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PubMed1979

Reduction of gamma-aminobutyric acid (GABA)-mediated transmission by a convulsant benzodiazepine.

In contrast to other benzodiazepine, Ro 5-3663 produces convulsions in mice. The CD50 of 7.0 mg/kg i.v. falls between that of picrotoxin and pentylenetetrazol. An electrophysiological study was made of the effects of this convulsant benzodiazepine on spinal reflexes and on ganglionic depolarization evoked by gamma-aminobutyric acid (GABA). In the unanesthetized spinal cat, Ro 5-3663 (15 mg/kg i.v.)depressed the dorsal root potentials and abolished the dorsal root reflexes evoked by muscle and cutaneous afferent inputs. The monosynaptic reflex was typically depressed, whereas polysynaptic potentials were enhanced. Diazepam reversed the depression of the dorsal root reflex and dorsal root potential produced by the convulsant benzodiazepine and reduced the enhancement of the polysynaptic potential. Presynaptic inhibition was attenuated by the convulsant, whereas strychnine-sensitive postsynaptic inhibition was slightly potentiated. Ro 5-3663 reduced the amplitude and duration of the GABA-evoked negative surface potential recorded from the superior cervical ganglion. The results indicate that the convulsant benzodiazepine acts in an opposite manner to the depressant benzodiazepines and support the hypothesis that these two types of compounds act through a modulation of GABAergic mechanisms.

Animals↗

PubMed1993

The regulation of presynaptic inhibition during co-contraction of antagonistic muscles in man.

1. The size of the soleus, tibialis anterior and medial gastrocnemius H reflexes were measured at different levels of EMG activity in ankle plantar- and dorsiflexors. At similar levels of EMG activity in the agonist muscle, the soleus and tibials anterior H reflexes were found to be smaller during co-contraction than during an isolated agonist contraction. In contrast to this, the medial gastrocnemius H reflex had the same size during co-contraction as during an isolated plantarflexion at comparable EMG levels. 2. Peaks occurred at monosynaptic reflex latency in the post-stimulus time histogram (PSTH) of firing of soleus and tibialis anterior motor units following stimulation of their respective motor nerves. These homonymous Ia peaks were found to be smaller during co-contraction than during isolated agonist contraction, whereas that of medial gastrocnemius motor units was unchanged. As the monosynaptic peak in the PSTH may give an indirect measure of the size of the monosynaptic EPSP in the motoneurone, it is suggested that these findings reflect a differential control of presynaptic inhibition of soleus and tibialis anterior motor units with respect to medial gastrocnemius motor units. 3. The monosynaptic Ia facilitation of the soleus H reflex evoked by a stimulation of the femoral nerve, was also found to be smaller during co-contraction of tibials anterior and soleus than during isolated plantarflexion. This suggests that presynaptic inhibition of heteronymous Ia fibres from the quadriceps muscle projecting to soleus motoneurones is regulated in the same way as presynaptic inhibition of homonymous Ia fibres during co-contraction. 4. The femoral nerve-induced monosynaptic facilitation of the soleus H reflex was found to decrease with increasing tonic levels of both co-contraction and isolated dorsi- and plantarflexion. The amount of facilitation decreased to the same degree with increasing levels of dorsiflexion and co-contraction. For the same level of EMG in the dorsiflexors there was thus no difference in the amount of facilitation whether the dorsiflexors were activated separately or in a co-contraction. 5. Whereas the soleus H reflex increased in size 50 ms prior to the onset of a dynamic plantarflexion, it did not change prior to the onset of a co-contraction. The femoral nerve-induced facilitation increased prior to the plantarflexion, but decreased prior to the co-contraction.(ABSTRACT TRUNCATED AT 400 WORDS)

Adult↗

PubMed1992

The short latency muscle reflex in the diagnosis of disc disease affecting roots L4 and L5.

A segmental monosynaptic reflex that can be evoked by using voluntary muscle contraction to facilitate it is of use in diagnosis. In a group of 15 healthy volunteers the reflex response from tibialis anterior proved to be 31.08 +/- 2.48 msec with a side difference of 0.41 +/- 0.36 msec and from peroneus longus 29.90 +/- 2.20 msec with a side difference of 0.38 +/- 0.25 msec. Of 21 patients with radiologically proven disc herniation (of root L4 in 5 and of root L5 in 16) 16 showed a delay of more than 2.5 SD of the side difference or no response at all. It is hope that this simple and speedy method will be routinely adopted as complement to standard electromyography.

Adult↗

PubMed1990

Physiology and clinical applications of hand muscle reflexes.

Hand muscle reflexes to stretch or electric stimulation of mixed nerves consist of two main components, the short latency reflex (SLR, M1) or Hoffmann reflex (HR) and the long latency reflex (LLR, M2). The SLR is most likely a spinal, monosynaptic reflex and all the evidence presently available supports a transcortical pathway of the LLR. Investigations in normal subjects demonstrate that the LLR is a reflex mediated by fast conducting muscle and cutaneous afferents. Group II muscle afferents do not significantly contribute to this reflex and it cannot be explained by repetitive excitation of spinal oligosynaptic pathways. These findings should not be uncritically generalized to other muscle groups, because the central and peripheral mechanisms apparently differ according to the body region and mode of stimulation. The LLR of hand muscles is most likely involved in skillful movements of the fingers. It is believed to assist rapid compensatory responses to unexpected disturbances. In addition to the main component of the LLR, which is called LLR II, the study of electrically elicited thenar reflexes following stimulation of the median nerve disclosed further LLR components, the LLR I and the LLR III. The latter reflexes are rarely seen in normal subjects but have a significance in several diseases. Several abnormalities could be demonstrated in different diseases. Enhanced HR and reduced LLR are found in spasticity of various origin. Enhanced LLR I are frequently seen in Parkinson's disease, essential tremor and reflex myoclonus. Absent or reduced LLR II is found in Huntington's disease and in different focal brain lesions but not in symptomatic choreatic syndromes of other origin. Delayed latencies of the LLR II or absent LLR II have been described in multiple sclerosis. Enhanced LLR III may occur in cerebellar diseases. The method to elicit LLR of thenar muscles by electric stimulation may prove to be useful for clinical neurophysiology.

Electric Stimulation↗

PubMed2002

The physiological mechanisms of 2 Hz electroacupuncture: a study using blink and H reflex.

Our previous studies have shown that the cerebral cortex modulates the physiological mechanisms of acupuncture. However, the role of the brain stem and spinal cord in acupuncture remains unclear. The present study investigated the action of the brain stem and spinal cord in acupuncture. A total of eight healthy adult volunteers were studied. Electrical stimulation of the supraorbital nerve in the supraorbital foramen was used to evoke the blink reflex. Electrical stimulation of the posterior tibial nerve in the right popliteal fossa was used to evoke the H reflex. Electroacupuncture (EA) of 2 Hz was applied to the Zusanli acupoint in the right or left leg. The area of the R1 and R2 components of the blink reflex, and the greatest H/M ratio and H-M interval of the H reflex were measured before EA, during EA and at various post-EA periods. These data were analyzed quantitatively by a computerized electromyographic examination system. The results indicate that EA did not change the R1 and ipsilateral R2 components of the blink reflex. EA depressed the contralateral R2 component of the blink reflex 10 minutes and 40 minutes after the start of EA, but not after 5 minutes. EA applied to the Zusanli acupoint did not change the H/M ratio or the H-M interval of the H reflex. The results of this study indicate that 2 Hz EA of the Zusanli acupoint does not change the R1 component of the blink reflex, and the H/M ratio and the H-M interval of the H reflex, suggesting that 2 Hz EA does not change the monosynaptic reflex in the brain stem and spinal cord in humans. We also found that EA at 2 Hz depressed the contralateral but not the ipsilateral R2 component of the blink reflex, suggesting that longer pathways, perhaps including the cerebral cortex, may play a role in the physiological mechanisms responsible for the effectiveness of acupuncture.

Adult↗

PubMed1989

General pharmacology of beraprost sodium. 1st communication: effect on the central nervous system.

Beraprost sodium (sodium (+/-)-(1R*,2R*,3aS*,8bS*)-2,3,3a,8b-tetrahydro-2- hydroxy-1-[(E)-(3S*)-3-hydroxy-4-methyl-1-octen-6-ynyl]-1H- cyclopenta[b]benzofuran-5-butyrate, TRK-100) is an orally active epoprostenol (prostaglandin I2, PGI2) analogue. Its effect on the central nervous system (CNS) was studied. 1. When orally administered in mice, beraprost sodium at 0.3 mg/kg caused a flush of skin, a suppression of spontaneous motility, and a fall of body temperature. At 1 mg/kg and more, it showed obvious sedation, prolongation of hexobarbital hypnosis, and analgesic action in acetic acid-induced writhing test. However, even at 3 mg/kg beraprost sodium neither induced ataxia nor had anticonvulsant activity. Hypothermia was also observed in rabbits at 1 mg/kg (p.o. and i.v.). 2. When intravenously administered, beraprost sodium exerted long-lasting action on the CNS, while its pharmacological effects resembled those of PGI2. 3. Oral administration of beraprost sodium did not inhibit aggregation toxicity induced by methamphetamine (20 mg/kg i.p.) in mice. Beraprost sodium at doses higher than 1 mg/kg enhanced aggregation toxicity induced by methamphetamine (5 mg/kg i.p.), while intracerebral ventricular administration of beraprost sodium failed to enhance it. 4. In rat spinal reflex, intravenous administration of beraprost sodium (0.1 mg/kg) slightly enhanced monosynaptic reflex and at a high dose (1 mg/kg) suppressed polysynaptic reflex. 5. In the rabbit EEG, intravenous administration of beraprost sodium at a high dose (1 mg/kg) showed some effects such as the continuous pattern of wakefulness and a fall in power of the EEG.(ABSTRACT TRUNCATED AT 250 WORDS)

Analgesics↗

PubMed1986

The effect of percutaneous motor cortex stimulation on H reflexes in muscles of the arm and leg in intact man.

The technique of electrical stimulation of the brain via scalp electrodes has been used to activate corticospinal pathways in intact man. The intensity of stimulation was adjusted to be below the threshold necessary to evoke a direct electromyographic response when the muscles being tested were totally relaxed. Changes in spinal cord excitability were measured using H-reflex (monosynaptic) testing. By this means it was found that subthreshold scalp stimulation can produce a descending corticospinal volley even in the absence of a direct muscle response. The time course of changes in spinal cord excitability was evaluated by evoking test H reflexes at different intervals relative to the scalp stimulus. In wrist and finger flexor muscles of seven subjects, a single subthreshold scalp shock produced an initial peak facilitation of the H reflex which on average lasted for 2.5 ms. The end of the initial facilitation was marked by a return of the H reflex towards basal levels and on one occasion by a frank inhibition. It is suggested that the initial facilitation is produced by arrival at the motoneurones of monosynaptic excitatory post-synaptic potentials (e.p.s.p.s) and is truncated by the subsequent arrival of disynaptic inhibitory post-synaptic potentials (i.p.s.p.s). The initial facilitation was followed by a second phase of facilitation of the H reflex. The second phase was weaker, more variable and longer lasting (from 5 to 20 ms) than the first phase. The threshold of scalp stimulus intensity required to produce an effect on the H reflex was the same for the first and second phases of facilitation. Several possible explanations are discussed for the mechanism responsible for the late and long-lasting facilitation. In two subjects wrist and finger extensor muscles were studied. The time course of H-reflex changes was similar to that of the flexors except that the initial facilitation was followed by a frank inhibition in both subjects. In one subject thenar muscles and tibialis anterior were studied and behaved similarly to wrist and finger flexor muscles. Effects on the soleus H reflex was studied in seven subjects. In five of these subjects, in contrast to the other muscles studied, the initial event was an inhibition of the H reflex. This inhibition also could be seen preceding the usual period of facilitation in averaged rectified surface electromyogram (e.m.g.) records when scalp stimuli were given during weak voluntary activation of soleus.(ABSTRACT TRUNCATED AT 400 WORDS)

Arm↗

PubMed1983

Effect of core cooling on short and long latency reflex responses.

Subjects were immersed in 10 degrees C water until the rectal temperature dropped to 35 degrees C. Reflexes of wrist flexors were tested before and after cooling with tendon taps and torque motor produced perturbations. Comparison of pre- and post-cooling reflex responses showed that the longer latency reflex (LLR) was delayed in onset more than the short latency monosynaptic reflex (SLR) response. This implies that a portion of the LLR pathway is separate and distinct from the SLR pathway.

Adult↗

PubMed1983

Effect of a synthetic enkephalin analogue on spinal nociceptive messages in humans.

The effects of a single dose (1.0 mg. i.v.) of a synthetic methionine enkephalin, FK 33-824 (FK) on spinal nociceptive pathways were studied in 3 normal subjects and in 3 paraplegic patients. In normal patients, FK 33-824 produced an increased threshold of a nociceptive flexor reflex of the lower limb as well as a decrease in the slope of the recruitment curve of this reflex as a function of stimulus intensity. The inhibition of a monosynaptic reflex induced by conditioning noxious cutaneous stimulation was also reduced by FK 33-824. In patients, administration of FK 33-824 resulted in marked depression of supraliminal nociceptive reflexes, showing a direct spinal effect of this opioid. In all subjects, FK 33-824 also produced severe side effects. All these effects were naloxone-reversible (0.03 mg/kg. i.v.). The clinical implications of these data are discussed.

Adult↗

PubMed1992

The pharmacological properties of CS-722, a newly synthesized centrally acting muscle relaxant.

The pharmacological properties of (R)-4-chloro-2-(2-hydroxy-3-morpholinopropyl)-5-phenyl-4-isoxaz olin-3-one hydrochloride (CS-722), a newly synthesized, centrally acting muscle relaxant, were studied in rats. The drug CS-722 reduced the radio frequency decerebrate rigidity in a dose-dependent manner (25-100 mg/kg, p.o.); it inhibited the increase in discharges from Ia afferent fibers, gamma-motor activity, which was induced by stimulation of the reticular formation. The compound, however, showed no effect on the basal discharge of Ia afferent fibers. The polysynaptic reflex was depressed by CS-722, with less influence on the monosynaptic reflex in intact and spinal preparations and CS-722 did not prolong thiopental-induced sleeping time. In rats anesthetized with halothane, CS-722 did not affect the electroencephalogram (EEG) arousal response, which was elicited by stimulation of the reticular formation. The results of this study suggest that CS-722 can exert a muscle relaxant action, at a dose range at which depression of the ascending reticular activating system was negligible. The results also suggest that depressions of the gamma-motor system and the polysynaptic reflex may contribute to the muscle relaxant action of CS-722.

Animals↗

PubMed1991

Effect of naloxone on transmission in excitatory and inhibitory spinal reflex pathways.

The effect of systemic administration of naloxone on transmission in hindlimb reflex pathways was investigated in acute low spinal cats by conditioning monosynaptic reflexes. A marked enhancement of excitatory effects from cutaneous, joint, group II and III muscle afferents was observed in posterior biceps and semitendinosus motoneurones in 4 out of 6 experiments. In contrast, inhibitory synaptic effects in gastrocnemius and soleus motoneurones were not enhanced except weakly in one experiment. The effects of naloxone are different from those observed after spinal cord lesions interrupting axons of a previously described group of upper lumbar propriospinal neurones, which tonically suppress reflex transmission in the acute low spinal state. It is postulated that the suppression exerted by this group of neurones is not dependent on endogenous opioid peptides.

Animals↗

PubMed1984

The effect of calcium ions on the responses to motoneurons to substance P and eledoisin-related peptide in the toad and rat spinal cord.

The effects of changes in the external calcium ion concentration [Ca2+]0 on segmental reflexes and the responses of motoneurons to bath applied agonists have been studied in the toad and rat spinal cords in vitro. Reducing [Ca2+]0 enhanced polysynaptic reflexes in the toad, with maximal discharges occurring at 0.3 mM. Monosynaptic reflexes in the rat were reduced by lowering [Ca2+]0. Responses of toad motoneurons to substance P and eledoisin-related peptide were enhanced by lowering [Ca2+]0, maximum responses occurring at 0.3 mM. Lowering [Ca2+]0 also enhanced responses to L-glutamate but the effect was smaller and less consistent. This effect of Ca2+ was abolished by the addition of tetrodotoxin to the bathing solution. Toad motoneuron responses to gamma-aminobutyrate and glycine were not affected by alterations in [Ca2+]0. Rat motoneuron responses to substance P and eledoisin-related peptide were also enhanced by reductions in [Ca2+]0 but the effect was more pronounced in younger (less than 5 days post partum) than older (5-10 days post partum) animals. These results are consistent with the idea that motoneuron responses to peptides in normal solutions result from activation of receptors on both motoneurons and interneurons: enhancement of the responses by lowering [Ca2+]0 results from the potentiation of the transynaptic component.

Animals↗

PubMed1999

An in vitro functionally mature mouse spinal cord preparation for the study of spinal motor networks.

An in vitro isolated whole spinal cord preparation has been developed in 'motor functionally mature' mice; that is mice of developmental maturity sufficient to weight-bear and walk. In balb/c mice this stage occurs at around postnatal day 10 (P10). Administration of strychnine elicited synchronous activity bilaterally in lumbar ventral roots. Rhythmic alternating locomotor-like activity could be produced by application of a combination of serotonin (5-HT), N-methyl-d-aspartate (NMDA), and dopamine in animals up to P12. Using a live cell-dead cell assay, it is demonstrated that there are primarily viable cells throughout the lumbar spinal cord. The viability of descending pathways was demonstrated with stimulation of the mid-thoracic white matter tracts. In addition, polysynaptic segmental reflexes could be elicited. Although usually absent in whole cord preparations, monosynaptic reflexes could invariably be elicited following longitudinal midline hemisection, leading to the possible explanation that there might be an active crossed pathway producing presynaptic inhibition of primary afferent terminals. The data demonstrate that this functionally mature spinal cord preparation can be used for the study of spinal cord physiology including locomotion.

Animals↗

PubMed1989

The most desirable conformation of phenylethylamine (PEA) moiety stimulating noradrenergic neurons: effects of PEA, methamphetamine, phenelzine, methylphenidate, nomifensine and mazindol on rat spinal reflexes.

1. The effects of phenylethylamine (PEA) and PEA-related substances on the rat spinal monosynaptic reflex (MSR) were examined. According to the flexibility of the PEA moiety in the molecule, these drugs were classified into three groups, i.e. non-rigid, rigid and semi-rigid groups. 2. PEA, methamphetamine and phenelzine (non-rigid group) showed opposite effects on the MSR, an increase at low doses and a decrease at high doses. The former effect was antagonized by pretreatment with the alpha 1-blocker, prazosin. 3. Nomifensine and mazindol (rigid group), which share the similar spatial relationships between the aromatic moiety and nitrogen, increased the MSR, and this effect was blocked by prazosin. 4. In the semi-rigid group the same result was obtained for methylphenidate but not for 1-methyl-2-benzylpiperidine, which might have difficulty in having the similar conformation of PEA moiety as methylphenidate because of its methyl group. 5. From these results, it appears that the effects of PEA and amphetamines on the MSR are determined by the spatial relationships between the amino group and the aromatic moiety and that the enhancement of the MSR might be induced through alpha 1-adrenergic transmission.

Animals↗

PubMed2003

Tricyclic analogs cyclobenzaprine, amitriptyline and cyproheptadine inhibit the spinal reflex transmission through 5-HT(2) receptors.

The centrally acting muscle relaxant cyclobenzaprine decreases the amplitude of monosynaptic reflex potentials by inhibiting the facilitatory descending serotonergic influences in the spinal cord. Interestingly, the structure of cyclobenzaprine is much similar to those of amitriptyline and cyproheptadine. In the present study, we attempted to elucidate the relationship between 5-HT(2) receptor antagonistic and inhibitory effects of cyclobenzaprine, amitriptyline, cyproheptadine and ketanserin on the spinal reflexes. Cyclobenzaprine, amitriptyline, cyproheptadine, and ketanserin significantly inhibited facilitatory effects of 1-(2,5-dimethoxy-4-iodophenyl)-2-aminopropane (DOI) on flexor reflexes and mono- and polysynaptic spinal reflex potentials in spinalized rats. In intact rats, these drugs significantly reduced the mono- and polysynaptic reflex potentials. 5-HT depletion significantly prevented the depression of the spinal reflex potentials induced by these drugs. These results suggest that the inhibitory effects of cyclobenzaprine, amitriptyline, and cyproheptadine on mono- and polysynaptic reflex potentials are due to the inhibition of descending serotonergic systems through 5-HT(2) receptors in the spinal cord.

Amitriptyline↗

PubMed1991

Intact inhibition of the stretch reflex during general tetanus.

Tetanus toxin at lethal doses (2-10 x 10(3) mouse minimal lethal doses per kg body weight, mMLD/kg) was injected i.v. into 10 cats under pentobarbital anaesthesia. After the appearance of the first sign of generalized tetanus the animal was anaesthetized by a mixture of urethane and chloralose. Experiments were performed several hr thereafter when the toxin action was anticipated to be optimal. The stretch reflexes were elicited manually, by the contraction of the antagonistic muscles or by a stretch device. In toxin treated animals the spontaneous electromyographic activity was inhibited by strong stretching of the tested muscle or by that of the antagonistic muscle. The stretch reflex of the extensor muscle elicited by a contraction of the flexor muscle was inhibited by electrical stimulation of the flexor afferent fibres. The stretch reflex elicited by a stretch device as well as the electrically elicited monosynaptic reflex were inhibited by conditioning stimulation of the antagonistic nerve. The inhibition curves were almost the same as those of healthy animals. It is concluded that the spinal inhibitions, such as antagonistic group Ia, autogenic group Ib, groups II and III and the presynaptic inhibitions, were kept intact in severe general tetanus.

Anesthesia↗

PubMed1979

Subject instruction and long latency reflex responses to muscle stretch.

1. Surface electromyographic recordings were made in eight normal subjects from the isometrically contracting elbow flexors before and during forcible extension of the elbow through 7 degrees in 50-150 msec. 2. Weh the subjects were instructed prior (2-5 sec) to a forthcoming stretch to 'resist' or to 'let go', they could reliably enhance or suppress e.m.g. activity occurring between 40 and 70 msec from commencement of the stretch. Such e.m.g. activity represents a 'long-latency' (or 'M2') reflex response: it occurs with a latency longer than the spinal segmental monosynaptic reflex, but shorter than a voluntary reaction time. When the subjects were given their instructions (by means of a light) at the moment the stretch commenced, however, none of them could adjust the long-latency reflex appropriately. 3. It is concluded that central, evaluative processes commencing at the time of a perturbation cannot influence long-latency reflex responses to that perturbation.

Elbow↗

PubMed1984

Facilitation of soleus-coupled Renshaw cells during voluntary contraction of pretibial flexor muscles in man.

Recurrent inhibition to soleus motoneurones, brought about by a conditioning H-reflex discharge, was estimated in human subjects by a subsequent test H reflex. Changes in recurrent inhibition during voluntary ankle dorsiflexion were evaluated by comparing the amplitude of the test H reflex to a reference H reflex: both reflexes were subjected to the same type of influences which modified soleus monosynaptic reflex excitability during pretibial flexor contraction, but only the test H reflex was subject to the recurrent inhibition evoked by the conditioning H-reflex discharge. During tonic or phasic ramp contractions of the pretibial flexors the inhibition of the test H reflex, as compared to rest, was more marked than that of the reference H reflex. Evidence is presented that this may indicate a facilitation of soleus-coupled Renshaw cells. Since this facilitation of soleus-coupled Renshaw cells was also observed before ramp contraction, it is, at least in part, supraspinal in origin. Within the range of forces studied (8-45% of maximum force) there was no evidence that the facilitation of soleus-coupled Renshaw cells increased along with increased force of the pretibial flexor voluntary contraction. During voluntary phasic ankle dorsiflexion, facilitation of soleus-coupled Renshaw cells was maximum at the moment when soleus motoneurones were most facilitated by the stretch-induced soleus I a discharge. There was no evidence for changes in Renshaw cell excitability during ballistic contractions. It is suggested that this facilitation of soleus-coupled Renshaw cells may be one of the mechanisms preventing the occurrence of a soleus stretch reflex during a voluntary ankle dorsiflexion. Such a mechanism could become important if reciprocal inhibition, via I a inhibitory interneurones, were not strong enough, e.g. because of a weak gamma-drive to the contracting muscles.

Adult↗