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PubMed1986

Paradoxical changes in spinal cord reflexes following the acute administration of acrylamide.

Acrylamide (ACR) produces a central-peripheral distal axonopathy when administered chronically. This is characterized functionally by decreases in the monosynaptic reflex (MSR) and dorsal root potential (DRP) and alterations in the characteristics of the dorsal root reflex (DRR). Acute administration of ACR inhibits the oxidative enzyme complex NADH-tetrazolium reductase and slows retrograde axoplasmic transport. This study was carried out to determine if the spinal cord reflexes are also affected following acute administration of ACR. Dose-response studies revealed a dose-dependent increase in both the MSR and DRR. A single injection of 50 mg/kg ACR caused an increase in both the MSR and DRR within 15 min and continued for over 3 h. These data are paradoxical since chronic administration of ACR results in decreased function. Two possible mechanisms are proposed. First, calcium ion regulation may be involved in both the acute and chronic effects of ACR on spinal cord reflexes. Second, a depolarization of the neurons is occurring just prior to cell injury or death.

Acrylamide↗
PubMed1986

Inhibitory effects of galanin on the isolated spinal cord of the newborn rat.

The effects of galanin, a 29-amino-acid peptide, on spinal reflexes were studied. In the isolated hemisected spinal cord of the newborn rat, galanin (0.1-5 microM) depressed the monosynaptic reflex that was induced by dorsal root stimulation and recorded from the corresponding ventral root. In the isolated spinal cord-tail preparation of the newborn rat, galanin (0.3-0.6 microM) depressed the nociceptive reflex that was induced by application of capsaicin to the tail and recorded from a lumbar ventral root. In both preparations the inhibitory effects of galanin were reversible and the full recovery of the reflexes was observed within 3-20 min after removal of the peptide. The mechanisms of action of galanin on the spinal reflexes and the physiological role of the peptide in the spinal cord are discussed.

Animals↗
PubMed1987

Effects of antihistamines on the spinal reflex in rats.

The effect of antihistamines on the spinal reflex in rats was studied. When H1-blocking agents such as pyrilamine, promethazine and diphenhydramine were given intravenously, both monosynaptic reflex (MSR) and polysynaptic reflex potentials (PSR) were inhibited in a dose-dependent fashion without affecting the dorsal root reflex and dorsal root-dorsal root potential. The extent of suppression of the MSR and PSR measured in spinal rats was smaller than that of intact rats. When H1-blocking agents (0.25-5.0 nmol) were applied by intraspinal microinjection close to the motoneuron, the MSR and PSR were depressed dose-dependently. Simultaneous application of carbachol partially blocked the inhibitory effects of H1-blocking agents induced by intraspinal microinjection. Also, the motoneuron discharges evoked by microinjection of glutamic acid or acetylcholine were depressed by simultaneous administration of any of H1-blocking agents tested. However, H2-blocking agents, such as cimetidine and ranitidine, given either intravenously or intraspinally had a scarcely measurable effect on the spinal reflex. The depression of H1-blocking agents on the spinal reflex is due to a direct inhibition of the motoneuron on the one hand. On the other hand, there is also an involvement of higher centers in the central nervous system increasing potential depression.

Animals↗
PubMed1980

[Effect of stimulation of the locus coeruleus and adjacent portions of the brain stem on inhibition of segmental reflexes].

Rhythmic stimulation of locus coeruleus and neighbouring regions of the pontine reticular formation diminished the inhibitory action from high-threshold spinal cutaneous and muscular afferents on the extensor monosynaptic reflex in anesthetized decerebellized cats. After preliminary reserpine treatment the effects evoked by locus coeruleus stimulation were selectively depressed while those from neighbouring regions of the brain stem remained unchanged. A selective depression of the effect in a reserpine treated animals suggests the monoaminergic nature of the effect.

Animals↗
PubMed1974

The modification of lumbar motoneurone excitability by stimulation of a putative 5-hydroxytryptamine pathway.

1 Changes in lumbar motoneurone excitability were monitored by recording spinal reflex activity from the ventral roots of rats anaesthetized with fluothane.2 Electrical stimulation of nucleus raphes medianus increased the amplitude of the monosynaptic reflex via a pathway having a slow conduction velocity. Stimulation elsewhere in the lower brain stem was less effective. This increase in motoneurone excitability was potentiated by the intravenous injection of L-tryptophan and reduced by intravenous injections of lysergic acid diethylamide (LSD), methysergide or Cinanserin.3 Extracellular field potential responses to stimulation of dorsal or ventral roots were recorded with six barrelled microiontophoresis electrodes. Stimulation of nucleus raphes medianus and iontophoretic application of 5-hydroxytryptamine (5-HT) both increased the excitability of lumbar motoneurones as reflected by an increase in field potential amplitude.4 Responses to both stimulation of raphe nuclei and iontophoretic application of 5-HT were reduced by iontophoretic application of Cinanserin and methysergide.5 The similarities of the responses of lumbar motoneurones to applied 5-HT and activity within the raphe-spinal pathway are discussed. It is suggested that activity within the raphe-spinal pathway can increase lumbar motoneurone excitability via the release of 5-HT in the ventral horn of the spinal cord.

Animals↗
PubMed1991

Amphetamine-antagonistic properties of 4-phenyl-1,2,3,4- tetrahydroisoquinoline: inhibition of spinal reflex-enhancing effects of methamphetamine, phenylethylamine and nomifensine.

The antagonistic effects of 4-phenyl-1,2,3,4-tetrahydroisoquinoline (4PTIQ) against S(+)-methamphetamine, phenylethylamine and nomifensine were studied by measurement of spinal monosynaptic reflex potential (MSR). S(+)-Methamphetamine, phenylethylamine and nomifensine enhanced the amplitude of MSR in C1-spinalized rats through release of noradrenaline from the terminals of descending fibers and consequent activation of alpha 1-adrenoceptors. Although 4PTIQ alone did not change the amplitude of the MSR, 4PTIQ inhibited the enhancement of MSR induced by S(+)-methamphetamine and related compounds. The MSR of rats with an intact spinal cord was enhanced by conditioning stimulation of the ipsilateral locus ceruleus. The MSR enhancement produced by the stimulation was blocked by prazosin but unaffected by 4PTIQ, showing that 4PTIQ does not have an alpha 1-blocking action. These results suggest that the antagonistic effects of 4PTIQ on MSR enhancement by S(+)-methamphetamine, phenylethylamine and nomifensine are due to its blocking of noradrenaline release produced by these amphetamine-like agents.

Amphetamine↗
PubMed1978

[Effects of psychotropic drugs on the spinal ventral root reflexes in cats. A comparison of the depressant actions in intact and spinal preparations (author's transl)].

Effects of the typical psychotropic drugs such as neuroleptics, tricyclic antidepressants and benzodiazepines on the monosynaptic reflex (MSR) and polysynaptic reflex (PSR) were investigated using intact and spinal cats. Drugs used were chlorpromazine, levomepromazine, perphenazine, prochlorperazine, droperidol, haloperidol, amitriptyline, imipramine, diazepam and flurazepam. Neuroleptics depressed the ventral root reflexes markedly to slightly in both preparations. The inhibitory effects of these drugs on MSR of intact cats were stronger than those on MSR of spinal cats, and the activity was slightly higher than that of PSR depression in intact preparations. In intact cats, those depressants effects of neuroleptics on PSR produced various characteristic action patterns in comparison with MSR inhibition. Tricyclic antidepressants were similar in the mode of action to the dimethylamino side-chain groups in phenothiazines, but the inhibitory effects of ventral root reflexes were distinctly weaker than that of neuroleptics. Benzodiazepines depressed only PSR without MSR inhibition, especially in spinal cats. Thus, it is suggested that the structure-activity relationship considered, a classification of the psychotropic drugs can be given according to the inhibitory activities on spinal ventral root reflexes in intact and spinal cats.

Action Potentials↗
PubMed1990

Depression of the flexor reflex by systemic morphine increases in chronically spinalized rats.

The effect of i.v. morphine on the spinal nociceptive flexor reflex was examined in decerebrate, unanesthetized rats in which the spinal cord was acutely or chronically transected. In acutely spinalized rats i.v. morphine dose dependently depressed the flexor reflex with an ED50 of 1.4 mg/kg. In rats in which the spinal cord was transected 1-3 days prior to the electrophysiological experiments, i.v. morphine had a similar depressive effect (ED50 = 1.1 mg/kg). However, 4-6 days after spinalization there was a 4-fold increase in morphine's depressive effect (ED50 = 0.35 mg/kg). The sensitivity to morphine was further increased 7-10 days post-spinalization with ED50 of 0.17 mg/kg. This supersensitivity was maintained up to 30-60 days. The reflex depression caused by morphine in both acutely and chronically spinalized rats could be reversed by naloxone. Morphine i.v. did not influence the monosynaptic reflex in either acutely or chronically spinalized rats. The present results support the clinical finding that patients with spinal lesions have an increased sensitivity to the antinociceptive and reflex depressive effects of systemic and intrathecal morphine.

Animals↗
PubMed1983

The afferent volleys responsible for spinal proprioceptive reflexes in man.

1. To define the neural volleys responsible for the Achilles tendon jerk and the H reflex, muscle afferent activity was recorded using micro-electrodes inserted percutaneously into appropriate fascicles of the tibial nerve in the popliteal fossa.2. The response of soleus muscle afferents to tendon percussion consisted of a dispersed volley, starting 3.5-7.0 ms after percussion, increasing to a peak over 6.5-11.0 ms, and lasting 25-30 ms, depending on the strength of percussion. Electrical stimuli to the sciatic nerve at a level adequate to evoke an H reflex but subthreshold for the M wave produced a more synchronized volley, the fastest fibres of which had conduction velocities of 62-67 m/s, and the slowest 36-45 m/s.3. The wave of acceleration produced by percussion subthreshold for the ankle jerk spread along the skin at over 150 m/s. Midway between the bellies of the gastrocnemii it consisted of a damped oscillation with four to five separate phases and maximum amplitude approximately one-twentieth of that recorded on the Achilles tendon.4. With ten primary spindle endings, tendon percussion subthreshold for the ankle jerk elicited two to five spike discharges per tap, the shortest interspike intervals being 4-7 ms. Tendon percussion elicited single discharges from two Golgi tendon organs, and altered the discharge pattern of a single secondary spindle ending. The degree of dispersion of the multi-unit muscle afferent volley can be explained by the pattern of discharge of primary spindle endings.5. Percussion on the Achilles tendon evoked crisp afferent volleys in recordings from nerve fascicles innervating flexor hallucis longus, tibialis posterior, the intrinsic muscles of the foot and the skin of the foot. Electrical stimuli delivered to the tibial nerve in the popliteal fossa at a level sufficient for the H reflex of soleus produced either a volley in muscle afferents from the intrinsic muscles of the foot or a volley in cutaneous afferents from the foot.6. For comparable stimuli in the two positions, the H reflex was inhibited but the Achilles tendon jerk enhanced when the ankle was dorsiflexed from 105 degrees to 90 degrees .7. The duration of the rise times of the excitatory post-synaptic potentials (e.p.s.p.s) produced in soleus motoneurones by electrical stimulation, and by tendon percussion subthreshold for the H reflex and the ankle jerk respectively, was estimated from post-stimulus time histograms of the discharge of voluntarily activated single motor units in soleus. The mean e.p.s.p. rise times were 1.9 ms for electrical stimulation and 6.6 ms for tendon percussion. There was evidence that the duration of the electrically evoked e.p.s.p. was curtailed by an inhibitory post-synaptic potential (i.p.s.p.) of only slightly longer latency than the e.p.s.p.8. The mechanically induced and electrically induced afferent volleys are not homogeneous volleys in group I a afferents from triceps surae. The afferent volleys differ in so many respects that it is probably invalid to compare the H reflex and tendon jerk as a measure of fusimotor activity. It is suggested that neither reflex can be considered a purely monosynaptic reflex.

Achilles Tendon↗
PubMed2001

Gait disorder in spasticity and Parkinson's disease.

The central programming, timing, and reciprocal mode of leg muscle activation during gait are basically intact in patients with spastic paresis. Exaggerated monosynaptic reflexes are associated with a loss of the functionally essential polysynaptic reflex mechanisms, both being dependent on supraspinal control. When this control is either not yet matured (small children) or impaired (spastic paresis), inhibition of monosynaptic stretch reflexes is missing in combination with a reduced facilitation of polysynaptic reflexes. A spinal or cerebral lesion associated with paresis is followed by a transformation of motor units (and most probably shortening of muscle fibers leading to muscle contracture), such that tension development in the muscle occurs in a simpler fashion. Calf muscle tension during gait is normally determined by modulated gastrocnemius or soleus EMG activity. In the spastic leg, calf muscle tension is associated with the stretching of the tonically activated muscle. This regulation of muscle tension at a lower level is efficient insofar as it enables the patient to support body weight during gait. Consequently, physiotherapeutic approaches should be applied primarily and antispastic drug therapy secondarily in mobile patients; whereas antispastic drugs may relieve muscle spasms and improve nursing care in immobilized patients.

Cerebral Palsy↗
PubMed1990

Persistence of renal nerve and spinal reflex activities and visceral motility after asphyxial anoxia.

Phrenic and renal nerves activities, spinal reflex (knee jerk and the evoked monosynaptic reflex response from the 5th lumbar ventral root), motility of the stomach, duodenum, jejunum and colon, and motility of urinary bladder during and after the lethal asphyxia were studied in cats under intraperitoneal urethane (400 mg/kg) and chloralose (40 mg/kg) anesthesia. Asphyxial anoxia produced one or two peaks of elevation of systemic arterial pressure (SAP) followed by a progressive decrease of SAP and narrowing of pulse pressure and eventual complete cardiovascular arrest. The phrenic nerve activity increased markedly during the final asphyxial SAP elevation; it then decreased along with the decline of SAP and ceased permanently when the SAP reached about 50 mmHg. The renal nerve activity increased along with each phase of pressure elevation. During the terminal stage of progressive SAP fall, the renal nerve activity fluctuated up and down 2-3 times before the SAP dropped to zero, and the activity persisted for an average of 202 sec thereafter. Data suggest that the motoneurons of the phrenic nerve in the cervical spinal cord and medulla oblongata are more vulnerable to asphyxia than the motoneurons responsible for the spinal reflex in the pathway from medulla, the intermediolateral column of the spinal cord and the celiac ganglion. During anoxia, the lumbar spinal reflex showed an initial inhibition then potentiation afterward. Even after the SAP had reached zero, the spinal reflex could still be elicited for one to a few minutes. This suggests that the spinal cord can function sometime after complete cardiac arrest subsequent to asphyxia. The motility of the stomach, duodenum, jejunum, colon and urinary bladder usually decreased during the period of pressure elevation. However, the activity was enhanced during the terminal stage of pressure decline. The enhancement of the colon and bladder motility, spasmodic in nature, was particularly prominent, more so than the others. After complete cardiovascular arrest, the motility of the above viscera became temporary quiescent but about 10 minutes later, it resumed activity again with an enhancement of action in some of the animals. The motility, persisted from few minutes to over six hours. These phenomena indicate that despite a complete deprivation of circulatory and respiratory supports, or death of the animal, the viscera can still contract for a certain period of time.

Animals↗
PubMed1980

Physiological development of a monosynaptic connection involved in an adult insect behavior.

Locust flight is an exclusively adult behavior whose neural basis has been extensively studied. The coordinated neural pattern underlying this behavior appears rapidly at the end of postembryonic development. This paper examines the ontogeny of elements of the nervous system involved in the behavior. Alternative extreme hypotheses are: 1) the neurons and synapses involved develop concomitant with the behavior, or 2) they are constructed early in development, and are activated at the appropriate time by, for example, the release of inhibition. These hypotheses were evaluated by selecting a synapse that is important in adult flight, and monitoring its physiological features during postembryonic development. The synapse between the forewing Stretch Receptor (SR) and the First Basalar (BA) motor neuron, two uniquely identified neurons, mediates a monosynaptic reflex which operates only in flight. The EPSP, initiated by SR in BA, was recorded intracellularly during the last four of six postembryonic instars. As early as third instar, the monosynaptic EPSP is present and appears to be as effective as in the adult. It also decrements and summates similarly in younger animals and adults. Therefore, some flight system synapses are present and effective throughout most of postembryonic development, and thus do not develop concomitant with the behavior.

Animals↗
PubMed1998

Prolonged GABA(B) receptor-mediated synaptic inhibition in the cat spinal cord: an in vivo study.

In pentobarbitone-anaesthetised spinal cats, a comparison was made of the effects of intravenous bicuculline hydrochloride, a GABA(A)-receptor antagonist, and several (-)-baclofen (GABA(B)-receptor) antagonists (CGP 35348, 4638 , 56999A) on the prolonged inhibition of extensor-muscle monosynaptic reflexes, recorded from lumbar ventral roots, by brief or continuous tetanic stimulation of low-threshold afferent fibres of hindlimb flexor muscles. Two components of brief tetanus inhibition were detected. Whilst possibly of similar central latency, the inhibition associated with GABA(B) receptors had a longer time course than that reduced by bicuculline. Furthermore, whereas bicuculline reduced primary afferent depolarization, generated by the inhibitory volleys, and detected as dorsal-root potentials, such potentials were generally enhanced by intravenous baclofen antagonists. The inhibition of reflexes during and after continuous (333 Hz) tetanic flexor-nerve stimulation appeared to be predominantly associated with the activation of GABA(B) receptors. In the period following continuous tetanic flexor-nerve stimulation, during which monosynaptic extensor reflexes were reduced in amplitude, the action potentials of the intraspinal terminations of extensor-muscle group-Ia afferent fibres were reduced in duration, as detected by the time course of the recovery of the threshold to extracellular microstimulation following the arrival of an orthodromic impulse. A reduction in termination action-potential duration also accompanied the reduction by microelectrophoretic (-)-baclofen of the release of excitatory transmitter from group-Ia terminations, both presynaptic effects being blocked by microelectrophoretic baclofen antagonists. However, the reduction of the duration of the action potential of individual group-Ia terminations, which followed continuous flexor-nerve stimulation, was not sensitive to the baclofen antagonist CGP 55845A, but was diminished by bicuculline methochloride. Intravenously administered bicuculline hydrochloride, however, had little or no effect on the inhibition of reflexes following continuous flexor-nerve stimulation. These observations are discussed in the context of possible intraspinal pathways and pre- and postsynaptic mechanisms for GABA(A) and GABA(B) receptor-mediated inhibition of the monosynaptic excitation of spinal motoneurones and of the functional significance of central GABA(B) receptor-associated inhibitory processes, given the relatively minimal effects on motor activity and behaviour produced by baclofen antagonists that penetrate the mammalian blood-brain barrier.

Animals↗
PubMed1992

In vitro studies of prolonged synaptic depression in the neonatal rat spinal cord.

1. Synaptic transmission between dorsal root afferents and alpha-motoneurones was studied in the in vitro hemisected spinal cord preparation isolated from neonatal rats. 2. Repetitive stimulation of the dorsal roots depressed the monosynaptic reflex recorded from the homologous ventral roots. The depression developed within the first five to six pulses in a stimulus train and stabilized at a plateau-like level for many seconds of stimulation. 3. The magnitude of the reflex depression depended on the stimulation interval and was capable of reducing the reflex to 17% of its undepressed control during 5 Hz stimulus trains. Complete recovery from depression was obtained at stimulation intervals greater than or equal to 30 s. 4. Monosynaptic excitatory postsynaptic potentials (EPSPs) were recorded intracellularly after reduction of the activity in polysynaptic pathways by addition of mephenesin to the bathing media. These EPSPs exhibited a prolonged, frequency-dependent synaptic depression. The depression reduced the amplitude of the EPSP to 25% of the undepressed control during 5 Hz stimulus trains, and was alleviated completely at stimulus interval greater than or equal to 60 s. 5. The prolonged EPSP depression was not altered by blockade of glycinergic and type-A gamma-aminobutyric acid (GABAA-ergic) receptors underlying postsynaptic inhibition in the spinal cord. Injection of current steps to motoneurones before and during the prolonged depression revealed similar values of the membrane time constant and input resistance. These excluded changes in the passive properties of the motoneurone membrane as an explanation for the observed synaptic depression. 6. Extracellular recordings of terminal potentials and their accompanying synaptic fields from motor nuclei in the ventrolateral cord revealed that the frequency-dependent depression in the synaptic fields was not preceded by any detectable changes in the amplitude or the shape of the terminal potential, suggesting that the depression cannot be attributed to impairment of action potential invasion to the afferent terminals. 7. Reduction of the basic level of transmitter release in the spinal cord by increasing the Mg2+/Ca2+ ratio of the bathing solution or by application of 2 microM of L(-)baclofen markedly diminished the synaptic potential depression at all the stimulation intervals tested in this study. Recovery from depression was evident for stimulation intervals greater than or equal to 5 s. Under these conditions, short tetanic trains (5 pulses at 25 Hz) revealed a substantial facilitation and potentiation of the EPSPs. 8. We suggest that prolonged depression of synaptic potentials in the neonatal rat reflects decreased transmitter output from the activated afferent terminals.(ABSTRACT TRUNCATED AT 400 WORDS)

Action Potentials↗
PubMed1975

[Intercentral relations in rat spinal cord with local depression of the inhibitory processes].

The changes in certain reflex responses of the rat spinal cord after local depression of inhibitory processes by tetanus toxin (the so-called phenomenon of "determinative dispatch station") were studied. It is shown that the tonic and rhythmic activity generated by this locus in the lumbar part of the spinal cord evokes generalized activity of all spinal motoneurons with similar time characteristics. The depression of its neurons by glycine removes this phenomenon. The excitation of "determinative dispatch station" neurons in cervical segments causes a pathologically enhanced scratch reflex in the ipsilateral hind limb. The enhancing of the scratch reflex is not connected with the depression of inhibitory processes of lumbar motoneurons. The formation of the "determinative dispatch station" in cervical segments produces both excitatory and inhibitory influences on monosynaptic reflexes of the lumbar flexor motoneurons. The role of local inhibitory processes depression in the functioning of the nervous system is discussed.

Animals↗
PubMed1979

[Contribution of Hoffmann's reflex, evoked on the soleus muscle, to the study of nerve conduction velocity from birth to age 5].

We tried to appreciate the maturation of the peripheric nervous system, in children from two days to five years old, by electrophysiological technics. Hoffmann's monosynaptic reflex is recorded on the soleus muscle and conduction velocity is calculated on the motor tibial nerve. So, we can follow the conduction velocities on the proximal and distal part of this nerve, from birth to five years of life. The conduction velocities develop in a parallel and approximately exponential way. The proximal conduction velocity remains always faster than the distal one but their difference decreases during the first 18 months of life and then remains constant. The evolution of the proximal conduction velocity explains that the conduction time slightly but significantly decreases during the first year of life in contrast to the increase of the nerve length. So, during the first year of life, nervous system maturation gets on very quickly and anticipates the skeletal growth.

Age Factors↗
PubMed1988

The spinal reflex of chronic spinal rats is supersensitive to 5-HTP but not to TRH or 5-HT agonists.

The effects of thyrotropin-releasing hormone (TRH), 5-methoxy-N,N-dimethyltryptamine (5-MeODMT) and L-5-hydroxytryptophan (5-HTP) were studied on the monosynaptic reflex (MSR) and the polysynaptic reflex (PSR) in acute and chronic spinal rats. Radioimmunoassay showed that while chronic spinal transection (for 2 weeks) caused the complete depletion of TRH in the ventral lumbar enlargement a certain level of TRH was maintained in the dorsal lumbar enlargement. This result suggested the existence of TRH-containing neurons in the dorsal horn other than the medullary raphe neurons descending to the spinal cord. The latency to the start of the MSR was shortened in chronic spinal rats and the amplitudes of the MSR and PSR were significantly greater than those in acute spinal rats. There was no obvious difference in the effects of TRH and 5-MeODMT on spinal reflexes of acute and of chronic spinal rats although marked supersensitivity to 5-HTP was observed in both the MSR and the PSR in chronic spinal rats. The supersensitivity to 5-HTP was considered to be due to a lack of 5-hydroxytryptamine (5-HT) uptake into 5-HT-containing nerve terminals rather than to a change in 5-HT receptors. It is suggested that TRH and 5-HT do not show any mutual requirement for each other in their effects on the spinal reflex since co-depletion of TRH and 5-HT did not change the effects of TRH and 5-MeODMT in chronic spinal rats. The coexistence of 5-HT and TRH in the descending spinal pathway is not considered to be significant for the control of spinal reflexes at the postsynaptic level.

5-Hydroxytryptophan↗