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PubMed1987

GABAergic modulation of a substance P-mediated reflex of slow time course in the isolated rat spinal cord.

The effects of gamma-aminobutyric acid (GABA) and other drugs which interact with GABA receptors were studied on a reflex of slow time course in the spinal cord preparation isolated from the neonatal rat. A single shock to a dorsal root (L3-L5) elicited a stereotyped series of reflexes, consisting of fast and slow components, recorded from the contralateral ventral root of the corresponding segment. The slow component, i.e. the contralateral slow ventral root potential (v.r.p.) had a time-to-peak of 2-5 s and lasted 20-30 s. Bath-application of GABA (5-20 microM) or muscimol (0.05-0.5 microM) caused a decrease in the amplitude of the contralateral slow v.r.p. without producing any change in the d.c. potential recorded from the ventral root. The monosynaptic reflex recorded from the ipsilateral ventral root was not changed by the drugs at these concentrations. Diazepam (0.1-1 microM) potentiated the depolarizing response of the dorsal root to GABA and markedly depressed the contralateral slow v.r.p. Neither the d.c. potential of the ventral root nor the dorsal root was changed by diazepam. The monosynaptic reflex was also unaffected by the drug. Bicuculline (1 microM) suppressed the GABA-induced depolarization recorded from the dorsal root whilst it markedly potentiated the contralateral slow v.r.p. Baclofen at concentrations from 0.01 to 0.1 microM reduced the contralateral slow v.r.p. The inhibitory action of baclofen on the contralateral slow v.r.p. was more marked than on the monosynaptic reflex. 7 The depolarization of the ventral root induced by a brief application of substance P (SP) was depressed by muscimol, diazepam and baclofen, whereas the depolarization was potentiated by bicuculline. 8 The present results suggest that an intraspinal GABAergic inhibitory mechanism plays a role in the modulation of certain slow spinal reflexes. They also support the hypothesis that SP released from certain primary afferent fibres is a neurotransmitter involved in the contralateral slow v.r.p.

Animals↗
PubMed1988

Temperature-dependence of reflex transmission in the neonatal rat spinal cord, in vitro: influence on strychnine- and bicuculline-sensitive inhibition.

The amplitude, latency and rise time of the monosynaptic reflex, recorded from the spinal cord of the neonatal rat in vitro, was temperature-dependent with optimal conditions occurring at 25 degrees C. The reflex was inhibited when conditioning stimuli were applied to an adjacent dorsal root at 1-150 msec before the monosynaptic reflex was evoked; the inhibition had both an early and a late phase. The early phase of inhibition occurred at conditioning-test intervals of 1-20 msec with peak inhibition occurring at 7 msec. Raising the temperature of the bath to 31 degrees C or exposing the cord to strychnine blocked the early phase of inhibition. The late phase of inhibition occurred at conditioning-test intervals greater than 20 msec, was unaffected by temperature and was blocked by bicuculline. The early phase of inhibition therefore appears to be postsynaptic in origin and mediated by glycine while the late component of inhibition may be presynaptic in origin and mediated by gamma-aminobutyric acid (GABA).

Animals↗
PubMed1976

Reflex effects and postsynaptic membrane potential changes during epileptiform activity induced by penicillin in decapitate spinal cords.

The administration of a convulsant dose of penicillin enhanced the transmission of monosynaptic reflexes in spinal cords in which reflex transmission was feeble before the drug treatment, but it had little effect in cords where monosynaptic reflexes were powerful to begin with. Post-tetanic potentiation was not altered by penicillin. Polysynaptic reflexes were invariably enhanced by convulsant amounts of penicillin. Postsynaptic ("direct") inhibition was not affected in the seizure-free intervals in spinal cords treated with penicillin, but it seemed to be suppressed during tonic seizures. The disability of reflex inhibition during ictal discharges may be due to presynaptic depolarization of inhibitory terminals. Recurrent inhibition was partially suppressed in spinal cords treated with penicillin. Neurons in the dorsal and intermediate gray matter were sometimes excited, sometimes inhibited, and sometimes unaffected by seizure activity of their segment. Motoneurons in the ventral horns invariably participated in the interictal and ictal activity. The timing of clonic seizure sequences coincided with bursts of Renshaw cell discharges. Action potential of abnormal amplitude and configuration were frequently observed in convulsing motoneurons. Paroxysmal depolarizing shifts (PDSs) of motoneurons were similar to those observed by other investigators in neurons in experimental epileptic foci of the cerebral cortex, except that spinal PDSs were not followed by hyperpolarizing waves.

Animals↗
PubMed1994

The effects of intrathecal neuropeptide Y on the spinal nociceptive flexor reflex in rats with intact sciatic nerves and after peripheral axotomy.

We examined the effects of intrathecally administered neuropeptide Y on the spinal nociceptive flexor reflex in decerebrate, spinalized, unanesthetized rats with intact sciatic nerves, or 11-39 days after unilateral transection of the sciatic nerve. In rats with intact sciatic nerve, intrathecal neuropeptide Y at low doses (10 and 100 ng) caused a brief facilitation of the flexor reflex. At a dose of 300 ng, the effect of neuropeptide Y on the flexor reflex was biphasic, i.e. a brief facilitation followed by slight depression. At higher doses (1 and 10 micrograms), the effect of neuropeptide Y was mainly inhibitory, causing substantial and usually prolonged depression of the flexor reflex magnitude. The reflex depression caused by intrathecal neuropeptide Y was not reversed by the opioid antagonist naloxone or the alpha 2 adrenoceptor antagonist atipamezole. Intrathecal neuropeptide Y at doses up to 1 and 10 micrograms had no effect on reflex facilitation caused by conditioning stimulation of C-fibers, intrathecal substance P or neurokinin A. Topical application of neuropeptide Y (1 microgram/microliter) failed to influence the monosynaptic reflex in normal rats. Eleven to 16 days after peripheral axotomy, the initial excitation of the flexor reflex to intrathecal neuropeptide Y was significantly enhanced in axotomized compared with normal rats. However, the depressive effect of neuropeptide Y on the flexor reflex was unchanged. Neuropeptide Y did not influence the monosynaptic reflex in axotomized rats at this period. In experiments performed on rats in which the sciatic nerve had been transected 31-39 days previously, the facilitatory effect of neuropeptide Y on the flexor reflex remained enhanced compared with normal rats. Furthermore, the inhibitory effect of neuropeptide Y also increased as 100 ng intrathecal neuropeptide Y was able to produce reflex depression in a similar fashion as 300 ng neuropeptide Y normally and the reflex depression caused by 1 microgram neuropeptide Y was stronger and longer lasting than in normal rats. Intrathecal neuropeptide Y (100 ng-10 micrograms) in rats with intact sciatic nerves caused a moderate decrease in spinal cord dorsal surface blood flow as measured with a laser Doppler flowmeter. This effect of neuropeptide Y was unchanged in axotomized rats. The present results support previous observations that spinal application of neuropeptide Y in normal rats caused antinociception. As the depressive effect of neuropeptide Y is independent of spinal opioid and alpha 2-adrenergic systems, it may be mediated by its own receptors.(ABSTRACT TRUNCATED AT 400 WORDS)

Animals↗
PubMed1991

Monosynaptic Interjoint Reflexes and their Central Modulation During Fictive Locomotion in Crayfish.

An in vitro preparation of the crayfish nervous system has been utilized to study an interjoint reflex pathway and its variability during rhythmic locomotor activity. The coxo-basal chordotonal organ (CBCO) is a joint stretch receptor spanning the second joint of walking legs in crayfish, where it encodes joint movements and position. Mechanical stimulation (stretch and release) of the CBCO and electrical stimulation of the CBCO nerve elicits reflex responses in promotor and remotor motor neurons innervating muscles moving the basal thoraco-coxal (TC) leg joint. Promotor and remotor motor neurons receive monosynaptic excitatory inputs from at least four CBCO afferents, including both stretch- and release-sensitive CBCO afferents. In a tonic preparation, in which there is no tendency to produce alternating bursts of activity in antagonistic motor neurons, the reflex responses were evoked during each cycle of imposed movement. However, when the preparation became rhythmic and produced bouts of fictive locomotion, the reflex responses were unstable and their gain was phasically modulated. Paired recordings indicate that such a modulation of the monosynaptic interjoint reflex could be due to both a phasic change in the excitability of the motor neurons and presynaptic inhibition that reduces the excitatory input from CBCO primary afferents.

Journal Article↗
PubMed1985

Stance and gait perturbations in children: developmental aspects of compensatory mechanisms.

The leg muscle EMG responses following perturbations during stance and gait were analysed in children between 1 and 8 years of age in order to study the development of those reflex systems responsible for the compensatory movements necessary to maintain body equilibrium. Single monosynaptic reflex potentials followed by a long-lasting (about 500 msec) polysynaptic gastrocnemius EMG response, along with coactivation of all antagonistic leg muscles, were characteristic of the EMG reactions following a treadmill acceleration impulse in early infancy. From 4 years of age on, the monosynaptic reflex potentials disappeared when perturbations were induced during gait. In addition, the polysynaptic reflex response became shorter (about 100 msec) and a reciprocal mode of leg muscle activation occurred, with a consequently more rapid and effective compensation of perturbation impulses. In older children with a disorder of the motor system acquired at an early age, a partial persistence of the immature motor responses could be observed, irrespective of whether the impairment was a cerebral lesion or a muscular dystrophy. It is concluded that the coactivation pattern is due to the immaturity of those nervous structures mediating afferent information necessary for the control of bipedal stance and gait. Furthermore, the existence of mutual inhibition of monosynaptic and polysynaptic spinal reflex responses, dependent on the function of supraspinal motor centres, can be assumed.

Cerebral Palsy↗
PubMed1983

The effect of transection and cold block of the spinal cord on synaptic transmission between Ia afferents and motoneurones.

Composite excitatory postsynaptic potentials were elicited in lumbar motoneurones by Ia afferents from muscles of the triceps surae group. These excitatory postsynaptic potentials were examined in the same cell before, during and after interruption of descending spinal pathways. After transection or cold block of the spinal cord at T12-T13, the amplitude of composite excitatory postsynaptic potentials showed no significant change for a period of up to seven hours after transection. However, there was a reduction in amplitude of the monosynaptic reflex in the extensor motoneurones which may be due to an observed hyperpolarization and reduction in membrane time constant in these neurones. The reduction in amplitude of the monosynaptic reflex observed in spinal shock can be attributed to the effects of these changes, rather than to a decrease in the size of the monosynaptic excitatory postsynaptic potential.

Afferent Pathways↗
PubMedDate not supplied

Birth hypoxia and spinal reflex in newborn babies.

Birth hypoxia is detrimental to neuronal function. In this study, its effect on spinal monosynaptic reflex was investigated on two different age groups of human newborn babies using few non-invasive electrophysiological parameters. A total of 57 newborns (25 hypoxic + 32 non-hypoxic) were the study subject. Out of which, 31 newborns (11 hypoxic + 20 non-hypoxic) were examined within 48 hours of birth, and the rest 26 (14 hypoxic + 12 non-hypoxic) were examined between 48h and 120h (five days) of birth. H-reflex latency (HRL), distal motor latency (DL), and H-reflex conduction velocity (HRCV), were estimated for understanding the transmission of impulse in the monosynaptic reflex pathway. Moreover, Hmax, Mmax, and H/M ratio were observed for studying the spinal motor neuronal excitability. The injurious effect of hypoxia was detected on HRL, HRCV, Hmax and H/M ratio in babies who were examined within 48h of birth. The HRL was significantly increased and other parameters were significantly reduced. In the older group of babies, however, Hmax was the only parameter affected by hypoxia. The relatively older babies of hypoxic or non-hypoxic group had higher Hmax and H/M ratio compared to younger ones of their own group.

Action Potentials↗
PubMed1959

Recurrent facilitation of spinal reflexes.

Antidromic volleys in muscle nerves may facilitate monosynaptic reflexes originating from neighboring motoneurons. This facilitation has been studied in spinal cats. It is at its peak with a conditioning-test interval of 20 to 30 msec., and can last 50 to 100 msec. The threshold of facilitation is about the same as that of recurrent inhibition. Both phenomena appear to be activated by stimulation of the large motor axons. The latency of facilitation seems to be longer than that of recurrent inhibition by approximately 1 msec., suggesting the presence of at least one more synaptic delay. Facilitation often follows an inhibition of variable depth and duration. Frequently, however, the facilitation is not preceded by inhibition, and therefore it cannot be a rebound effect. The pharmacological properties of facilitation resemble those of recurrent inhibition. Dihydro-beta-erythroidine(1) partially blocks facilitation; the peak is decreased and occurs earlier, and the duration is shortened. Eserine increases the duration of facilitation and inhibition and sometimes enhances their magnitude. It is concluded that recurrent facilitation is mediated by the cholinergic axon collaterals, and that at least two interneurons are located between collateral and motoneuron. Possible mechanisms of facilitation are discussed.

Animals↗
PubMedDate not supplied

Physiologic loading of the anterior cruciate ligament does not activate quadriceps or hamstrings in the anesthetized cat.

We attempted to elicit quadriceps and hamstring electromyographic responses in seven chloralose-anesthetized cats by loading the ACL with controlled anterior displacement of the tibia on the femur using rigid fixation and an MTS testing machine. We did not detect reflex activity in the quadriceps or hamstring muscles of any of the cats in response to anterior tibial displacements of up to 4 mm, with rise times ranging from 1.0 to 0.1 seconds. In four of the cats we loaded the ACL using a wire loop. Loads of up to 125 N (4 to 5 times body weight) produced no reflex activity in any of the four animals, although we consistently observed monosynaptic reflex responses to tendon taps. Whole nerve recordings from the posterior articular nerve revealed substantial activity from afferents in response to tugging on the ACL, although we could not differentiate receptors in the ACL from those in other periarticular tissues. Thus, while traction on the intact ACL causes signals in the afferent nerves, those signals are not translated into direct monosynaptic reflexes.

Animals↗
PubMed1992

[Effects of tizanidine, a central muscle relaxant, upon spinal reflexes].

Effects of intravenous administration of tizanidine upon spinal reflexes were studied in cats anesthetized with urethane-chloralose. Both extensor and flexor monosynaptic reflexes and polysynaptic flexor reflex were inhibited by intravenous administration of tizanidine in a dose of 10-50 micrograms.kg-1. The inhibition was dose-dependent. After strychnine administration, polysynaptic flexor reflex was augmented, but the inhibition by tizanidine administration was unaffected. In spinal cats, inhibitory effect of tizanidine upon monosynaptic reflex was weaker than in intact cats. Viscero-intercostal reflex elicited by electrical stimulation of A delta afferent fibers in the greater splanchnic nerve was also inhibited by intravenous tizanidine (25 micrograms.kg-1). The degree of inhibition decreased in parallel with increase in the intensity of stimulus applied to the greater splanchnic nerve.

Animals↗
PubMed1999

Effects of intrathecal clonidine injection on spinal reflexes and human locomotion in incomplete paraplegic subjects.

We studied the effect of the intrathecal (i.t.) injection of clonidine (30, 60 and 90 microg) on the polysynaptic spinal reflexes (PSR) elicited by electrical stimulation of flexor reflex afferents (FRA), monosynaptic reflex and gait of 11 subjects with spinal cord injuries. The effect of clonidine administration on gait velocity, stride amplitude and duration was measured in eight subjects who were able to walk. Five subjects were able to walk after intrathecal injection of clonidine and three were not able to stand up. Three subjects improved their gait velocity after clonidine administration; one (S6) increased his stride amplitude; the two others decreased their cycle durations. The tibialis anterior seemed to be more regularly activated during gait. Spasticity was reduced dramatically (P<0.0001) after i.t. clonidine injection, but there was no statistically significant difference in the soleus H reflex (no effect on Hmax/Mmax). Clonidine administration decreased the amplitude of the early PSR (90-120 ms, N=4) and the threshold and maximal integrated EMG corresponding to the late response (140-450 ms, N=7). This effect was dose dependent (30, 60 and 90 microg). Placebo injection (N=4) caused no change. The changes in spinal reflexes, with a large reduction in spasticity, no change in motoneurone excitability and a large decrease in PSR, suggest that clonidine acts at a premotoneuronal level, possibly by presynaptic inhibition of group II fibres. The increase in gait velocity in three subjects could have been due to reduced spasticity or activation of spinal circuitry.

Adrenergic alpha-Agonists↗
PubMedDate not supplied

H reflex amplitude. Effect of leg muscle activity.

The H reflex is a monosynaptic reflex whose latency can be used to evaluate pathology of the S1 nerve root and axon. Little has been written about the use of the H reflex amplitude in evaluating S1 nerve root and axon. Little has been written about the use of the H reflex amplitude in evaluating S1 nerve physiology. Although amplitude measurement of evoked potentials is useful in the evaluation of other sensory and compound muscle action potentials, this single case study shows it to be an unreliable parameter with which to evaluate the integrity of S1 nerve fibers, because muscle activity in antagonist and agonist affects the amplitude and in some instances abolishes it.

Action Potentials↗