Superficial Peroneal Nerve Stimulation Research Articles

Erosion of Stumble Correction Evoked with Superficial Peroneal Nerve Stimulation in Older Adults during Walking.

In healthy young adults, electrical stimulation of the superficial peroneal cutaneous nerve (SPn) innervating the dorsum of the foot has been shown to elicit functionally relevant reflexes during walking that are similar to those evoked by mechanical perturbation to the dorsum of the foot during walking and are referred to as stumble corrective (obstacle avoidance) responses. Though age-related differences in reflexes induced by mechanical perturbation have been studied, toe clearance has not been measured. Further, age-related differences in reflexes evoked by electrical stimulation of SPn have yet to be determined. Thus, the purpose of this study was to characterize age-related differences between healthy young adults and older adults with no history of falls in stumble correction responses evoked by electrical stimulation of the SPn at the ankle during walking. Toe clearance relative to the walking surface along with joint displacement and angular velocity at the ankle and knee and EMG of the tibialis anterior, medial gastrocnemius, biceps femoris and vastus lateralis were measured. The combined background and reflex toe clearance was reduced in the older adults compared with the young in mid-early swing (p = 0.011). These age-related differences likely increase fall risk in the older adult cohort. Further, age-related changes were seen in joint kinematics and EMG in older adults compared with the young such as decreased amplitude of the plantarflexion reflex in early swing in older adults (p < 0.05). These altered reflexes reflect the degradation of the stumble corrective response in older adults.

Superficial peroneal neuromodulation of nonobstructive urinary retention induced by prolonged pudendal afferent activity in cats.

The purpose of this study is to determine whether superficial peroneal nerve stimulation (SPNS) can improve nonobstructive urinary retention (NOUR) induced by prolonged pudendal nerve stimulation (PNS). In this exploratory acute study using eight cats under anesthesia, PNS and SPNS were applied by nerve cuff electrodes. Skin surface electrodes were also used for SPNS. A double lumen catheter was inserted via the bladder dome for bladder infusion and pressure measurement and to allow voiding without a physical urethral outlet obstruction. The voided and postvoid residual (PVR) volumes were also recorded. NOUR induced by repetitive (4-13 times) application of 30-min PNS significantly (P < 0.05) reduced voiding efficiency by 49.5 ± 16.8% of control (78.3 ± 7.9%), with a large PVR volume at 208.2 ± 82.6% of control bladder capacity. SPNS (1 Hz, 0.2 ms) at 1.5-2 times threshold intensity (T) for inducing posterior thigh muscle contractions was applied either continuously (SPNSc) or intermittently (SPNSi) during cystometrograms to improve the PNS-induced NOUR. SPNSc and SPNSi applied by nerve cuff electrodes significantly (P < 0.05) increased voiding efficiency to 74.5 ± 18.9% and 67.0 ± 15.3%, respectively, and reduced PVR volume to 54.5 ± 39.0% and 88.3 ± 56.0%, respectively. SPNSc and SPNSi applied noninvasively by skin surface electrodes also improved NOUR similar to the stimulation applied by a cuff electrode. This study indicates that abnormal pudendal afferent activity could be a pathophysiological cause for the NOUR occurring in Fowler's syndrome and a noninvasive superficial peroneal neuromodulation therapy might be developed to treat NOUR in patients with Fowler's syndrome.

Superficial peroneal neuromodulation of persistent bladder underactivity induced by prolonged pudendal afferent nerve stimulation in cats.

The purpose of this study is to determine whether superficial peroneal nerve stimulation (SPNS) can reverse persistent bladder underactivity induced by prolonged pudendal nerve stimulation (PNS). In 16 α-chloralose-anesthetized cats, PNS and SPNS were applied by nerve cuff electrodes. Skin surface electrodes were also used for SPNS. Bladder underactivity consisting of a significant increase in bladder capacity to 157.8 ± 10.9% of control and a significant reduction in bladder contraction amplitude to 56.0 ± 5.0% of control was induced by repetitive (4-16 times) application of 30-min PNS. SPNS (1 Hz, 0.2 ms) at 1.5-2 times threshold intensity (T) for inducing posterior thigh muscle contractions was applied either continuously (SPNSc) or intermittently (SPNSi) during a cystometrogram (CMG) to determine whether the stimulation can reverse the PNS-induced bladder underactivity. SPNSc or SPNSi applied by nerve cuff electrodes during the prolonged PNS inhibition significantly reduced bladder capacity to 124.4 ± 10.7% and 132.4 ± 14.2% of control, respectively, and increased contraction amplitude to 85.3 ± 6.2% and 75.8 ± 4.7%, respectively. Transcutaneous SPNSc and SPNSi also significantly reduced bladder capacity and increased contraction amplitude. Additional PNS applied during the bladder underactivity further increased bladder capacity, whereas SPNSc applied simultaneously with the PNS reversed the increase in bladder capacity. This study indicates that a noninvasive superficial peroneal neuromodulation therapy might be developed to treat bladder underactivity caused by abnormal pudendal nerve somatic afferent activation that is hypothesized to occur in patients with Fowler's syndrome.

Superficial peroneal neuromodulation of nonobstructive urinary retention in cats

To determine if superficial peroneal nerve stimulation (SPNS) can improve nonobstructive urinary retention (NOUR). In α-chloralose anesthetized cats, NOUR was induced by repetitive application (4-16 times) of 30-minute tibial nerve stimulation (TNS: 5 Hz frequency, 0.2 ms pulse width) at 4 to 6 times threshold intensity (T) for inducing toe twitches. SPNS (1 Hz, 0.2 ms) at 2 to 4 times threshold intensity (T) for inducing posterior thigh muscle contractions was applied either continuously (SPNSc) during a cystometrogram (CMG) or during voiding (SPNSv) by a surgically implanted cuff electrode or by skin surface electrodes to determine if the stimulation reduced NOUR induced by prolonged TNS. During control CMGs, efficient (86.4% ± 5.5%) voiding occurred with a postvoid residual (PVR) volume equal to 14.9% ± 6.2% of control bladder capacity. NOUR elicited by prolonged TNS significantly (P < .05) increased bladder capacity to 168.6% ± 15.5% of control, reduced voiding efficiency to 30.4% ± 4.8%, and increased PVR to 109% ± 9.2% of control. Using the implanted cuff electrode, SPNSc and SPNSv significantly (P < .05) increased voiding efficiency to 66.7% ± 7.4% and 65.0% ± 5.9%, respectively, and reduced PVR to 52.2% ± 11.4% and 64.3% ± 11.6%, respectively. SPNSc but not SPNSv significantly (P < .05) reduced bladder capacity to 133.4% ± 15% of control. Transcutaneous SPNSv but not SPNSc also significantly (P < .05) reversed the TNS-induced NOUR responses. This study shows that SPNS is effective in reversing NOUR induced by prolonged TNS. Transcutaneous SPNS provides the opportunity to develop a noninvasive neuromodulation therapy for NOUR to treat more patients than current sacral neuromodulation therapy.

An excitatory reflex from the superficial peroneal nerve to the bladder in cats.

This study in α-chloralose-anesthetized cats discovered an excitatory peroneal nerve-to-bladder reflex. A urethral catheter was used to infuse the bladder with saline and record bladder pressure changes. Electrical stimulation was applied to the superficial peroneal nerve to trigger reflex bladder activity. With the bladder distended at a volume ~90% of bladder capacity, superficial peroneal nerve stimulation (PNS) at 1-3 Hz and threshold (T) intensity for inducing muscle twitching on the posterior thigh induced large-amplitude (40-150 cmH2O) bladder contractions. PNS (1-3 Hz, 1-2T) applied during cystometrograms (CMGs) when the bladder was slowly (1-3 ml/min) infused with saline significantly (P < 0.01) reduced bladder capacity to ~80% of the control capacity and significantly (P < 0.05) enhanced reflex bladder contractions. To determine the impact of PNS on tibial nerve stimulation (TNS)-induced changes in bladder function, PNS was delivered following TNS. TNS of 30-min duration produced long-lasting poststimulation inhibition and significantly (P < 0.01) increased bladder capacity to 140.5 ± 7.6% of the control capacity. During the post-TNS inhibition period, PNS (1-3 Hz, 1-4T) applied during CMGs completely restored bladder capacity to the control level and significantly (P < 0.05) increased the duration of reflex bladder contractions to ~200% of control. The excitatory peroneal nerve-to-bladder reflex could also be activated by transcutaneous PNS using skin surface electrodes attached to the dorsal surface of the foot. These results raise the possibility of developing novel neuromodulation therapies to treat underactive bladder and nonobstructive urinary retention.

Interlimb Reflexes Induced by Electrical Stimulation of Cutaneous Nerves after Spinal Cord Injury.

Whether interlimb reflexes emerge only after a severe insult to the human spinal cord is controversial. Here the aim was to examine interlimb reflexes at rest in participants with chronic (>1 year) spinal cord injury (SCI, n = 17) and able-bodied control participants (n = 5). Cutaneous reflexes were evoked by delivering up to 30 trains of stimuli to either the superficial peroneal nerve on the dorsum of the foot or the radial nerve at the wrist (5 pulses, 300 Hz, approximately every 30 s). Participants were instructed to relax the test muscles prior to the delivery of the stimuli. Electromyographic activity was recorded bilaterally in proximal and distal arm and leg muscles. Superficial peroneal nerve stimulation evoked interlimb reflexes in ipsilateral and contralateral arm and contralateral leg muscles of SCI and control participants. Radial nerve stimulation evoked interlimb reflexes in the ipsilateral leg and contralateral arm muscles of control and SCI participants but only contralateral leg muscles of control participants. Interlimb reflexes evoked by superficial peroneal nerve stimulation were longer in latency and duration, and larger in magnitude in SCI participants. Interlimb reflex properties were similar for both SCI and control groups for radial nerve stimulation. Ascending interlimb reflexes tended to occur with a higher incidence in participants with SCI, while descending interlimb reflexes occurred with a higher incidence in able-bodied participants. However, the overall incidence of interlimb reflexes in SCI and neurologically intact participants was similar which suggests that the neural circuitry underlying these reflexes does not necessarily develop after central nervous system injury.

Stimulus Point Distribution in Deep or Superficial Peroneal Nerve for Treatment of Ankle Spasticity

To develop effective electrical stimulation treatment to reduce spasticity, we examined the optimal stimulus point of the common peroneal nerve. The locations of selective stimulus points for the deep peroneal nerve or superficial peroneal nerve fiber were examined in 25 healthy subjects in both legs (50 legs) using the ratio of the tibialis anterior (TA) to the peroneus longus (PL) M-wave amplitude (TA/PL ratio). In addition, we measured reciprocal Ia inhibition in ten healthy subjects. The amount of inhibition was determined from short-latency suppression of the soleus (Sol) H-reflex by conditioning stimuli to the deep or superficial peroneal nerve. The paired t-test was used for statistical analysis. The mean TA/PL ratio during deep peroneal nerve stimulation was significantly different from superficial peroneal nerve stimulation (p < 0.001). The mean stimulus point for the deep peroneal nerve was located 7 ± 5 mm distal and 3 ± 6 mm anterior from the distal edges of the head of fibula and was markedly different from the stimulus point for the superficial peroneal nerve (20 ± 7 mm distal and 12 ± 8 mm posterior). During deep peroneal nerve stimulation, the mean conditioned H-reflex was depressed to 83.8 ± 10.7% of the unconditioned value of the H-reflex. In contrast, during superficial peroneal nerve stimulation, the mean conditioned H-reflex increased to 105.3 ± 5.2%. These values were significantly different (p < 0.001). In the present study, we revealed a stimulus area of the deep peroneal nerve. Also, we observed the inhibitory effects of stimulation upon the deep peroneal nerve at individual stimulus point. Our results appear to indicate that localized stimulation of the deep peroneal nerve is more useful for the reduction of ankle spasticity.

Load‐related modulation of cutaneous reflexes in the tibialis anterior muscle during passive walking in humans

Although cutaneous reflexes are known to be strongly modulated in a phase-dependent manner during walking in both human and cat, it is not clear whether the movement-related or the load-sensitive afferent feedback plays a more important role in regulating this modulation. To address this issue in humans, we investigated modulation of the cutaneous reflex in the tibialis anterior muscles (TA) of 17 subjects during passive walking with a load (0%, 33%, 66% unloading of body weight) and without a load (100% unloading). These walking tasks were performed passively with a robotic gait trainer system. Cutaneous reflexes in TA, elicited by electrical stimulation to the distal tibial (Tib) and superficial peroneal (SP) nerves, were recorded during 10 different phases of the walking cycle, and the middle latency responses (MLR, 70-120 ms) were analysed. During loaded walking, the magnitudes of the MLR induced by Tib nerve stimulation were strongly increased during the late stance-to-early swing phase irrespective of the amount of load (phase modulation), a phenomenon that also occurred without background electromyogram in the TA. Predominant suppression of the MLR following SP nerve stimulation at the early stance phase changed to facilitation at the late stance. By contrast, the MLR following either Tib or SP nerve stimulation was not at all modulated by the stepping phase during both unloaded walking (100% unloading) and standing. These results suggest that phasic changes in the load-related afferent information in concert with rhythmic lower limb movement play a key role in modulating cutaneous reflexes during walking.

Modulations of interlimb and intralimb cutaneous reflexes during simultaneous arm and leg cycling in humans

Objective We investigated to what extent intralimb and interlimb cutaneous reflexes are altered while simultaneously performing arm and leg cycling (AL cycling) under different kinematic and postural conditions. Methods Eleven subjects performed AL cycling under conditions in which the arm and leg crank ipsilateral to the stimulation side were moved synchronously (in-phase cycling) or asynchronously (anti-phase cycling) while sitting or standing. Cutaneous reflexes following superficial radial or superficial peroneal nerve stimulation (2.0–2.5 times radiating threshold, 5 pulses at 333 Hz) were recorded at 4 different pedal positions from 12 muscles in the upper and lower limbs. Cutaneous reflexes with a peak latency of 80–120 ms were then analyzed. Results The magnitude of interlimb and intralimb cutaneous reflexes in the arm and leg muscles was significantly modulated depending on the crank position for the relevant limb (phase-dependent modulation). A significant correlation between the magnitude of the cutaneous reflex and background EMG was observed in the majority of muscles during static contraction, but not during AL cycling (task-dependent modulation). No significant difference was found in comparisons of the magnitude of intralimb and interlimb cutaneous reflexes obtained during in- and anti-phase AL cycling. Qualitatively, the same results were obtained during AL cycling while sitting or standing. In addition, the modulation of cutaneous reflexes in arm muscles was identical among in-phase, anti-phase and isolated arm cycling. Results were the same for leg muscles. Conclusions Cutaneous reflexes in arm muscles are little influenced by rhythmic movement of the legs and vice versa during AL cycling. It is likely that neural components that control interlimb reflexes are loosely coupled during AL cycling while sitting or standing. Significance Our results provide a better understanding of the coordination between the upper and lower limbs during rhythmic movement.

Topography of spinal neurons active during hindlimb withdrawal reflexes in the decerebrate cat

There exists a spatial organization of receptive fields and a modular organization of the flexion withdrawal reflex system. However, the three dimensional location and organization of interneurons interposed in flexion reflex pathways has not been systematically examined. We determined the anatomical locations of spinal neurons involved in the hindlimb flexion withdrawal reflex using expression of the immediate early gene c-fos and the corresponding FOS protein. The flexion withdrawal reflex was evoked in decerebrate cats via stimulation of the tibial or superficial peroneal nerve.Animals that received stimulation had significantly larger numbers of cells expressing FOS-like immunoreactivity (42.7±2.3 cells/section, mean±standard error of the mean) than operated unstimulated controls (18.6±1.4 cells/section). Compared with controls, cells expressing FOS-like immunoreactivity were located predominantly on the ipsilateral side, in laminae IV–VI, at L6 and rostral L7 segments, and between 20% and 60% of the distance from the midline to the lateral border of the ventral gray matter. Labeled neurons resulting from tibial nerve stimulation were medial to neurons labeled following superficial peroneal nerve stimulation in laminae I–VI, but not VII. The mean mediolateral positions of labeled neurons from both nerves shifted medially as the transverse plane in which they were viewed was moved from rostral to caudal and as the coronal plane in which they were viewed was moved from dorsal to ventral. The mediolateral separation between populations of labeled cells was consistent with primary afferent projections and the location of reflex encoders. This topographical segregation corresponding to different afferent inputs is a possible anatomical substrate for a modular organization of the flexion withdrawal reflex system.

Electrical stimulation of the human common peroneal nerve elicits lasting facilitation of cortical motor-evoked potentials.

Motor-evoked potentials (MEP) in the tibialis anterior (TA) muscle were shown to be facilitated by repetitive electrical stimulation of the common peroneal (CP) nerve at intensities above motor threshold. The TA electromyogram (EMG) and ankle flexion force were recorded in response to transcranial magnetic stimulation (TMS) of the leg area of the motor cortex to evaluate the excitability of cortico-spinal-muscular pathways. Repetitive stimulation of the CP nerve at 25 Hz for 30 min increased the MEP by 50.3 +/- 13.6% (mean +/- S.E.) at a TMS intensity that initially gave a half-maximum MEP (MEPh). In contrast the maximum MEP (MEPmax) did not change. Ankle flexion force (103 +/- 21.9%) and silent period duration (75.3 +/- 12.9%) also increased. These results suggest an increase in corticospinal excitability, rather than total connectivity due to repetitive CP stimulation. Facilitation was evident after as little as 10 min of stimulation and persisted without significant decrement for at least 30 min after stimulation. The long duration of silent period following CP stimulation (99.2 +/- 14.8 ms) suggests that this form of stimulation may have effects on the motor cortex. To exclude the possibility that MEPh facilitation was primarily due to sensory fibre activation, we performed several control experiments. Preferentially activating Ia muscle afferents by vibration in the absence of motor activity had no significant effect. Cutaneous afferent activation via stimulation of the superficial peroneal nerve increased the amplitude of responses at MEPmax rather than MEPh. Concurrent tendon vibration and superficial peroneal nerve stimulation failed to facilitate TA MEP responses. In summary, repetitive electrical stimulation of the CP nerve elicits lasting changes in corticospinal excitability, possibly as a result of co-activating motor and sensory fibres.

Neurology (63)

Effect of electrical stimulation of peripheral nerves on neuropathic pain. (Inabe Orthopedic Clinic, Inabe, Japan) Spine 2000;25:1886–1892.Responses of wide dynamic range neurons in the lumbosacral dorsal horn to input from C fibers were studied in urethane chloralose‐anesthetized cats. The posterior tibial nerve and sciatic nerve were stimulated simultaneously to examine the effect on the C fiber responses elicited by superficial peroneal nerve stimulation. Simultaneous stimulation of the posterior tibial nerve and sciatic nerve was performed with superficial peroneal nerve C fiber stimulation. This study demonstrated that electrical stimulation of peripheral nerves leads to inhibitory input to the pain pathways at the spinal cord level.

Cutaneous reflexes during human gait: electromyographic and kinematic responses to electrical stimulation.

The functions of ipsilateral cutaneous reflexes were studied with short trains of stimuli presented pseudorandomly to the superficial peroneal (SP) and tibial nerves during human gait. Electromyograms (EMGs) of tibialis anterior (TA), soleus, lateral and medial gastrocnemius, vastus lateralis (VL), and biceps femoris (BF) muscle were recorded, together with ankle and knee joint angles. Net reflex EMG responses were quantified in each of the 16 parts of the step cycle according to a recently developed technique. After SP nerve stimulation, TA muscle showed a significant suppression during swing phase that was highly correlated to ankle plantarflexion. BF and VL muscles were both excited throughout swing and significantly correlated to knee flexion during early swing. Tibial nerve stimulation caused dorsiflexion during late stance, but plantarflexion during late swing. We argue that SP nerve reflexes are indicative of a stumbling corrective response to nonnoxious electrical stimulation in humans. The correlated kinematic responses after tibial nerve stimulation may allow smooth movement of the swing leg so as to prevent tripping during swing and to assist placing and weight acceptance at the beginning of stance.

Retention of a backward classically conditioned reflex response in spinal cat.

Retention of a backward classically conditioned reflex response was investigated in the spinal cat preparation. Facilitation of the flexion reflex was induced by the pairing of superficial peroneal nerve stimulation (30 Hz, 0.5 s), the US (unconditioned stimulus), with saphenous nerve stimulation (10 Hz, 1.5 s), the CS (conditioned stimulus). Both the US and CS were supramaximal for activation of A delta cutaneous afferent fibers. Experimental animals received 30 paired trials (US preceded CS by 0.25 s) with an intertrial interval (ITI) of three min. Control animals received the same stimuli but in an explicitly unpaired manner. Following acquisition, all animals received 30 additional CS-alone trials at five min intervals. This paradigm, which incorporated ITIs longer than those which had been used previously in backward conditioning studies, induced a long-lasting potentiation of the flexion reflex which appeared to be specific to spinal reflex pathways activated by A alpha cutaneous fibers. The relevancy of these results to a more specific understanding of backward and forward classical conditioning in the spinal cat is discussed.

Retention of a classically conditioned reflex response in spinal cat

Retention of classically conditioned flexion reflex facilitation was examined in unanesthetized, decerebrate, acute spinal cats. Flexion reflex facilitation, recorded from the tibialis anterior muscle, was obtained by pairing saphenous nerve stimulation (the conditioned stimulus) with superficial peroneal nerve stimulation (the unconditioned stimulus). The flexion reflex declined in control animals receiving the same number of nerve stimuli over the same time span, but in an explicitly unpaired sequence. To investigate retention, conditioned stimuli were presented at 5-min intervals following acquisition for a 2 1/2-h period. During this time a significant difference between conditioning and control groups was maintained even to the last trial, with no indication that the difference was subsiding over time. The results support the possibility that a classical conditioning paradigm applied to the spinal cord can induce alterations in spinal reflexes of long duration. Furthermore, the results appear to rule out post-tetanic potentiation as a mechanism producing the observed long-term effects.

Classical conditioning of a flexor nerve response in spinal cats: effects of tibial nerve CS and a differential conditioning paradigm.

Previous studies have shown flexor nerve response increases produced by classical conditioning procedures in spinal cats when the conditioned stimulus (CS) was delivered to the superficial peroneal nerve and the unconditioned stimulus (US) was delivered to the ankle skin. In this study, these effects were produced when the CS was delivered to the whole tibial nerve or to the medial plantar branch. The finding that response increases followed by extinction effects could be obtained when either the superficial peroneal or the tibial nerve was utilized allowed the assessment of the effects of a differential conditioning paradigm. The responses to CS-US presentations on the superficial peroneal nerve increased, whereas responses to CS presentations on the tibial nerve remained unchanged. However, lack of extinction effects in the superficial peroneal data suggested that stimulation of the tibial nerve potentiated superficial peroneal evoked responses. Furthermore, responses evoked by stimulation of either nerve increased when paired trials were given on the tibial nerve. These data demonstrate that stimulation of the tibial nerve potentiates responses to superficial peroneal nerve stimulation but that superficial peroneal nerve stimulation has no effect on responses to CS presentations to the tibial nerve.

Presynaptic effects of morphine and methionine-enkephalin in feline spinal cord

The effects of morphine (applied either iontophoretically in substantia gelatinosa or injected intravenously) and met-enkephalin (iontophoretically) were examined on the terminal excitabilities of single sural C, post-A δ and A δ afferents, in cats that were decerebrated and then spinalized. Small amounts of morphine (0.1–2.0 mg/kg or 15–80 nA) and met-enkephalin (15–80 nA) produced an increase in the threshold for antidromic activation of these sural fibres. In these doses, the opiate and the opioid peptide potentiated the enhancement of sural afferent terminal excitability produced by superficial peroneal (SP) nerve stimulation. The above effects of both agonists were antagonized by small doses of naloxone (0.05–0.15 mg/kg or 20–40 nA). In large amounts, morphine (3.2–6.4 mg/kg or 50–150 nA) and met-enkephalin (60–150 nA) increased the excitabilities of the sural afferent terminals and antagonized the enhancement of the terminal excitability produced by SP nerve stimulation. These actions by large doses of the agonists were not consistently antagonized by naloxone. In some experiments in which the peripheral nerves, except a few post-A δ fibres from which recordings were made, were left intact, intraarterially injected bradykinin (10 μg, to a hind limb) produced a decrease in threshold for antidromic activation of the post-A δ fibres and converted the increase in threshold produced by small amounts of morphine and met-enkephalin into a decrease in threshold. Morphine (0.8–6.4 mg/kg or 30–200 nA) did not consistently alter the excitabilities of muscle group I afferent terminals. The results of these studies indicate that morphine- and met-enkephalin-induced analgesia is, at least, partly due to the ability of the agents to potentiate “presynaptic inhibition” of nociceptive pathways in the spinal cord.

Morphine and met-enkephalin effects of sural aδ- afferent terminal excitability

Morphine (30–80 nA) and met-enkephalin (30–80 nA) decreased the excitability of single sural Aδ afferent terminals and potentiated the enhancement of the terminal excitability produced by superficial peroneal nerve stimulation, in mid-collicular decerebrate and spinalized cats. Naloxone (20–40 nA) antagonized the actions of both substances on the unconditioned and the terminalned terminal excitabilities. These results indicate that morphine and met-enkephalin hyperpolarize Aδ sural afferent terminals and facilatate the terminal depolarization during presynaptic inhibition. This enhancement of presynaptic inhibition may be, at least partly, responsible for the analgesic action of these agents.