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At least 703 records · Page 39Linked to original sources

PubMed2002

Inter-trial variation of soleus H reflex in humans: implication for supraspinal influence.

Inter-trial variation in soleus H reflex amplitude for different effort modes, elicited at different test-stimulus intensities, was studied in fifteen healthy subjects. Regardless of test-stimulus intensity, weak isometric plantarflexion and dorsiflexion at 20% of maximum voluntary contraction caused significant potentiation and depression of the H reflex amplitude. In addition, both facilitation and inhibition of the soleus H reflex was associated with considerable inter-trial variability of the H reflex amplitude that varied proportionally with test-stimulus intensity. As inter-variability of the H reflex was independent of that of M response, the results indicate that: 1) supra-spinal input influences loop-gain fluctuations of the monosynaptic-reflex arc; and 2) smaller test stimuli may be more efficacious for exploration of motoneuronal excitability because of reduction in variability in H reflex amplitude.

Adolescent↗

PubMed2001

An investigation of the Jendrassik manoeuvre.

Several mechanisms were investigated by which the Jendrassik manoeuvre might potentiate tendon jerk and H-reflexes, recorded here as surface EMG from the triceps surae muscle group. If fusimotor activation is involved, then, after muscle conditioning designed to leave spindles in a slack state, interposing a Jendrassik manoeuvre before reflex testing should have increased reflex amplitude by restoring spindle sensitivity; but this was not the case. The Jendrassik manoeuvre failed to increase facilitation of the soleus H-reflex by a quadriceps volley, contrary to expectations if it operates by presynaptic disinhibition. There was no increase in the level of ongoing EMG during a Jendrassik manoeuvre, indicating that it does not operate by direct facilitation of motoneurones. The Jendrassik manoeuvre produced less reflex potentiation when spindles had a high rate of resting discharge. A remaining, untested mechanism is the modulation of oligosynaptic pathways that may contribute to the largely monosynaptic reflex response.

Electromyography↗

PubMed1985

Noradrenergic modulation of sensorimotor processes in intact rats: the masseteric reflex as a model system.

The masseteric jaw closure reflex was utilized as a model system with which to gauge the functional activity of central noradrenergic neurons. This system was chosen because it is a simple monosynaptic reflex the neuronal substrate of which receives a dense noradrenergic input. The modulatory effects of norepinephrine (NE) on this response in the intact, chloral hydrate-anesthetized rat were studied with a variety of pharmacological strategies. Initially, a reflex facilitation was obtained with the catecholamine precursor L-DOPA. Manipulations with greater specificity of action on the noradrenergic system were then employed. First, we used the presynaptic alpha-2 noradrenergic agonist clonidine, which acts to decrease noradrenergic transmission. Clonidine attenuated the amplitude of the reflex, and this suppression was blocked by pretreatment with the alpha-2 antagonist yohimbine. The effects of yohimbine itself were then examined, and a biphasic effect was obtained. At low doses, at which it preferentially acts as an antagonist at presynaptic alpha-2 receptors and increases noradrenergic transmission, yohimbine enhanced the reflex. At higher doses, at which it also displays postsynaptic alpha-1 antagonist activity, yohimbine depressed the reflex. This reflex modulation by yohimbine was blocked by pretreatment with the alpha-1 antagonist prazosin. The anatomical site of the observed effect was then localized to the direct noradrenergic innervation of the reflex circuitry by locally destroying, with 6-hydroxydopamine, the noradrenergic terminals in the trigeminal motor nucleus mediating the response. This significantly attenuated the reflex modulation by yohimbine, without affecting elicitation of the reflex itself.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

PubMed1999

The modulation of presynaptic inhibition in single muscle primary afferents during fictive locomotion in the cat.

The aim of this study is to understand the functional organization of presynaptic inhibition in muscle primary afferents during locomotion. Primary afferent depolarization (PAD) associated with presynaptic inhibition was recorded intra-axonally in identified afferents from various hindlimb muscles in L6-L7 spinal segments during fictive locomotion in the decerebrate cat. PADs were evoked by the stimulation of peripheral muscle nerves and were averaged in the different epochs of the fictive step cycle. Fifty-three trials recorded from 39 muscle axons (37 from group I and two from group II) were retained for analysis. The results showed that there was a significant phase-dependent modulation of PAD amplitude (p < 0.05) in a majority of muscle afferents (30 of 39, 77%). However, not all stimulated nerves led to significantly modulated PADs in a given axon (36 of 53 trials, 68%). We also observed that the pattern of modulation (phase for maximum and minimum PAD amplitude and the depth of modulation) varied with each recorded afferent, as well as with each stimulated nerve. We further evaluated the effect of PAD modulation on the phasic transmission of the monosynaptic reflex (MSR) and found that PADs decreased the MSR amplitude in all phases of the fictive step cycle, independent of the PAD pattern in individual group I fibers. We conclude that (1) PAD modulation patterns of all group I fibers contacting motoneurons led to an overall reduction in monosynaptic transmission, and (2) individual PAD patterns could participate in the control of transmission in specific reflex pathways during locomotion.

Animals↗

PubMed1986

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.

Animals↗

PubMed2006

Levetiracetam suppresses long-loop reflexes at the cortical level.

Posthypoxic coma is often associated with cortical and brainstem hyperexcitability. Five months following cardiopulmonary resuscitation after myocardial infarction and ventricular arrhythmia, a 47-year-old man presented with posthypoxic cerebral dysfunction, minimal responsiveness, severe spastic-dystonic tetraparesis, and stimulus-sensitive muscle spasms upon acoustic and sensory stimulation. Neurophysiological examination revealed increased long-loop reflexes in abductor pollicis brevis muscle following median nerve stimulation at the wrist, consistent with cortical hyperexcitability. Exaggerated startle responses provided evidence of concomitant brainstem disinhibition. Levetiracetam up to 3,000 mg per day suppressed transcortical long-loop reflexes in a dose-dependent manner without concomitant suppression of the H-reflex and only mild attenuation of the startle response. The present findings suggest a suppressive effect of levetiracetam on cortical neurons in the absence of a spinal effect on monosynaptic reflexes, and thus support the drug's efficacy in posthypoxic cortical hyperexcitability.

Coma↗

PubMed1999

Changes in reflex responses of the masseter and digastric muscles during sleep in freely behaving rabbits.

The aim of this study was to clarify the modulation of motoneuron excitability in masticatory muscles during sleep. For this purpose, changes in the reflex responses of the masseter and digastric muscles between sleep and wakefulness were studied in freely behaving rabbits. Stimulation of the jaw closing muscle spindle afferents induced the masseteric monosynaptic reflex (MMR). During quiet sleep (QS), which gradually replaced quiet wakefulness, the mean MMR amplitude showed no change. During active sleep (AS). MMR amplitudes were markedly reduced, but they were confounded by the occasional occurrence of facilitation in the amplitude. The facilitatory reflexes were often related to rapid eye movements (REMs). However, the excitatory input probably did not originate from the same region as the REM generator, since the REM and the large MMR did not always occur simultaneously. On the other hand, jaw opening reflexes remained inhibited. The results indicated that there is mainly a difference in the excitability between the two groups of motoneurons during AS; masseter motoneuron activity was inhibited but occasionally facilitated by excitatory inputs occurring in association with REMs, however, the digastric motoneuron activity was remained inhibited. The excitatory inputs may induce dysfunctional muscle contraction of the jaw closing muscles as seen in bruxism.

Animals↗

PubMed1999

Spinal neurokin3 receptors facilitate the nociceptive flexor reflex via a pathway involving nitric oxide.

The present study examined the effects of intrathecal administration of neurokinin3 receptor agonists on the electrically-evoked nociceptive flexor reflex in decerebrate and spinalized adult rats. The reflex was evoked by stimulating the isolated sural nerve at an intensity that activates C fibers and was measured by recording the number of compound potentials in the ipsilateral hamstring muscles. Intrathecal senktide (1-30 nmol), a neurokinin3 receptor agonist, dose-dependently facilitated the reflex reaching a maximum effect of 230% of the baseline reflex at 10 nmol. SR 142801 (60 nmol), a non-peptide neurokinin3 receptor antagonist, blocked facilitation of the reflex induced by 10 nmol senktide, providing further support that the effect of senktide is mediated by neurokinin3 receptors. The intrathecal administration of senktide (10 nmol) did not alter the monosynaptic reflex elicited by stimulating the L5 dorsal root at an intensity that was at the threshold for activating A fibers. This indicates that the senktide-induced facilitation of the nociceptive flexor reflex was not at the level of the motor neuron. Pretreatment with N(G)-nitro-L-arginine methyl ester (30 nmol), a nitric oxide synthase inhibitor, attenuated the effect of senktide, indicating that facilitation of the reflex by senktide is also mediated by the production of nitric oxide. Data from the present work have shown that spinal neurokinin3 receptors facilitate the nociceptive flexor reflex through a pathway that involves interneurons and the production of NO. Therefore, neurokinin3 receptors are likely to be involved in enhancing nociceptive neurotransmission at the level of the spinal cord.

Animals↗

PubMed1998

Effects of the novel tricyclic quinoxalinedione derivatives, SM-18400 and its analogs, on N-methyl-D-aspartate (NMDA) receptor-mediated synaptic transmission in the isolated neonatal rat spinal cord in vitro.

We examined the effects of novel tricyclic quinoxalinedione derivatives, SM-18400 ((S)-9-chloro-5-[p-aminomethyl-o-(carboxymethoxy)phenylcarbamoylmethy l]-6,7-dihydro-1H,5H-pyrido[1,2,3-de]quinoxaline-2,3-dione hydrochloride trihydrate) and its analogs (i.e., ID-17263 and ID-17332), on the N-methyl-D-aspartate (NMDA) receptor-mediated polysynaptic reflex (PSR) in the isolated spinal cord of neonatal rats in vitro. Application of SM-18400 selectively suppressed the PSR activity in a concentration-dependent manner without affecting the monosynaptic reflex (MSR). Differential suppression of the PSR was also obtained with ID-17263, ID-17332 and other known NMDA receptor glycine-binding site antagonists, 5,7-dichlorokynurenate (5,7-diClkyn) and L-689,560 (4-trans-2-carboxy-5,7-dichloro-4-phenylaminocarbonylamino-1,2,3,4 -tetrahydroquinoline). Relative potencies of the test drugs for inhibition of the PSR were as follows: SM-18400 >> L-689,560 > ID-17332 > ID-17263 > 5,7-diClkyn. In addition, the inhibitory effects of SM-18400 on PSR were markedly antagonized by simultaneous application of D-serine, an agonist for NMDA receptor glycine-binding sites. These findings suggest that SM-18400 is a potent NMDA receptor glycine-binding site antagonist and blocks the NMDA receptor-mediated synaptic neurotransmission in the spinal cord in vitro.

Aminoquinolines↗

PubMed1996

On the mechanism of the post-activation depression of the H-reflex in human subjects.

It was demonstrated that the soleus H-reflex was depressed for more than 10 s following a preceding passive dorsiflexion of the ankle joint. This depression was caused by activation of large-diameter afferents with receptors located in the leg muscles, as an ischaemic block of large-diameter fibres just below the knee joint abolished the depression, whereas a similar block just proximal to the ankle joint was ineffective. The depression of the H-reflex was not caused by changes in motoneuronal excitability, as motor-evoked potentials by magnetic brain stimulation were not depressed by the same passive dorsiflexion. Therefore it was concluded that the long-lasting depression is due to mechanisms acting at presynaptic level. The transmission of the monosynaptic Ia excitation from the femoral nerve to soleus motoneurones was not depressed by the ankle dorsiflexion. The depression thus seems to be confined to those afferents that were activated by the conditioning dorsiflexion. In parallel experiments on decerebrate cats, more invasive methods have complemented the indirect techniques used in the experiments on human subjects. A similar long-lasting depression of triceps surae monosynaptic reflexes was evoked by a preceding conditioning stimulation of the triceps surae Ia afferents. This depression was accompanied by a reduction of the monosynaptic Ia excitatory postsynaptic potential recorded intracellularly in triceps surae motoneurones, but not by changes in the input resistance or membrane potential in the motoneurones. Stimulation of separate branches within the triceps surae nerve demonstrated that the depression is confined to those afferents that were activated by the conditioning stimulus. This long-lasting depression was not accompanied by a dorsal root potential. It is concluded that the long-lasting depression is probably caused by a presynaptic effect, but different from the "classical" GABAergic presynaptic inhibition which is widely distributed among afferent fibres and accompanied by dorsal root potentials. It is more probably related to the phenomenon of a reduced transmitter release from previously activated fibres, i.e. a homosynaptic post-activation depression. The consequences of this post-activation depression for the interpretation of results on spinal mechanisms during voluntary movements in man are discussed.

Adult↗

PubMed1990

Motor outflow to cervical motoneurons from raccoon motorsensory cortex.

Motor outflow from forelimb motorsensory cortex (MsI) to forelimb muscle motoneurons in raccoon has been investigated using three approaches: 1) determination of latencies for cortically evoked efferent discharge in forelimb nerves; 2) determination of latencies for cortical facilitation of forelimb monosynaptic reflexes; and 3) intracellular recording of cortically evoked synaptic potentials. All three approaches indicated a major polysynaptic pathway (minimally disynaptic) for corticofugal facilitation or inhibition of cervical motoneurons. Suggestive evidence for a monosynaptic connection between forelimb MsI and cervical motoneurons was found for only one motoneurons. Nevertheless, the motor pathway between MsI and cervical motoneurons was shown to be more efficacious (defined on the basis of central delays) than in the cat under similar experimental conditions. The results are discussed in terms of organization changes in forelimb MsI which appear to be related to the extent to which certain mammals use their forelimbs for manipulating and exploring objects.

Action Potentials↗

PubMed1998

Inhibition of masseteric electromyographic activity during oral respiration.

Although the effects of oral respiration on the growth and development of craniofacial structure have been studied previously, little is known about how altered respiration affects the activity of the jaw-closing muscles. Obstruction of the nasal airway in the cat significantly inhibited the masseteric stretch reflex and discharges of masseteric motor units but did not affect the electromyographic activity of the diaphragm. This inhibition was greater during inspiration than during expiration. In addition, the amplitude of the masseteric monosynaptic reflex elicited by electrical stimulation of the mesencephalic trigeminal nucleus showed no significant change in association with the altered respiratory mode. These findings suggest that masseteric electromyographic activity is inhibited during oral respiration and that the gamma-system is involved in this inhibition.

Action Potentials↗

PubMed1989

[Effect of tractotomy on the reflex activity of the lumbar segment of the spinal cord severed after sectioning of the sciatic nerve in the rat].

Electrical responses of the spinal cord roots of rats evoked by the preliminary cutting of nerve were investigated in 1, 3, 7 and 14 days after tractotomy. Mean amplitude of the monosynaptic reflex discharges in ventral roots on the side of nerve section is substantially higher 7 and 14 days after the tractotomy, than that of these responses 1 and 3 days after it.

4-Aminopyridine↗

PubMed1989

FES and spasticity.

A model of hemiplegic spasticity based on electromyographical and biomechanical parameters measured during passive muscle stretching is presented. Two components of spasticity can be distinguished--phasic and tonic. This classification depends on the pattern of stretch reflex activity which can be either phasic or tonic as well as on the muscle stretch/tension characteristic. Stretch reflex, as a control loop, is in phasic spasticity characterized by increased sensitivity to velocity of stretching. In tonic spasticity, sensitivity to length of stretching is increased. After the injury, phasic spasticity appears first and invokes monosynaptic reflex pathways. The intensity of tonic spasticity increases with the duration of disability and hence causes changes in muscle fiber biomechanical properties. The model mentioned above has been used to evaluate the effects of FES on spasticity. Hemiplegic patients with implanted peroneal nerve stimulator for gait correction were followed up for one year starting a week before implantation. Long-term use of FES resulted in decrease of tonic spasticity in both ankle joint antagonistic muscle groups. In stimulated tibialis anterior muscle, the phasic type of spasticity increased. To obtain the correlation between changes in spasticity and functional abilities of patients, the maximal voluntary isometric contraction of both muscle groups was also measured. An improvement in voluntary strength was also observed. This can be taken as additional evidence that tonic spasticity is of greater physiological and clinical significance than phasic spasticity. It may be concluded that use of FES can decrease tonic spasticity and, if applied early after the injury, can prevent the appearance of tonic spasticity.

Adult↗

PubMed1997

Functional analysis of the sensory motor pathway of resistance reflex in crayfish. I. Multisensory coding and motor neuron monosynaptic responses.

An in vitro preparation of the fifth thoracic ganglion of the crayfish was used to study in detail the negative feedback loop involved in the control of passive movements of the leg. Release-sensitive primary afferents of from the coxo-basipodite chordotonal organ (CBCO), a proprioceptor whose strand is released by upward movement of the leg, monosynaptically connect to depressor motor neurons (Dep MNs). Extracellular identification of sensory units from the CBCO neurogram allowed us to determine the global coding of a sine-wave movement, imposed from the most released position of the CBCO strand. Intracellular recordings from sensory terminals (CBTs) and ramp movement stimulations applied to the CBCO strand allowed us to characterize two groups of release-sensitive CBCO fibers. The first group, divided into two subgroups (phasic and phaso-tonic), is characterized by discontinuous firing patterns: phasic CBTs fired exclusively during release movements; phaso-tonic CBTs displayed both a phasic firing and a tonic discharge during the more released plateaus. The second group was continuously firing whatever the movement, with higher frequencies during the release phase of the movement stimulation. All CBTs displayed a marked sensitivity for release movements while only the phaso-tonic ones showed a clear sensitivity to maintained positions. Surprisingly, no pure tonic sensory fibers were encountered. Systematic intracellular recordings from all resistant Dep MNs, performed in high divalent cation saline, allowed us to describe two shapes of monosynaptic resistance reflex responses. A phasic response was characterized by bursts of excitatory postsynaptic potentials (EPSPs) occurring exclusively during CBCO strand release movements. A phaso-tonic response was characterized by a progressive depolarization occurring all along the release phase of the stimulation: during maintained released positions, the amplitude of the sustained depolarization was position dependent; in addition, each release movement produced a phasic burst of EPSPs in the MN. The parallel study of the Dep MN properties failed to point out any correlation between the type of reflex response recorded from the MN and the MN intrinsic properties, which would indicate that the type of MN response is entirely determined by the afferent messages it receives.

Animals↗

PubMed1989

Pathophysiology of the spinal cord studied in vitro.

We describe the use of isolated hemisected mouse spinal cords for pathophysiological investigations and analyze the responses evoked and recorded with suction electrodes in spinal roots. Dorsal root (DR) recordings from preparations in control solution show a directly evoked fiber volley (FV); an early postsynaptic spike generated by neurons in spinal gray matter and picked up by volume conduction (DRR1); and a 'slow' dorsal root potential (DRP). The 'conventional' dorsal root reflex (here termed DRR2) was absent or very small in control medium but became very prominent in elevated bath [Ca2+]. DRP and DRR2 but not DRR1 are depressed by GABAA antagonists. Recordings from VR contain the electrotonically conducted VRepsp and superimposed monosynaptic reflex discharge (VRR1). Rarely in control medium but regularly in elevated bath [Ca2+] a GABA-dependent late reflex (VRR2) appears (see also Duchen, 1986). The effects of varying bath concentrations of K+, Ca2+ and Mg2+ on evoked responses are briefly summarized. Irregularly timed spontaneous discharges appear in DR and VR recordings when [Ca2+] is elevated above 1.8 or 2.4 mM, and when [Mg2+] is lowered to 0.4 mM. In hypoxic solution synaptically transmitted responses fail in 10 to 20 min, but persist longer when [Ca2+] is elevated. Unexpectedly, spreading depression (SD)-like responses were recorded in some preparations during hypoxia. Following hypoxia, after synaptically transmitted responses recovered, spontaneous activity developed in DR and VR recordings.

Action Potentials↗

PubMed1987

Inhibitory effect of acupuncture on the finger flexion reflex induced by finger tip vibration.

The effect of acupuncture on finger flexion reflex, caused by mechanical vibration applied to the finger tip, was studied by using the cross-correlation function. A stainless steel acupuncture needle was inserted into the acupuncture point called "Wai-Kuan" for 10 min. Acupuncture inhibited the reflex and suppressed the two modes seen in the cross-correlogram between unitary EMG activity of the muscle flexor digitorum superficialis and finger tip vibration with random frequency. The recovery of the primary mode, which may be via the spinal monosynaptic reflex loop, was significantly earlier than the recovery of the secondary mode, which may be via the supraspinal reflex long loop. This suggests that the distinct inhibitory effect of acupuncture takes place on the reflex at spinal and supraspinal levels.

Action Potentials↗

PubMed1991

Reciprocal Ia inhibition between elbow flexors and extensors in the human.

1. Reciprocal inhibition between elbow flexor and extensor muscles (biceps and triceps brachii) has been investigated in nine healthy subjects. Two techniques were used to assess changes in motoneurone excitability after stimulation of antagonist muscle afferents: (1) monosynaptic reflexes elicited by a mechanical stimulation of the distal muscle tendon (tendon tap); (2) post-stimulus time histograms (PSTH) of voluntarily activated motor units. 2. Electrical stimulation of the antagonist muscle nerve produced a short-latency and short-lasting inhibition of the flexor and extensor motoneurones. The amount of this inhibition was found to be similar in both motor nuclei. 3. The inhibition could be evoked with conditioning electrical stimuli as low as 0.7 x motor threshold (MT) or by very weak tendon taps applied to the antagonist tendon. In the former case the threshold of this inhibition was found to be consistently increased after raising the threshold of Ia afferent fibres by a long-lasting muscle vibration. Since a contribution from cutaneous afferent fibres was ruled out, it is concluded that this inhibition was Ia in origin. 4. Post-stimulus time histograms of voluntarily activated triceps and biceps motor units were made following electrical stimulation of homonymous and antagonist muscle afferents. This enabled an estimate of the central synaptic delay of the inhibitory process. An average central delay of 0.94 ms in excess of that of monosynaptic facilitation was found, thus suggesting that the inhibitory process could be mediated by only one interneurone. 5. A conditioning reflex discharge elicited in the antagonist muscle by a tendon tap depressed or suppressed this inhibition. This depression was maximal when the reflex discharge was elicited 10-20 ms before the conditioning stimulus for the inhibition and never lasted more than 30 ms. It is argued that the only mechanism compatible with such a depression is the inhibitory activity of Renshaw cells acting on the pathway mediating reciprocal inhibition. 6. We conclude that group Ia afferent fibres from elbow extensor and flexor muscles project monosynaptically onto Ia inhibitory interneurones to mediate disynaptic reciprocal inhibition of antagonist motoneurones.

Adult↗