Tachykinins mediate changes in spinal reflexes after activation of unmyelinated muscle afferents in the rat.

The effect of intrathecally applied tachykinin antagonist D-NicLys1, 3-Pal3, D-Cl2Phe5, Asn6, D-Trp7.9, Nle11-substance P, spantide II, on the long-term increase of spinal cord excitability after activation of unmyelinated muscle afferents was studied in decerebrate, spinalized, unanaesthetized rats. A conditioning stimulus train (1 Hz, 20 s) that activated unmyelinated fibres in the gastrocnemius muscle nerve facilitated the flexor reflex for about 1 h, which was strongly blocked by pretreatment with spantide II (3 micrograms). The present results indicate that the facilitation of the flexor reflex by conditioning stimulation of a muscle nerve is mediated by tachykinins and possibly other neuropeptides which may be released from the central terminals of these unmyelinated afferents.     

Spinal substance P and N-methyl-D-aspartate receptors are coactivated in the induction of central sensitization of the nociceptive flexor reflex.

We have studied the effects and interactions of the neurokinin-1 receptor antagonist CP-96,345 and the N-methyl-D-aspartate receptor/channel blocker MK-801, both applied intravenously, on the flexor reflex and on the facilitation of the flexor reflex by conditioning stimulation of cutaneous C-afferents in decerebrate, spinalized, unanesthetized rats. The flexor reflex was evoked by subcutaneous electrical stimuli applied to the sural nerve innervation area 1/min at an intensity that activated C-fibers and was recorded as electromyogram from the ipsilateral hamstring muscles. The magnitude of the baseline flexor reflex was usually highly stable in the course of the experiments without experimental manipulations. The same stimulus was used as a conditioning train (0.9 Hz, 20 shocks) and caused a brief facilitation of the flexor reflex, which was maximal 0.5 and 1 min after stimulation (255.1 +/- 23.6% over baseline). During the course of the conditioning stimulus train, the reflex magnitude was gradually increased (wind-up). MK-801 (0.1 and 0.5 mg/kg) consistently depressed the polysynaptic flexor reflex. At a dose of 0.5 mg/kg, but not 0.1 mg/kg, MK-801 reduced the wind-up and blocked the facilitation of the flexor reflex induced by the conditioning stimulus by 90%. The facilitatory effect of 7 pmol intrathecal substance P was also partially reduced by MK-801. CP 96,345 (1 and 3 mg/kg) did not depress the flexor reflex, but dose-dependently antagonized reflex facilitation by the conditioning stimulus train, similarly to its antagonism of intrathecally applied 7 pmol substance P-induced facilitation.(ABSTRACT TRUNCATED AT 250 WORDS)     

NK-1, but not NK-2, tachykinin receptors mediate plasma extravasation induced by antidromic C-fiber stimulation in rat hindpaw: demonstrated with the NK-1 antagonist CP-96,345 and the NK-2 antagonist Men 10207.

The effects of intradermal injection of CP-96,345 and Men 10207, selective antagonists for NK-1 and NK-2 tachykinin receptors, respectively, on the extravasation of plasma protein induced by antidromic stimulation of unmyelinated sensory fibers in the sciatic nerve was studied in rat hindpaw. Activation of unmyelinated fibers by antidromic sciatic nerve stimulation (1 Hz, 5 min) consistently evoked a localized plasma extravasation of Evans blue on the skin area of the hindpaw innervated by the sciatic nerve, which was not inhibited by intradermal injection of saline or Men 10207 (9 and 35 nmol). In contrast, CP-96,345 (3 and 9 nmol, but not 1 nmol), injected intradermally 15 min prior to nerve stimulation dose-dependently inhibited this response. Plasma extravasation induced by intravenously injected substance P was also inhibited by CP-96,345. Since CP-96,345 is a highly selective antagonist for NK-1 tachykinin receptors, it is suggested that the plasma extravasation induced by antidromic C-fiber stimulation and by systemically applied tachykinins is mediated by NK-1 tachykinin receptors.     

Tachykinns mediate changes in spinal reflexes after activation of unmyelinated muscle afferents in the rat

The effect of intrathecally applied tachykinin antagonist D-NicLys¹, 3-Pal³, D-Cl² Phe⁵, Ama⁶, Trp^7,8, Nle¹¹-substance P, spantide II, on the long-term increase of spinal cord excitability after activation of unmyelinated muscle afferents was studied in decerebrate, spinalized, unanaesthetized rats. A conditioning stimulus train (1 Hz, 20 s) that activated unmyelinated fibres in the gastrocnemius muscle nerve facilitated the flexor reflex for about 1 h, which was strongly blocked by pretreatment with spantide II (3 µg). The present results indicate that the facilitation of the flexor reflex by conditioning stimulation of a muscle nerve is mediated by tachykinins and possibly other neuropeptides which may be released from the central terminals of these unmyelinated afferents.     

Intrathecal neurokinin A facilitates the spinal nociceptive flexor reflex evoked by thermal and mechanical stimuli and synergistically interacts with substance P

The neuropeptide neurokinin A was injected intrathecally and its effect on the spinal nocifensive flexor reflex was examined. The reflex, which was evoked by electrical, thermal or mechanical stimulation of the foot and was recorded from the ipsilateral hamstring muscles, was substantially facilitated by 7 pmol intrathecally injected neurokinin A. The facilitatory effect of neurokinin A to thermal stimulation was, however, significantly stronger than to electrical or mechanical stimuli. Furthermore, co-administration of neurokinin A with substance P induced a significant synergistic facilitation of the reflex. It is suggested that neurokinin A, like substance P, may be released in association with activation of polymodal C-nociceptors.     

Intrathecal neurokinin A facilitates the spinal nociceptive flexor reflex evoked by thermal and mechanical stimuli and synergistically interacts with substance P.

The neuropeptide neurokinin A was injected intrathecally and its effect on the spinal nociceptive flexor reflex was examined. The reflex, which was evoked by electrical, thermal or mechanical stimulation of the foot and was recorded from the ipsilateral hamstring muscles, was substantially facilitated by 7 pmol intrathecally injected neurokinin A. The facilitatory effect of neurokinin A to thermal stimulation was, however, significantly stronger than to electrical or mechanical stimuli. Furthermore, co-administration of neurokinin A with substance P induced a significant synergistic facilitation of the reflex. It is suggested that neurokinin A, like substance P, may be released in association with activation of polymodal C-nociceptors.     

Facilitation of the human nociceptive reflex by stimulation of Aβ-fibres in a secondary hyperalgesic area sustained by nociceptive input from the primary hyperalgesic area

Hyperalgesia was induced in healthy volunteers by topical capsaicin applied on the dorsum of the foot within the receptive field of the sural nerve. Under presence of hyperalgesia different normally non-noxious conditioning stimuli were applied to the hyperalgesic area and the polysynaptic nociceptive spinal reflex and pain ratings were used to assess central excitability. The nociceptive reflex was measured in the knee extensor and flexor muscles evoked by electrical stimulation of the sural nerve trunk at an intensity of 1.5 times the initial reflex threshold (an intensity above the pain threshold). Thermal stimulation of the primary hyperalgesic area (re)established both on-going spontaneous pain and secondary hyperalgesia. Thus, increased nociceptive reflexes were recorded and increased pain intensity reported when Aβ-fibres in the secondary hyperalgesic area were activated concurrently with the reflex testing after a non-noxious thermal stimulation of the primary hyperalgesic area. The Aβ-fibre activation was achieved by continuous low-intensity electrical stimulation (40 Hz) that was initiated after on-going pain produced by the thermal stimulation had waned. The same measurement without prior thermal conditioning stimulation of the primary area resulted in no reflex facilitation, indicating rapid changes in the central excitability with existence of on-going nociceptive activity. This indicates that the development and maintenance of secondary hyperalgesia are dependent on sustained peripheral nociceptive activity. The study also shows that a central summation of nociceptive and non-nociceptive afferent activity can occur once secondary hyperalgesia is present.     

Morphine-sensitive late components of the flexion reflex in the neonatal rat

The 8-15-day-old rat spinal cord was isolated together with peripheral nerves innervating a hindlimb. Multiunit neural discharges in response to electrical stimulation of a cutaneous nerve (sural, plantar of superficial peroneal nerve) were recorded from a flexor nerve (deep peroneal nerve or nerve innervating the hamstring muscles). Attempts were made to find relations between the magnitude of the flexion reflex discharges and the sizes of the volleys in the myelinated or unmyelinated afferent fibers. The neonatal flexion reflex discharges due to myelinated fiber volleys were exaggerated when compared with those in the adult rats. Higher stimulus strengths recruited later components of the flexion reflex discharges. The observed increment of the flexion reflex discharges was precisely associated with the recruitment of unmyelinated afferent fibers in the nerve. These late flexion reflex discharges were shown to be depressed by the opiate analgesic morphine in a naloxone-reversible manner.     

Effects of flexor reflex afferent stimulation on the soleus H reflex in patients with a complete spinal cord lesion: evidence for presynaptic inhibition of Ia transmission

Summary The effects of electrically stimulating the Flexor Reflex Afferent (FRA) on the soleus H reflexes were investigated in 34 paraplegic patients having a clinically complete spinal cord lesion. Conditioning stimuli (5–50 mA) were applied to the ipsilateral or contralateral sural nerve. The conditioning-test interval ranged from 20 to 1000 ms. A late ipsilateral flexor reflex (EMG) was found in all patients. A late contralateral extension reflex was sporadically observed in only 3 patients. The excitability curves usually showed two phases of ipsilateral H reflex inhibition and contralateral H reflex facilitation, one between 50 and 130 ms and the other after over 200 ms. These intervals correspond to early and late flexion reflexes. With high intensity stimulation the early and late ipsilateral inhibition fused. An early low threshold ipsilateral facilitation occured in 9 patients. The contralateral late facilitation was followed by prolonged inhibition in 10 patients. Changes in presynaptic inhibition were assessed by measuring the heteronymous monosynaptic Ia facilitation from quadriceps to soleus. For methodological reasons, it was only possible to investigate the effect of contralateral conditioning volleys which was performed in 5 patients. A significant and regular reduction of the heteronymous Ia facilitation was found in 4 patients. This reduction is taken to indicate that the FRA evokes presynaptic inhibition of Ia transmission to alpha motoneurones. Presynaptic inhibition was also indicated by the enhancement of a vibratory stimulus induced inhibition in 2 subjects. These results are consistent with the hypothesis that the reflex organization in patients with a spinal cord section is similar to that of the acute spinal cat injected with DOPA.     

Reflex responses evoked in the adrenal sympathetic nerve to electrical stimulation of somatic afferent nerves in the rat

The present study was initiated to determine the role of somatic A (myelinated) and C (unmyelinated) afferent fibers in both responses of increases and decreases in adrenal sympathetic nerve activities during repetitive mechanical pinching and brushing stimulations of the skin in anesthetized rats with central nervous system (CNS) intact. Accordingly, changes in adrenal sympathetic nerve activity resulting from repetitive and single shock electrical stimulation of various spinal afferent nerves, especially the 13th thoracic (Th13) spinal nerve and the sural nerve, were examined in urethane/chloralose-anesthetized rats. Repetitive electrical stimulation of A afferent fibers in Th13 spinal or sural nerve decreased the adrenal nerve activity similarly as brushing stimulation of skin of the lower chest or hindlimb did, while repetitive stimulation of A plus C afferent fibers of those nerves increased the adrenal nerve activity as pinching stimulation of those skins did. Single shock stimulation of spinal afferent nerves evoked various reflex components in the adrenal nerve: an initial depression of spontaneous activity (the early depression); the following reflex discharge due to activation of A afferent fibers (the A-reflex); a subsequent reflex discharge due to activation of C afferent fibers (the C-reflex); and following post-excitatory depressions. These reflexes seem to be mediated mainly via supraspinal pathways since they were abolished by spinal transection at the C1-2 level. Although the supraspinal A- and C-reflexes could be elicited from stimulation of a wide variety of spinal segmental afferent levels, the early depression was more prominent when afferents at spinal segments closer to the level of adrenal nerve outflow were excited. It is suggested that the decreased responses of the adrenal nerve during repetitive electrical stimulation of A afferent nerve fibers are attributable to summation of both the early depression and post-excitatory depression evoked by single shock stimulation, while the increased responses during repetitive stimulation of A plus C afferent fibers are attributable to summation of the C-reflex after single shock stimulation. In spinalized rats, repetitive stimulation of Th13 always increased the adrenal nerve activities regardless of whether A fibers alone or A plus C fibers were stimulated, just as brushing and pinching of the lower chest skin always increased them. The increased responses in spinal animals seem to be related to the fact that single electrical stimuli of Th13 produced A- and C-reflexes of spinal origin without clear depressions.     

The effect of intrathecal galanin on the flexor reflex in rat: increased depression after sciatic nerve section

The effect of intrathecal galanin (GAL) on the hamstring flexor reflex to sural nerve stimulation was compared in rats with intact and unilaterally sectioned sciatic nerves. GAL had a biphasic effect on the flexor reflex in rats with intact nerves, including facilitation, facilitation followed by depression and pure depression, in a dose-dependent manner. In axotomized rats, the depressive effect of GAL was significantly increased, occurring at lower drug concentrations. Furthermore, the degree of depression was significantly stronger with a more rapid onset after nerve section. It is concluded that along with an increase in GAL-like immunoreactivity in primary afferents, the inhibitory function of this neuropeptide is enhanced following axotomy. This functional change may be due to both pre- and postsynaptic mechanisms.     

The brief and the prolonged facilitatory effects of unmyelinated afferent input on the rat spinal cord are independently influenced by peripheral nerve section

Single C-fibre strength stimuli applied to the sciatic nerve in the decerebrate spinal rat evoke three separate bursts of activity in posterior biceps/semitendinosus flexor alpha motorneurones which are associated with the arrival in the spinal cord of volleys in the A-beta, A-delta and C-afferent fibres. Repetitive stimulation of the sciatic nerve at 1 Hz for 20 s generates a progressive wind-up of response and an after-discharge lasting up to 10 s. Twelve to fourteen days after section of the sciatic nerve, stimuli applied central to the section evoke a larger than normal response in the posterior biceps/semitendinosus flexor motorneurones and repetitive stimulation (1 Hz, 20 s) produces an after-discharge which is four times longer than that produced by stimulation of the intact nerve. In addition to the direct excitatory effects of sciatic nerve stimulation on the flexor motorneurones which lasts for seconds, conditioning stimuli to the sciatic nerve at C-fibre strength (1 Hz, 20 s) produce a facilitation of the flexor reflex evoked by a standard pressure stimulus to the ipsilateral and contralateral toes which lasts for 70 min. However, although the direct excitatory effects of stimulating a sectioned sciatic nerve on the posterior biceps/semitendinosus flexor motorneurones are exaggerated, the facilitation of the cutaneous flexion reflex evoked by stimulating sectioned sciatic nerves (1 Hz, 20 s) only lasts for 17 min. These results show that the mechanism which produces the rapid effects of sciatic nerve stimulation on the flexor reflex circuit can be separated from the mechanism which produces the prolonged facilitation.(ABSTRACT TRUNCATED AT 250 WORDS)     

The effects of morphine administered intrathecally on the somatosympathetic reflex discharges in anesthetized cats

The effect of intrathecally applied morphine or naloxone on the sympathetic A and C reflexes evoked by stimulation of somatic myelinated A and unmyelinated C afferent nerves was investigated in anesthetized cats. Intrathecal application of morphine in the lumbar spinal region depressed the C reflex elicited by stimulation of a hindlimb nerve (superficial peroneal, SP) without affecting the C reflex elicited by stimulation of a forelimb nerve (radial, RA). Also, intrathecal application of naloxone in the lumbar spinal region was found to reverse the intravenous morphine-induced depression of the C reflex elicited by stimulation of the SP nerve. The present results suggest that selective depression of morphine on the somatosympathetic C reflex is mediated at the spinal cord level.     

Substance P and calcitonin gene-related peptide synergistically modulate the gain of the nociceptive flexor withdrawal reflex in the rat

A comparison has been made between the effects of intrathecally administered L-glutamate, L-aspartate, substance P and calcitonin gene-related peptide (CGRP) on the excitability of rat flexor alpha-motoneurons activated monosynaptically by Ia afferents and polysynaptically by high mechano-threshold cutaneous afferents. At doses that do not modify the monosynaptic reflex, substance P, CGRP and some factor released from sural C-fibres increase the excitability of the nociceptive flexion reflex for prolonged periods in a multiplicative fashion. The excitatory amino acids have no such action. We suggest that one role for C-afferent neuropeptides is a long-acting gain modulation of nociceptive inputs into the spinal cord.     

Synaptic actions of cutaneous A delta and C fibers on primate hindlimb alpha-motoneurons

Postsynaptic potentials evoked in hindlimb alpha-motoneurons by stimulation of a cutaneous nerve (sural) with finely graded stimulus strengths were analyzed in the primate, monitoring the spinal cord potentials and afferent nerve volleys in the sural nerve. It was observed that activities in A alpha beta, A delta and C fibers of the cutaneous nerve elicited characteristic excitatory and/or inhibitory postsynaptic potentials (EPSPs and/or IPSPs) with different latencies and durations in extensor and flexor motoneurons. Volleys in A delta fibers of the cutaneous nerve produced EPSPs in 57% of flexor and 31% of extensor motoneurons tested, whereas IPSPs were produced by A delta volleys in 41% of flexor and 62% of extensor motoneurons. EPSPs with longer latencies and longer durations were evoked by cutaneous C fiber volleys in 55% of flexor and 34% of extensor motoneurons, whereas IPSPs due to C volleys were recorded in 9% of flexor and 14% of extensor motoneurons. A alpha beta and A delta volleys caused motoneurons to fire in several instances, and some motoneurons discharged repetitively during the depolarizations evoked by activities in C fibers of the nerve. Central latency for transmission in interneuronal chains in the spinal cord was estimated from the onset of the cord potential (N3 wave) to the onset of the postsynaptic potential evoked by A delta volleys. Ranges of central latencies of the EPSPs and IPSPs evoked by A delta volleys were 2.0-7.0 ms and 3.5-8.5 ms, respectively. It is postulated that there may be at least two interneurons interposed in the excitatory reflex pathway from A delta afferent fibers to motoneurons and the A delta inhibitory pathway may involve longer interneuronal chains. In a few motoneurons, however, sural volleys with strengths sufficient to activate A delta fibers produced EPSPs with a central latency of about 1 ms, suggesting activation of a disynaptic segmental pathway with one interposed interneuron. Stimulation of the sural nerve with strengths sufficient to activate cutaneous C fibers produced slow negative cord dorsum potentials with long latencies. It is proposed that primate motoneurons, which show characteristic postsynaptic potentials evoked by cutaneous A delta and C fiber volleys, may provide a suitable model for analyzing the role of high threshold cutaneous afferent fibers not only in the flexor withdrawal reflex but also in motor control functions.     

Effects of hip joint angle changes on intersegmental spinal coupling in human spinal cord injury

Pathological expression of movement and muscle tone in human upper motor neuron disorders has been partly associated with impaired modulation of spinal inhibitory mechanisms, such as reciprocal or presynaptic inhibition. In addition, input from specific afferent systems contributes significantly to spinal reflex circuits coupled with posture or locomotion. Accordingly, the objectives of this study were to identify the involved afferents and their relative contribution to soleus H-reflex modulation induced by changes in hip position, and to relate these effects with activity of spinal interneuronal circuits. Specifically, we investigated the actions of group I synergistic and antagonistic muscle afferents (e.g. common peroneal nerve, CPN; medial gastrocnemius, MG) and tactile plantar cutaneous afferents on the soleus H-reflex during controlled hip angle variations in 11 motor incomplete spinal cord injured (SCI) subjects. It has been postulated in healthy subjects that CPN stimulation evokes an inhibition on the soleus H-reflex at a conditioning test (C-T) interval of 2–4 ms. This short latency reflex depression is caused mainly by activation of the reciprocal Ia inhibitory pathway. At longer C-T intervals (beyond 30 ms) the soleus H-reflex is again depressed, and is generally accepted to be caused by presynaptic inhibition of soleus Ia afferents. Similarly, MG nerve stimulation depresses soleus H-reflex excitability at the C-T interval of 6 ms, involving the pathway of non-reciprocal group I inhibition, while excitation of plantar cutaneous afferents affects the activity of spinal reflex pathways in the extensors. In this study, soleus H-reflexes recorded alone or during CPN stimulation at either short (2, 3, 4 ms) or long (80, 100, 120 ms) C-T intervals, and MG nerve stimulation delivered at 6 ms were elicited via conventional methods and similar to those adopted in studies conducted in healthy subjects. Plantar skin conditioning stimulation was delivered through two surface electrodes placed on the metatarsals at different C-T intervals ranging from 3 to 90 ms. CPN stimulation at either short or long C-T intervals and MG nerve stimulation resulted in a significant facilitation of the soleus H-reflex, regardless of the hip angle tested. Plantar skin stimulation delivered with hip extended at 10° induced a bimodal facilitation reflex pattern, while with hip flexed (10°, 30°) the reflex facilitation increased with increments in the C-T interval. This study provides evidence that in human chronic SCI, classically key inhibitory reflex actions are switched to facilitatory, and that spinal processing of plantar cutaneous sensory input and actions of synergistic/antagonistic muscle afferents interact with hip proprioceptive input to facilitate soleus H-reflex excitability. These actions might be associated with the pathological expression of neural control of movement in individuals with SCI, and potentially could be considered in rehabilitation programs geared to restore sensorimotor function in these patients.     

Effects of a substance P analogue with antagonist properties ([D-Arg1, D-Trp7,9, Leu11]substance P) on spontaneous activity of the adrenal sympathetic nerve and its evoked reflex discharges in response to somatic afferent stimulation

The present study was designed to test the effect of a substance P (SP) antagonist, [D-Arg1, D-Trp7,9, Leu11]substance P (Spantide), on spontaneous efferent activity of adrenal sympathetic nerve and the two A- and C-sympathetic reflex components evoked in adrenal sympathetic nerve by stimulation of myelinated A- and unmyelinated C-afferent nerve fibers of a hindlimb nerve, respectively, in anesthetized rats. The spontaneous adrenal nerve activity and both of the A- and C-sympathetic reflex components were proportionally reduced by intrathecal application of the SP antagonist (0.038-0.76 nmol), although the same doses did not affect A- and C-somatic reflex components. These data suggest that the SP antagonist has a greater effect on SP-containing neurons related to the generation of spontaneous activity of sympathetic neurons and somato-sympathetic reflex pathways than on SP-containing primary somatic afferent nerves and somato-somatic reflex pathways.     

Effect of rhythmic arm movement on reflexes in the legs: modulation of soleus H-reflexes and somatosensory conditioning

During locomotor tasks such as walking, running, and swimming, the arms move rhythmically with the legs. It has been suggested that connections between the cervical and lumbosacral spinal cord may mediate some of this interlimb coordination. However, it is unclear how these interlimb pathways modulate reflex excitability during movement. We hypothesized that rhythmic arm movement would alter the gain of reflex pathways in the stationary leg. Soleus H-reflexes recorded during arm cycling were compared with those recorded at similar positions with the arms stationary. Nerve stimulation was delivered with the right arm at approximately 70 degrees shoulder flexion or 10 degrees shoulder extension. H-reflexes were evoked alone (unconditioned) or with sural or common peroneal nerve (CP) conditioning to decrease or increase soleus IA presynaptic inhibition, respectively. Both conditioning stimuli were also delivered with no H-reflex stimulation. H-reflex amplitudes were compared at similar M-wave amplitudes and activation levels of the soleus. Arm cycling significantly reduced (P < 0.05) unconditioned soleus H-reflexes at shoulder flexion by 21.7% and at shoulder extension by 8.8% compared with static controls. The results demonstrate a task-dependent modulation of soleus H-reflexes between arm cycling and stationary trials. Sural nerve stimulation facilitated H-reflexes at shoulder extension but not at shoulder flexion during static and cycling trials. CP nerve stimulation significantly reduced H-reflex amplitude in all conditions. Reflexes in soleus when sural and CP nerve stimulation were delivered alone, were not different between cycling and static trials; thus the task-dependent change in H reflex amplitude was not due to changes in motoneuron excitability. Therefore modulation occurred at a pre-motoneuronal level, probably by presynaptic inhibition of the IA afferent volley. Results indicate that neural networks coupling the cervical and lumbosacral spinal cord in humans are activated during rhythmic arm movement. It is proposed that activation of these networks may assist in reflex linkages between the arms and legs during locomotor tasks.     

Facilitation of transmission via inhibitory pathway 1a to spinal extensor motoneurons in response to stimulation of the forelimb nerves in cats

Activation of forelimb flexor reflex afferent in cats anesthetized with a mixture of Chloralose and Nembutal evoked temporospatial facilitation in the reciprocal inhibitory pathways to spinal extensor motoneurons. The amplitude of disynaptic reciprocal 1a inhibitory postsynaptic potentials (IPSP) evoked in the extensor motoneurons by activation of the most excitable fibers of the nerve supplying the antagonist muscle increased several-fold using conditioning stimulation of the forelimb nerve. Facilitation of 1a IPSP occurred on a background of IPSP evoked by descending inter-limb discharges. Facilitation of 1a IPSP had a latent period of 18–20 msec and could last to 60 msec. The possible role of inhibitory 1a interneurons in interlimb coordination is discussed. Translated from Rossiiskii Fiziologicheskii Zhurnal imeni I. M. Sechenova, Vol. 85, No. 3, pp. 430–435, March, 1999.     

Long spinal and pyramidal actions on hindlimb motoneurons of the marsupial brush-tailed possum, Trichosurus vulpecula.

The existence of descending propriospinal reflex linkages between forelimbs and hindlimbs has been established in the brush-tailed possum (Trichosurus vulpecula). In animals under chloralose anesthesia and with intact brain stem, forelimb volleys evoked facilitation of flexor and extensor monosynaptic reflexes of both hindlimbs, more pronounced on the ipsilateral side. Powerful inhibition of briefer latency and restricted to ipsilateral flexor digitorum longus (FDL) motoneurons was also brought about by forelimb volleys; at latencies exceeding 20-30 ms, FDL inhibition was usually replaced by facilitation. Distinctness of the two long spinal actions was shown by differences in forelimb receptive fields and in threshold of the executant afferent fibers. The field for reflex inhibition was located distally in the forepaw region, that for facilitation being wider, including deep as well as superficial tissues. Threshold of afferent fibers evoking inhibition was lower than that for facilitation. The descending long spinal actions were compared with those set up by repetitive stimulation of the motor cortex contralateral to the test hindlimb reflexes. In agreement with previous work, strong facilitation of most flexor or extensor motoneurons was produced, including those of quadriceps and ankle flexors, as well as gastrocnemius and hamstring motor nuclei; inhibition consistently appeared only in the FDL motoneuron pool. Weak and inconstant inhibitory action was occasionally observed in other motor pools. Pyramidal tract section abolished the cortical inhibition of FDL, but had little effect on facilitation; both long spinal actions were unchanged. Pyramid-sparing brain stem section greatly reduced both cortical and long spinal facilitatory action, but had little or no effect on FDL inhibition from either source. Interaction experiments demonstrated facilitation of weak inhibitory actions on FDL motoneurons of forelimb and cortical stimulation when elicited together, suggesting a sharing by the two inputs of common interneuronal elements. The observation is consistent with the notion that the long propriospinal system responsible for FDL inhibition from the forepaw might provide the pathway for pyramidal inhibition of the same group of motoneurons.