was devoted to measuring strEPSPs produced by MG motoneurons in response to repeated trials of MG muscle stretch applied through the servomotor as described above. Amplified and filtered records of motoneuron membrane potential (10×, DC –10 kHz), microelectrode current, dorsal root activity, muscle length and force were sampled (20 kHz) through separate A/D channels (Cambridge Electronic Design Power 1401) and stored on computer for later analysis using CED Spike 2 software. Events were averaged over replicate stimulus trials to improve the signal-to-noise ratio over multiple trials during which motoneuron resting membrane potential varied by no more than 4 mV. Voltages were measured from strEPSPs at the initial phase of stretch, at the end of the ramp or dynamic phase of stretch, and at the end of the hold or static phase of stretch (Fig. 1). At these points and throughout their entire duration, the strEPSPs closely resembled the waveform for rectified and integrated afferent activity evoked by MG muscle stretch (Fig. 1). The observed afferent activity profile matched that expected for group IA afferents in response to ramp–hold–release stretch (Matthews, 1972), including: (a) marked increase in firing rate near the onset or ‘initial’ phase of stretch, (b) increasing firing rate during the ‘dynamic’ rising phase of the ramp to its peak, (c) a sharp drop in firing rate after ramp peak, (d) sustained firing throughout the ‘static’ or hold phase of stretch, (e) cessation of firing during ramp release and rebound firing soon thereafter. These features suggest that in barbiturate-anaesthetized cats, the strEPSPs recorded in MG motoneurons were produced predominantly by monosynaptic excitation from spindle afferents. Stretching the MG muscle resulted in population-level activation of stretch-sensitive afferents and generation of an aggregate stretch-evoked excitatory post-synaptic potential (strEPSP) in MG motoneurons In an anaesthetized control animal, the intracellularly recorded strEPSP (top trace) averaged of 10 sequential trials of ramp–hold–release (middle trace) comprised distinct components in relation to the stretch stimulus (dashed vertical lines). The magnitude of the strEPSP was measured at specific points within each component (indicated by arrows and labels) The profile of the strEPSP closely resembled the profile of the rectified and filtered voltage recorded by bipolar electrodes positioned on the dorsal root (bottom trace, raw record in light trace superimposed by rectified and filtered record in dark line trace). Data were collected in cats anaesthetized by Nembutal. Measures of strEPSPs and motoneuron electrical properties were pooled within treatment groups (control or crush-regenerated), and treatment effects were tested statistically using nested ANOVA (individual experiments nested inside treatment groups). Tukey's honestly significant difference (HSD) post hoc test was used to test for the significance of comparisons of treatment effects (SYSTAT; Systat Software, Point Richmond, CA, USA). Data are reported as mean ± SEM unless indicated otherwise. In two cats with nerve crush, we directly determined whether reinnervated MG muscles recovered a stretch reflex, i.e. whether these muscles contracted in response to stretch. Methods employed are detailed in our earlier reports (Huyghues-Despointes et al. 2003). Briefly, cats were anaesthetized by inhalation of isoflurane (1.5–2.5%) carried in equal parts of compressed room air and compressed O2 combined through an air mixer. They were fitted with monitors for vital signs and prepared for study of the MG muscles in both hind limbs as described in the previous section, but no laminectomy was performed. Next, cats were decerebrated by removal of brain tissue rostral to mid-collicular transection in order to render them reflexive yet insensate when the gaseous anaesthesia was discontinued. The extent of stretch reflex recovery was assessed by bilateral comparisons within each individual cat of the reinnervated MG in the left hind limb and the normally innervated MG in the right hind limb. With right and left legs secured in fixed positions and the MG muscles attached through a force transducer to length-servo motors (described above; linear motors with encoder resolution 0.1 μm and maximum acceleration ca. 50 m s−2) to deliver ramp–hold–release stretches (amplitude 2 mm, ramp and release rate 40 mm s−1, hold duration 0.3 s) to the MG muscle at 4 s intervals. Stretches were applied before, during and after activation of the MG muscle in a crossed-extension reflex evoked by electrical stimulation (100 Hz) of the contralateral posterior tibial nerve (Fig. 2A). Stretch reflex measurements in decerebrate cats A, muscle force (top trace) was measured from MG muscles bilaterally during ramp–hold–release stretches (bottom trace). Background force was modulated using the crossed-extension reflex elicited by stimulating the contralateral posterior tibial nerve (dark bar middle trace). B, the force of the muscle stretch response during the dynamic component of the stretch (defined as in Fig. 1A) varied as a function of the background force. This plot shows the data taken from stretch responses in one trial of crossed-extension reflex in an MG muscle reinnervated after nerve crush (continuous line is best polynomial fit, dashed lines are 95% confidence interval; dotted vertical lines point to intersection with polynomial fit (open circles) where dynamic forces were identified at selected background forces (2, 3, 4 and 5 N). Records of MG muscle force obtained during muscle stretch were amplified (5×), filtered (DC to 1 kHz), digitized (sampling rate 1 kHz), and stored on computer for off-line analysis. Forces were measured at the maximum excursion of the ramp (dynamic force) and from the end of the hold phase of stretch (static force) corresponding to those same points measured from strEPSPs (see below). Force responses were then computed by subtracting the background force measured 50 ms prior to the ramp from the dynamic and static forces. Best polynomial fits (within 95% confidence limits) were obtained in plots of dynamic or static forces vs. background force (Fig. 2B; Huyghues-Despointes et al. 2003), and stretch forces were then measured from these polynomial functions for right and left MG muscles at selected background forces. In order to compare the extent of reflex action in the right and left MG muscles, force responses were plotted as a function of background force, and these relationships were compared between the two muscles (cf. Fig. 6). The stretch reflex increases with background force as progressively larger motor units are recruited (Matthews, 1986) and as intrinsic stiffness increases, so comparisons are only valid at matched background forces. Since the force responses consist of intrinsic and reflex components (Nichols & Houk, 1976; Huyghues-Despointes et al. 2003), it was also important to verify that the intrinsic mechanical properties of the muscles were not altered as a result of the recovery from nerve crush. We compared the intrinsic mechanical properties by measuring the force responses 10 ms after the beginning of ramp stretch, corresponding to initial or short-range stiffness (Fig. 6B). These responses were due solely to the intrinsic properties of the motor units active prior to stretch, since the stretch reflexes of triceps surae muscles have latencies of approximately 20 ms (Nichols & Houk, 1976). Since the muscles in this study were reflexive, it was not possible to measure the dynamic or static intrinsic response. In order to provide an estimate of the intrinsic components corresponding to the dynamic force responses, we used data obtained from MG muscles reinnervated following transection and repair of the muscle nerve (Huyghues-Despointes et al. 2003) (Fig. 6A). Although muscles reinnervated by cut nerves generated graded contraction in crossed-extension reflexes, their responses to stretch applied during these reflexes yielded force increments entirely attributable to intrinsic muscular stiffness as judged by comparison with responses obtained from muscles following dorsal rhizotomy (Huyghues-Despointes et al. 2003). Stretch reflexes recover to greater-than-normal levels following nerve crush In two acutely decerebrated cats, stretch forces generated during ramp–hold–release stretch (inset) were compared bilaterally for MG muscles that were untreated in the right leg (filled symbols) and reinnervated after nerve crush 1 year earlier in the left leg (open symbols). A, plot shows the dynamic component of the muscle force at the peak of ramp stretch vs. background muscle force immediately preceding stretch (cf. Fig. 2). The reflex component of dynamic force was that which exceeded the active intrinsic force estimated by the polynomial fit (dashed line) to data collected in an earlier study from a reinnervated MG muscle in cat (Huyghues-Despointes, 2003, see Methods). Dynamic reflex force was greater in reinnervated than in the contralateral untreated MG muscle at each of several background forces (vertical lines join bilateral forces measured from at 2, 3, 4, 5 and 6 N for each cat). B, plots of force responses from MG muscles in cats 1 and 2 obtained 10 ms following initiation of ramp stretch correspond to initial intrinsic (non-reflex) stiffness (see Methods). Data are expressed as force responses (y axis on left of plot) and as stiffness (force response divided by 0.4 mm stretch; y axis on right of plot). Initial stiffness was similar in both muscles in cat 2 and greater in the untreated muscle in cat 1. Therefore, differences in dynamic force between crush-reinnervated vs. normal muscles seen in A were due almost entirely to differences in the reflex component. The goal of experiments reported in this section of the paper was to determine what fraction of regenerated spindle afferents regained both responsiveness to muscle stretch and monosynaptic transmission onto motoneurons. These functions were measured from strEPSPs (see Fig. 1) recorded in cats that were anaesthetized in order to reduce confounding contributions from interneurons and motoneuron active conductances. Figure 3 shows that recovery of strEPSPs and their component responses was substantial but incomplete. The mean amplitudes of strEPSP components for each of four cats following nerve crush was smaller than for each of three control cats, with the exception of the static component in one cat. This tendency was expressed in comparisons of the pooled group means (Fig. 3D), which achieved statistical significance (nested ANOVA) for initial (P= 0.001) and dynamic (P= 0.03) components. The initial, dynamic and static components of strEPSPs following nerve crush (n= 39) recovered to, respectively, 68%, 68% and 72% of their corresponding values of control strEPSPs (n= 23). From these findings we suggest that roughly 70% of the spindle afferent population recovered function following nerve crush regeneration (see Discussion). strEPSPs recovered partially following crush, but failed to return to control values The tendency for incomplete strEPSP recovery was evident in the initial (A), dynamic (B) and static (C) components of the strEPSP (each column represents an experimental animal and numbers of strEPSPs sampled in each are shown in parentheses; all strEPSPs recorded in MG motoneurons in response to MG muscle stretch. D, summary of the three conditions shown in panels A–C further illustrates the changes in strEPSP magnitude in each component of the strEPSP (values are means ± SE; asterisks designate statistical significance (P < 0.03; nested ANOVA with Tukey post hoc test). Data were collected in cats anaesthetized by Nembutal. Figure 3 shows that on average, regenerated afferents sustained transmission throughout the duration of muscle stretch. That analysis, however, might have obscured incomplete recovery of the transmitted stretch signal resulting from the known failure of some spindle afferents to sustain firing during stretch (Brown & Butler, 1976; Hyde & Scott, 1983; Barker et al. 1988) or possible changes in the activity dependence of monosynaptic transmission (Mendell, 1988). These possibilities were tested by examining the relationships among strEPSP components. Figure 4 shows that initial, dynamic and static components of individual strEPSPs co-varied after crush regeneration as they did in untreated controls. There were no significant differences in slopes of the linear regressions (ANCOVA, P > 0.005) between initial vs. dynamic or static vs. dynamic components for the nerve crush group compared with the control group. Relationships among strEPSP components (initial, dynamic and static) were similar to normal after crush regeneration For all linear regressions (continuous and dashed lines) correlation coefficients (r) were significant (P < 0.05; Pearson correlation); slopes and elevations of regression lines were not significantly different between groups (P < 0.005, ANCOVA) for initial vs. dynamic components (A) or for static vs. dynamic (B). Data were collected in cats anaesthetized by Nembutal. Motoneurons sampled from control and nerve crush groups were characterized by properties that normally co-vary with monosynaptic EPSP size (Burke & Rymer, 1976; Zengel et al. 1985). Figure 5A shows nearly complete overlap in rheobase current and AHP half-decay time for motoneurons sampled from the two groups. Moreover, the normal tendency for these properties to vary inversely was evident after nerve crush. The motoneurons sampled from control and crush-regenerated groups were not significantly different, respectively, for either rheobase current (14.6 ± 1.7 and 16.5 ± 1.3 nA; ANOVA, P= 0.771) or AHP half-decay time (19.1 ± 1.6 and 18.1 ± 0.9 ms; P= 0.842). These observations suggest that motoneurons were similar in the two samples and that crushed motoneurons regained normal properties. Despite the similarity of motoneuron samples, Fig. 5B shows that strEPSPs in the crush group tended toward smaller values across the range of motoneuron rheobase current. These findings suggest that the decrease in strEPSP size was not explained by corresponding changes in postsynaptic properties. Motoneuron electrical properties returned to normal and were not associated with the decrease in strEPSPs after crush regeneration A, rheobase currents (Irh) and after-hyperpolarization (AHP) half-decay times co-varied and overlapped between normal and crush-regenerated samples of MG motoneurons. B, initial phase of strEPSPs declines with rheobase, and mean values in each 10 nA bin were smaller in crush" @default.
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• W1572547065 date "2011-10-14" @default.
• W1572547065 modified "2023-09-24" @default.
• W1572547065 title "Recovery of proprioceptive feedback from nerve crush" @default.
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• W1572547065 doi "https://doi.org/10.1113/jphysiol.2011.210518" @default.
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