女性球海绵体肌反射临床应用初探

目的:探讨女性球海绵体肌反射(BCR)及阴部神经短潜伏期体感诱发电位(SSEP)临床应用价值.方法:利用电生理技术对15例女性患者(女病例组)进行BCR及阴部神经SSEP的潜伏期、波幅检测,并与30例男性心因性阳痿患者(男病例组)和30例男性正常对照组(男对照组)进行比较.结果:女病例组BCR潜伏期比男病例组和男对照组BCR潜伏期延长,差异有统计学意义(P＜0.05),三组SSEP P41波潜伏期则无显著差异.结论:女病例组BCR潜伏期较男性组延长.国人女性BCR的检测和应用有待进一步探讨.     

Modulation of the vestibulo-ocular reflex by serotonin in the rat

The effects of intraventricular injection of serotonin (5-HT) and its agonists and antagonists on the amplitude of the vestibulo-ocular reflex were studied in chronic implanted rats. 5-HT (10^–5 M) triggers an increase of the amplitude of the reflex which lasts 30 min. Similar results are obtained when N,N-dimethyl-5-methoxytryptamine (10^–3 M) is introduced into the ventricular cannula. The increasing effects observed both with 5-HT and N,N-dimethyl-5-methyoxy-tryptamine are abolished by methiothepin, a potent antagonist of 5-HT receptors. Injection of indirect agonists like pargyline, a monoamine oxidase inhibitor, or fluoxetine, a potent inhibibitor of 5-HT reuptake, is followed by an increase of the amplitude of the vestibulo-ocular reflex. These results indicate that 5-HT can modulate the activity of the vestibulo-ocular pathway and muscular tone of extraocular muscles. Location and involvement of various modulating 5-HT sites are discussed.     

On the cutaneous receptors contributing to withdrawal reflex pathways in the decerebrate spinal rat

Previous studies indicate that the withdrawal reflex system in the rat has a “modular” organization, each reflex pathway performing a specific sensorimotor transformation. Here, we wished to clarify which cutaneous receptors contribute to this system and to determine whether there are differences in this respect between reflex pathways of different muscles. Withdrawal reflexes of the peroneus longus, extensor digitorum longus, and semitendinosus muscles were recorded with EMG techniques during high reflex excitability in decerebrate spinal rats (n=26). While maintained innocuous pressure on glabrous skin could elicit a sustained reflex activity in all muscles studied, vibration of glabrous skin (10–300 Hz) always failed to evoke a reflex response, suggesting that slowly adapting, but not rapidly adapting, low-threshold mechanoreceptive fibers from this type of skin contribute to withdrawal reflex pathways. Thermal stimulation in the innocuous range, i.e., cooling from 32 to 17°C, or warming the skin from 32 to 41°C, always failed to produce reflex responses, indicating that neither cold nor warm receptors contribute to withdrawal reflex pathways. When either cooling or warming the skin to the noxious temperatures of 1°C or above 45°C, respectively, a reflex discharge was often evoked in the muscles studied. Intradermal administration of histamine, a potent pruritogenic substance, produced very weak, or no, reflex response. In contrast, mustard oil produced vigorous reflex responses in all muscles studied. These findings suggest that some chemonociceptors contribute only weakly, or not at all, to withdrawal reflex pathways. The present data suggest that a selective set of cutaneous receptors contribute to withdrawal reflex pathways and that different withdrawal reflex pathways receive input from essentially the same cutaneous receptor types. Received: 13 March 1997 / Accepted: 27 June 1997     

Glutamate and AMPA receptor immunoreactivity in Ia synapses with motoneurons and neurons of the central cervical nucleus

Axonal tracing and high resolution immunocytochemistry were used to identify transmitter content and postsynaptic receptors in synapses between Ia primary afferents and motoneurons and in neurons of the central cervical nucleus (CCN), respectively, in the rat. The terminals, as well as the target neurons, were identified by postembedding immunogold detection of transganglionically or retrogradely, respectively, transported cholera toxin B subunit (CTB), and in adjacent sections postembedding immunogold was employed to demonstrate glutamate and AMPA receptors in the same synapses. A total of 390 CTB-labelled Ia boutons in apposition to CTB-labelled motoneurons, CCN neurons or unlabelled dendrites in the surrounding neuropil were traced in section series from two animals. A third animal was used as a control. In the motor nucleus, a majority of the synapses were with medium-sized dendrites, whereas in the CCN the distribution was skewed towards fine-calibre dendrites. In both nuclei, somatic and juxtasomatic synapses were quite infrequent (<10%). All of the CTB-labelled Ia boutons recovered in the sections incubated for glutamate (n=323) were enriched with glutamate immunoreactivity. One hundred and fifty of these disclosed synaptic contact in at least two ultrathin sections. In this sample, 50% (33–59%) appeared immunoreactive to receptor sub-units GluR1–4 in at least two ultrathin sections, whereas 35% were labelled in one section only. Distribution of gold particles relative to presynaptic and postsynaptic membrane profiles (n=23) revealed a close correlation between AMPA immunoreactivity and the postsynaptic membrane of the synapse. Finally, immunogold particles signalling GluR1 were observed much less frequently than particles signalling GluR2/3 or GluR4. Our results provide additional strong evidence that chemical transmission at Ia synapses is mediated by glutamate and identify GluR2/3 and GluR4 as important postsynaptic receptors. Electronic Publication     

Modulation of the jaw-opening reflex by stimulation of the vestibular nuclear complex in rats

The effect of stimulation of the vestibular nuclear complex (VN) on the jaw-opening reflex (JOR) was studied in anesthetized rats. The JOR was evoked by electrical stimulation of the inferior alveolar nerve, and was recorded as the electromyographic responses of the anterior belly of the digastric muscle, bilaterally. Conditioning electrical stimulation of the medial (MVN), lateral (LVN) and superior (SVN) vestibular nuclei facilitated the JOR bilaterally. Microinjection of monosodium glutamate into the SVN, LVN and MVN also facilitated the JOR bilaterally. In contrast, conditioning electrical stimulation of the inferior vestibular nucleus (IVN) inhibited the JOR ipsilaterally. Microinjection of monosodium glutamate into the IVN also inhibited the JOR ipsilaterally. These results suggest that the VN is involved in modulation of the JOR and plays an important role in controlling the jaw movements.     

Modulation of the masseteric monosynaptic reflex by stimulation of the vestibular nuclear complex in rats

The effect of stimulation of the vestibular nuclear complex (VN) on the masseteric monosynaptic reflex (MMR) was studied in anesthetized rats. The MMR was evoked by electrical stimulation of the mesencephalic trigeminal nucleus and was recorded, bilaterally, as the electromyographic responses of the masseter muscles. Conditioning electrical stimulation of the medial vestibular nucleus (MVN) facilitated the MMR bilaterally, as did microinjection of monosodium glutamate into the MVN. In contrast, conditioning electrical stimulation of the inferior vestibular nucleus (IVN) inhibited the MMR bilaterally. Microinjection of monosodium glutamate into the IVN also inhibited the MMR bilaterally. Conditioning electrical stimulation of the lateral and superior vestibular nuclei did not modulate the MMR. These results suggest that the MVN and the IVN are involved in modulation of the MMR and plays an important role in controlling jaw movements.     

A role for the basal ganglia in nicotinic modulation of the blink reflex

Summary In humans and rats we found that nicotine transiently modifies the blink reflex. For blinks elicited by stimulation of the supraorbital branch of the trigeminal nerve, nicotine decreased the magnitude of the orbicularis oculi electromyogram (OOemg) and increased the latency of only the long-latency (R2) component. For blinks elicited by electrical stimulation of the cornea, nicotine decreased the magnitude and increased the latency of the single component of OOemg response. Since nicotine modified only one component of the supraorbitally elicited blink reflex, nicotine must act primarily on the central nervous system rather than at the muscle. The effects of nicotine could be caused by direct action on lower brainstem interneurons or indirectly by modulating descending systems impinging on blink interneurons. Since precollicular decerebration eliminated nicotine's effects on the blink reflex, nicotine must act through descending systems. Three lines of evidence suggest that nicotine affects the blink reflex through the basal ganglia by causing dopamine release in the striatum. First, stimulation of the substantia nigra mimicked the effects of nicotine on the blink reflex. Second, haloperidol, a dopamine (D₂) receptor antagonist, blocked the effect of nicotine on the blink reflex. Third, apomorphine, a D₂ receptor agonist, mimicked the effects of nicotine on the blink reflex.     

Sympathetic activity in the recto-rectal reflex of the guinea pig

In the guinea pig, defecation is controlled by the myenteric plexus, whose activity is modulated by the sacral spinal and supraspinal centers. The purpose of this study is to clarify the control of defecation reflex by sympathetic nerves. The propulsive contractions of the rectum produced by rectal distension (recto-rectal excitatory reflex response) were abolished after transection of the Th 13 and/or the L 4 segment. This response was reproduced again after removal of the lumbar segments (L1-4), division of the lumbar dorsal roots (L1-4), the lumbar splanchnic nerves or lumbar colonic nerves (LCN). The frequency of efferent discharges of LCN was increased slightly by rectal distension and remarkably increased after Th 13 and/or L 4 transection. Thus, there occurs during the recto-rectal reflex not only mucosal intrinsic reflex and sacral excitatory reflex via the pelvic nerves but also a lumbar inhibitory reflex via the colonic nerves, whose center may be located in the upper lumbar segments.But, the activity of the inhibitory center was depressed by the supraspinal center, so that an excitatory reflex is produced more dominantly than an inhibitory one in normal animals. All these extrinsic reflexes coordinate the activity of the myenteric plexus in defecation reflex.     

Steroid hormone masculinization of neural structure in rats: a tale of two nuclei

We review the mechanisms by which steroid hormones masculinize two different regions of the central nervous system (CNS) in rats. Although in both cases, androgens induce a male phenotype, the detailed mechanisms are remarkably different in the two models. In the spinal nucleus of the bulbocavernosus (SNB), testosterone must be present during the perinatal period to spare motoneurons and their target muscles from cell death. This masculinization of the SNB system is through activation of androgen receptors, because XY rats with a defective gene for the androgen receptor fail to develop a masculine SNB system. Interestingly, the motoneurons are spared by androgen, even though they themselves do not possess androgen receptors during the critical period for their survival. Thus, steroids can act on one part of the body to secondarily masculinize the CNS. In the posterodorsal aspect of the medial amygdala (MePD), testosterone can induce masculine development even in adulthood, indicating that there is no critical period for steroids to affect sexual differentiation of this system. In the case of the MePD, both estrogen receptors and androgen receptors appear to mediate testosterone's masculinizing influence on neural structure. The extended neural plasticity of the MePD may reflect annual "reorganization" of the brain in the seasonally breeding ancestors of laboratory rats.     

Opioid modulation of reflex versus operant responses following stress in the rat

In pre-clinical models intended to evaluate nociceptive processing, acute stress suppresses reflex responses to thermal stimulation, an effect previously described as stress-induced "analgesia." Suggestions that endogenous opioids mediate this effect are based on demonstrations that stress-induced hyporeflexia is enhanced by high dose morphine (>5 mg/kg) and is reversed by naloxone. However, reflexes and pain sensations can be modulated differentially. Therefore, in the present study direct comparisons were made of opioid agonist and antagonist actions, independently and in combination with acute restraint stress in Long Evans rats, on reflex lick-guard (L/G) and operant escape responses to nociceptive thermal stimulation (44.5 degrees C). A high dose of morphine (>8 mg/kg) was required to reduce reflex responding, but a moderate dose of morphine (1 mg/kg) significantly reduced escape responding. The same moderate dose (and also 5 mg/kg) of morphine significantly enhanced reflex responding. Naloxone (3 mg/kg) significantly enhanced escape responding but did not affect L/G responding. Restraint stress significantly suppressed L/G reflexes (hyporeflexia) but enhanced escape responses (hyperalgesia). Stress-induced hyperalgesia was significantly reduced by morphine and enhanced by naloxone. In contrast, stress-induced hyporeflexia was blocked by both naloxone and 1 mg/kg of morphine. Thus, stress-induced hyperalgesia was opposed by endogenous opioid release and by administration of morphine. Stress-induced hyporeflexia was dependent upon endogenous opioid release but was counteracted by a moderate dose of morphine. These data demonstrate a differential modulation of reflex and operant outcome measures by stress and by separate or combined opioid antagonism or administration of morphine.     

Flexion reflex modulation during stepping in human spinal cord injury

The flexion reflex modulation pattern was investigated in nine people with a chronic spinal cord injury during stepping using body weight support on a treadmill and manual assistance by therapists. Body weight support was provided by an upper body harness and was adjusted for each subject to promote the best stepping pattern with the least manual assistance required by the therapists. The flexion reflex was elicited by sural nerve stimulation with a 30 ms pulse train at 1.2–2 times the tibialis anterior reflex threshold. During stepping, stimuli were randomly dispersed across the gait cycle which was divided into 16 equal bins. A long latency (>110 ms) flexion reflex was present in all subjects, while a short (>30 ms) and a medium latency (>70 ms) flexion reflex were present only in three subjects. For each response, the non-stimulated EMG was subtracted from the stimulated EMG at identical time windows and bins, normalized to the maximal corresponding EMG, and significant differences were established with a Wilcoxon rank-sum test. The long latency flexion reflex was facilitated at late stance and during the swing-to-stance transition phase. A reflex depression was present from heel strike until mid-stance and during the swing-to-stance transition phase. The short and medium latency flexion reflexes were depressed during mid-stance followed by facilitation during the stance-to-swing transition phase. Regardless of the latency, facilitatory flexion responses during the swing phase coincided with decreased activity of ipsilateral ankle extensors. The flexion reflex was modulated in a phase dependent manner, a behavior that was absent for the soleus H-reflex in most of these patients (Knikou et al. in Exp Brain Res 193:397–407, 2009). We propose that training should selectively target spinal reflex circuits in which extensor muscles and reflexes are involved in order to maximize sensorimotor recovery in these patients.     

Auditory neurons in the rat thalamic reticular nucleus

Summary In the thalamic reticular nucleus (TR) of the rat a cluster of neurons has been located which receives auditory inputs and acts as a source of inhibition for relay neurons of the medial geniculate nucleus (MG). These TR neurons (auditory thalamic reticular neurons; A-TR neurons) showed a repetitive burst of grouped discharge upon electrical stimulation of the inferior colliculus (IC) or of the auditory cortex. Many of them responded to tonal stimuli such as clicks or pips.Adjacent to the cluster of A-TR neurons there were the cluster of TR neurons receiving visual inputs (V-TR neurons) and that receiving somatosensory inputs (S-TR neurons). The cluster of A-TR neurons was situated ventrally to the cluster of V-TR neurons, both extending caudally from the level of the rostral tip of the dorsal lateral geniculate nucleus. The S-TR neurons distributed rostrally to the clusters of A- and V-TR neurons. Some of the sensory TR neurons, usually found around the boundaries between the clusters of different sensory modalities, were activated from stimulation of different central sensory pathways.Single electric shocks directly applied to the cluster of A-TR neurons suppressed discharges of relay neurons of the MG, either spontaneous or evoked by click stimuli or by electric shocks to the IC. The postexcitatory suppression of MG relay neurons was similar in time course to the suppression following electrical stimulation of A-TR neurons.Response latencies of the A-TR neurons to IC shocks were found to be 1.0–1.5 ms longer than those of the MG relay cells with respect to the modal and shortest values. It is suggested that A-TR neurons are intercalated in the axon collateral circuit of the thalamocortical projection arising from relay neurons of the MG.Dedicated to Dr. Kitsuya Iwama, Emeritus Professor of Osaka University Medical School, on the occasion of his retirement     

Influence of inferior olive on flexor reflex activity

Summary In Wistar rats we have studied the effect of inferior olive lesion or activation on the threshold of a flexor reflex elicited by a nociceptive stimulus applied to the hindpaw. When the inferior olive is lesioned by means of 3-acetylpyridine, the threshold value is significantly decreased. A recovery occurs in 3–4 weeks. When the inferior olive is activated by means of harmaline, the threshold value is significantly increased. These experiments suggest the inferior olive activity exerts an inhibitory effect on flexor reflex activity. The recovery of the threshold value depends, probably, on the plastic reorganization of the cerebellar circuits, which occurs after inferior olive lesion.     

NO-Dependent mechanisms of amygdalofugal modulation of hypothalamic autonomic neurons

Neurophysiological and histochemical experiments on rats were performed to study the effects of the central nucleus of the amygdala on the activity of cells in various areas of the hypothalamus. Electrical stimulation of the medial part of the nucleus evoked marked excitatory reactions in neurons in the medial part of the paraventricular nucleus of the hypothalamus and the rostral part of the lateral hypothalamic area. Intravenous administration of N^G-nitro-L-arginine methyl ester (L-NAME, 10 mg/kg) led to increases in evoked neuron responses. A series of histochemical studies following activation of the central nucleus demonstrated increases in the quantity and optical densities of NADP diaphorase (NADP-d)-positive neurons in the parvocellular zone of the paraventricular nucleus of the hypothalamus and the medial part of the lateral hypothalamic area. The activity of nitroergic cells in the ventrolateral part of the lateral hypothalamic area was suppressed in these conditions. These mechanisms may underlie the amygdalofugal modulation of the autonomic functions of the hypothalamus. __________ Translated from Rossiiskii Fiziologicheskii Zhurnal imeni I. M. Sechenova, Vol. 92, No. 8, pp. 957–966, August, 2006.     

Hypothetical anatomical model to describe the aberrant gag reflex observed in a clinical population of orally deprived children

In this 'clinical conundrum', we propose a hypothetical anatomical model to explain the abnormal gag reflex that is consistently observed in a clinical population of children experiencing feeding delays. This model is based on the presence of 'transient' connections formed during the normal development of autonomic brainstem circuitry involving the nucleus tractus solitarius (NTS). We propose that, as a result of normal feeding and swallowing, the activity of these transient fibers typically diminishes shortly after birth. In children who are orally deprived during infancy, these transient connections persist and the aberrant gag reflex is maintained into childhood. The most critical feature of the proposed model is the idea that swallowing during feeding initiates the retraction of the tactile 'transient' input to NTS. In the NICU feeding clinics, it has been suggested that triggering the gag reflex in neonates by tactile stimulation of non-oral body areas and anterior portions of the mouth directly or indirectly may contribute to oral feeding delays. To the contrary, we propose an anatomical model to suggest that oral feeding delays and lack of swallowing food, when experienced by neonates, actually contribute to the development of the aberrant gag reflex observed in later developmental stages.     

Excitatory amino acid receptors in the caudal ventrolateral medulla mediate a vagal cardiopulmonary reflex in the rat

Summary The importance of the caudal ventrolateral medulla (CVLM) in mediating vagal cardiopulmonary (Bezold-Jarisch reflex) reflex activity was studied in urethane-anaesthetized rats. Unilateral electrolytic lesion of the CVLM markedly attenuated Bezold-Jarisch reflex responses (hypotension and bradycardia) elicited by intravenous injections of 5-HT. Bilateral lesion of the CVLM virtually abolished the reflex responses. Microinjection of the excitatory amino acid (EAA) receptor antagonist kynurenate (KYN), but not the inactive analogue xanthurenate, into the CVLM markedly attenuated the reflex responses to 5-HT. The N-methyl-D-aspartate (NMDA) receptor antagonist, MK-801 also markedly attenuated reflex activity. Furthermore, lesions, KYN and MK-801 all tended to elevate resting blood pressure and to reduce resting heart rate. These findings support the hypothesis that the CVLM is an important medullary locus mediating cardiovascular reflex integration and that an EAA synapse in the CVLM is important in the cardiopulmonary reflex arc.     

Distribution of the tecto-thalamic projection neurons in the hereditary microphthalmic rat

Summary Tecto-thalamic projections in the hereditary bilaterally microphthalmic rat were studied by means of WGA-HRP injection into the dorsal lateral geniculate nucleus (LGNd) and the lateroposterior thalamic nucleus (LP). Histological study in the mutant rats showed that whereas LGNd and superficial layers of the superior colliculus (SC) suffered from a remarkable reduction in size, LP had no histological changes as compared to the normal animals. Unilateral injection of the tracer into the microphthalmic LGNd showed that WGA-HRP positive neurons were present mostly in the ipsilateral str. griseum superficiale (SGS) of the SC. However, the number of labeled SGS neurons of the microphthalmic animals was about 3% of the normal. Although cell bodies of the normal tecto-LGNd neurons in the SGS were spindle-form in shape and issued one or two proximal dendrites from each pole, the microphthalmic tecto-LGNd neurons showed an irregular contour and their dendrites were not so intensively labeled. Unilateral injections of WGA-HRP into the LP revealed that the tecto-LP neurons were mainly distributed in the ipsilateral str. opticum of the colliculus. (SO) in both normal and microphthalmic animals. However, the number of labeled SO cells in the microphthalmic rat was about one-half of the normal. Furthermore, the size of labeled tecto-LP neurons was smaller than that of the normal ones, and they showed irregular round to oval cell bodies with equivocally labeled dendrites, in contrast to the normal tecto-LP neurons with polygonal cell bodies extending three or more dendrites in a radial fashion. These results indicate that there exist the tecto-LGNd and -LP projection neurons in the microphthalmic rat and that their laminally segregated projection is fundamentally preserved. However, the number of the tecto-thalamic projection neurons, especially of the tecto-LGNd cells, was markedly diminished in the mutant tectum compared to normals.Abbreviations CST cortico-spinal tract - DRN dorsal raphe nucleus - DTN dorsal tegmental nucleus - LGNd pars dorsalis of the lateral geniculate nucleus - LLN nucleus of the lateral lemniscus - LM medial lemniscus - LP lateroposterior thalamic nucleus - MGN medial geniculate nucleus - MRF midbrain reticular formation - OT optic tract - P pretectal area - PAG periaqueductal gray - PB parabigeminal nucleus - PN pontine nuclei - PCS superior cerebellar peduncle - SGS superficial gray layer of the superior colliculus - SO stratum opticum of the superior colliculus - SN substantia nigra - Vm motor nucleus of the trigeminar nerve - Vs sensory nucleus of the trigeminar nerve     

Afterhyperpolarization modulation in lumbar motoneurons during locomotor-like rhythmic activity in the neonatal rat spinal cord in vitro

Motoneuron afterhyperpolarization (AHP) amplitude and somatic input conductance were monitored during pharmacologically induced, locomotorlike ventral root activity using an isolated neonatal rat spinal cord preparation (transected at the C1 level). Nonspontaneously firing motoneurons were selected for study. Single spikes were evoked at regular intervals by brief depolarizing current pulse injections, while somatic input conductance was monitored by hyperpolarizing current pulses. The induction of rhythmic ventral root activity was associated with tonic depolarization of motoneurons as well as superimposed rhythmically alternating membrane depolarization and hyperpolarization (locomotor drive potentials, LDPs). In 9 of 13 trials (six of eight cells) the peak amplitude of AHPs following current-evoked action potentials was reduced during both the hyperpolarized and the depolarized phases of the LDP, compared with the pre-locomotor condition. The peak AHP amplitude increased during the depolarized phase of the LDP in 4 of 13 trials (three of eight cells); however, in 3 of these 4 trials measurement of the AHP later in the course of its trajectory, using a half decay time (HDt) reference point, demonstrated AHP amplitude reduction during rhythmic activity compared with the prelocomotor condition. In seven of eight motoneurons the induction of rhythmic activity was associated with a decrease in input conductance. The pattern of AHP amplitude and conductance modulation during the two phases of the LDP was consistent for individual trials; however, there was considerable intertrial variation. The results suggest that AHP modulation during locomotor-like activity in this preparation can be mediated independently of supraspinal influences by intrinsic spinal cord mechanisms, and the observed AHP suppression does not appear to be the passive result of an increase in background conductance. The discrepancy between peak and HDt-based AHP amplitude measurements during the depolarized phase of the LDP in some trials may be due to competing effects of passively enhanced potassium currents and a mechanism that actively reduces the calcium-dependent potassium conductance. The possibility that both the AHP amplitude and the input conductance changes observed during locomotor-like activity reflect a regulation of potassium channels is discussed.     

Stretch reflex modulation during imposed static and dynamic hip movements in standing humans

The purpose of this study was to investigate the effects of hip proprioceptors on soleus stretch reflex excitability in standing humans. A custom-made device to stretch the ankle extensors was mounted on the lower leg portion of a gait orthosis and was used to elicit stretch reflex responses while standing. Six subjects with motor complete spinal cord injury (SCI) and six spinal intact subjects were placed in the orthosis, and stretch reflex responses were elicited when static and/or dynamic hip joint angle changes were imposed. We found that static hip extension significantly enhanced the stretch reflex responses as compared to the neutral position and the hip flexion position only in the SCI group. The EMG magnitude induced by hip extension was 142 ± 16.6% greater than that induced by the neutral position. When the leg was dynamically swung, the reflex responses also changed with the phase of the hip angle in the SCI group; in particular, the reflex amplitude was enhanced with hip extension and in the transition phase from flexion to extension. Although the magnitude of the changes was less than that in the SCI group, a similar type of modulation was found in the normal group. Given the fact that the persons with SCI had lost the neural connection between higher nervous center and the paralyzed lower limb muscles, the mechanism underlying the present results can be attributed to the peripheral afferent input due to the hip angle changes. We concluded that hip mediated afferent input has a significant influence on the excitability modulation of the soleus stretch reflex pathway. Such neural modulation may play a role in the mechanism responsible for the phase-dependent modulation of the stretch reflex while walking.