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At least 19 recordsLinked to original sources
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[Effect of polysynaptic flexion reflex on monosynaptic reflexes of calf muscles prior to and following intramuscular injection of ethylbenzatropine in drug-induced muscle rigidity].

In patients with drug-induced parkinsonism and in healthy subjects the effect of stimulation of low-threshold skin fibres of sural nerve producing the polysynaptic flexion reflex of the short head of the biceps femoris muscle on the monosynaptic H reflex of calf muscles was studied before and after administration of ethylbenzatropine. In healthy subjects stimulation of low-threshold skin nerve was followed by facilitation of H reflex in the time of 70 to 200 msec. from the conditioning stimulation to the test stimulation. After one single intramuscular dose of ethylbenzatropine this late facilitating effect disappeared. In patients with drug-induced parkinsonism stimulation of afferent fibres of flexion reflex failed to cause late facilitation of H reflex and one dose of ethylbenzatropine brought no changes. During systematic administration of the drug an evident tendency for facilitation of H reflex was observed, similarly as in healthy subjects. The results obtained in healthy subjects and in patients with drug-induced parkinsonism are explained as evidence of inhibitory action of noradrenaline in certain chains of spinal interneurons, since noradrenaline release in the spinal cord is determined by the striatal equilibrium between the cholinergic and dopaminergic systems. The corrective action of ethylbenzatropine would depend on its central action on certain spinal chains of interneurons determining transmission of impulses from dermal afferent nerves to alpha motoneurons.

H-Reflex↗
PubMed1990

Cutaneous nerve-evoked cholinergic inhibition of monosynaptic reflex in the neonatal rat spinal cord: involvement on M2 receptors and tachykininergic primary afferents.

The mechanisms of a cutaneous nerve-evoked inhibition of monosynaptic reflex were investigated in an isolated spinal cord-peripheral nerve preparation of the neonatal rat. Conditioning stimulation of the saphenous nerve, with five pulses at 50 Hz and a strength sufficient to activate C fibers, evoked an inhibition lasting about 20 s of the monosynaptic reflex that was elicited by stimulation of the nerve branch to quadriceps femoris muscle and recorded from the L3 ventral root. This inhibition of monosynaptic reflex was potentiated by an anticholinesterase, edrophonium, and mostly blocked by atropine. Application of acetylcholine, muscarine, bethanechol, carbachol, arecoline and oxotremorine induced an inhibition of monosynaptic reflex. From the effects of muscarinic antagonists, pirenzepine, AF-DX 116, and 4-diphenylacetoxy-N-methylpiperidine on the agonist-evoked and primary afferent-evoked inhibition of monosynaptic reflex it was concluded that the muscarinic receptors involved in the cutaneous nerve-evoked inhibition of monosynaptic reflex are of M2 type. When monosynaptic reflexes were evoked by two successive stimuli with intervals of 15 ms to 1 s, the second response was smaller than the first. This depression of monosynaptic reflex became less pronounced when the reflex was reduced by application of oxotremorine or arecoline or by conditioning stimulation of primary afferents, suggesting that the inhibition of monosynaptic reflex is presynaptic in nature. The late phase of the cutaneous nerve-evoked inhibition of monosynaptic reflex (5-20 s after conditioning stimulation) was markedly depressed by a tachykinin antagonist, spantide. Perfusion of the spinal cord with capsaicin (1 microM) for 1 h also abolished the late phase of the inhibition.(ABSTRACT TRUNCATED AT 250 WORDS)

Acetylcholine↗
PubMed1992

Serotonergic fibers induce a long-lasting inhibition of monosynaptic reflex in the neonatal rat spinal cord.

The transmitter mechanism of a long-lasting descending inhibition of the monosynaptic reflex was investigated in the isolated spinal cord of the neonatal rat. The monosynaptic reflex elicited by dorsal root stimulation was recorded extracellularly from a lumbar ventral root (L3-L5). Electrical stimulation of the upper thoracic part of the hemisected cord caused an inhibition lasting about 40 s of the monosynaptic reflex. This descending inhibition was markedly attenuated by perfusing the spinal cord with reserpine (1 microM) or 5,7-dihydroxytryptamine (10 microM) for 2-6 h. The perfusion with reserpine (1 microM) for 4 h significantly decreased the contents of 5-hydroxytryptamine, dopamine, and norepinephrine of the neonatal rat spinal cord, whereas the perfusion with 5,7-dihydroxytryptamine (10 microM) for 4 h decreased the contents of 5-hydroxytryptamine and dopamine. The descending inhibition was markedly potentiated by a 5-hydroxytryptamine uptake blocker, citalopram (10 nM), and was blocked by a 5-hydroxytryptamine antagonist, ketanserin (10-100 nM). Application of 5-hydroxytryptamine to the spinal cord induced an inhibition of the monosynaptic reflex, a later part of which was blocked by ketanserin. Ketanserin also moderately blocked inhibitions of the monosynaptic reflex caused by norepinephrine and dopamine. Phentolamine (10 microM) abolished the depressant actions of norepinephrine and dopamine, but did not affect that of 5-hydroxytryptamine or the descending inhibition. These results strongly suggest the involvement of 5-hydroxytryptamine, but not dopamine nor norepinephrine, in the descending inhibition. Besides ketanserin, the descending inhibition was blocked by ritanserin, haloperidol, and pipamperone, which have affinities to 5-hydroxytryptamine2 receptors, and also by spiperone and methiothepin, which are antagonists at both 5-hydroxytryptamine1 and 5-hydroxytryptamine2 receptors (all 1 microM). On the other hand, a 5-hydroxytryptamine1C and 5-hydroxytryptamine2 antagonist, mesulergine (1 microM), and 5-hydroxytryptamine3 antagonists, ICS 205-930 and quipazine (both 1 microM), did not depress either the descending inhibition or the 5-hydroxytryptamine-evoked inhibition of the monosynaptic reflex. The results with these antagonists favor the involvement of 5-hydroxytryptamine2 receptors although the results with mesulergine disagree with this notion. 5-Hydroxytryptamine1 agonists, such as 8-hydroxy-2-(di-n-propylamino)tetralin, buspirone, and 5-carboxyamidotryptamine, and a 5-hydroxytryptamine3 agonist, 2-methyl-5-hydroxytryptamine, induced a long-lasting inhibition of the monosynaptic reflex, which was blocked by ketanserin whereas a 5-hydroxytryptamine2 agonist, S-(+)-alpha-methyl-5-hydroxytryptamine, evoked a biphasic inhibition, in which only the later component was blocked by ketanserin.(ABSTRACT TRUNCATED AT 400 WORDS)

5,7-Dihydroxytryptamine↗
PubMed1979

Effect of propanolol on monosynaptic reflex activity during a task.

20 normal healthy subjects in a double-blind crossover experiment were given a table of either 40 mg propranolol or placebo half an hour before the beginning of the experiment. At rest and during the performance of a task, hert rate, Achilles tendon (T) and Hoffmann (H) reflexes were recorded. No increase in heart rate occurred during the task in the propranolol session. The increase of T-reflex amplitude, a common finding during the task under consideration, was larger in the propranolol session. No difference with H reflexes was found. It is concluded that the increase of T-reflex amplitudes during the task is caused only by fusimotor and not by sympathetic activity. It is speculated that if the sympathetic system plays a role at all, the effect on the T reflex is depressive rather than facilitating.

Adolescent↗
PubMed1989

The effects of postsynaptic inhibition on the monosynaptic reflex of the cat at different levels of motoneuron pool activity.

The motoneurons to the Soleus muscle in the decerebrate cat were activated by the crossed extensor reflex, elicited by stimulation of the contralateral common peroneal (CP) nerve. Monosynaptic reflexes were obtained from the Soleus motoneuron pool by stimulation of the cut L7-S1 dorsal roots. The amplitude of the reflex increased approximately linearly with the recruitment level of the motoneuron pool. Tonic postsynaptic inhibition was induced in the Soleus motoneuron pool by repetitive antidromic stimulation of the Lateral Gastrocnemius (LG) and Medial Gastrocnemius (MG) nerves at a rate of 17-47 stimuli/s. This reduced the size of the monosynaptic reflex at rest by at least 40%. However, when the motoneurons were active, the amplitude of the monosynaptic reflex obtained during repetitive stimulation of the LG-MG nerve increased with the recruitment level along the same curve as the control reflexes. Thus, tonic postsynaptic inhibition of the motoneurons per se cannot control the amplitude of the monosynaptic reflex independently of the recruitment level of the motoneuron pool. These experimental results verify predictions from computer simulations and suggest by exclusion that presynaptic inhibition is needed to control the amplitude of the monosynaptic reflex independently of the recruitment level of the motor pool.

Action Potentials↗
PubMed1976

Serotonin involvement in the blockade of bulbospinal inhibition of the spinal monosynaptic reflex.

Bulbospinal inhibition of the extensor quadriceps monosynaptic reflex (MSR) was antagonized by the serotonin precursor, 5-hydroxytryptophan (5-HTP, 75 mg/kg), in unanesthetized, mid-collicular, decerebrate cats. Fluoxetine HCl (Lilly 110140, 0.25 - 6 mg/kg), a specific serotonin neuronal uptake blocker, also blocked this inhibition as well as bulbospinal inhibition of the flexor posterior biceps-semi-tendinosus MSR. The serotonin antagonist, cyproheptadine HCl (5 mg/kg), partially reversed the above blocking actions of 5-HTP and fluoxetine and enhanced bulbospinal inhibition when administered alone in doses of 2.5-5 mg/kg. Imipramine HCl (0.125 - 4 mg/kg) was more potent in antagonizing bulbospinal inhibition of the dorsal root-ventral root MSR when administered intra-arterially to the spinal cord than when injected intra-arterially to the brain stem or intravenously, indicating that the spinal cord is the site of imipramine's action. These results support our earlier proposal that a 5-HT system antagonizes bulbospinal inhibition of the MSR. They also indicate that the 5-HT system is tonically active and exerts its blocking action in the spinal cord.

5-Hydroxytryptophan↗
PubMed1976

Tonic inhibitory influence of a supraspinal monoaminergic system on recurrent inhibition of an extensor monosynaptic reflex.

Recurrent inhibition of the extensor (quadriceps) monosynaptic reflex (MSR) was antagonized by a 5-hydroxytryptamine (5-HT) precursor, 5-hydroxytryptophan (5-HTP, 75 mg/kg), and a specific 5-HT neuronal uptake blocker, fluoxetine-HC1 (Lilly 110140, 0.25-6 mg/kg), in unanaesthetized decerebrate cats. This inhibition of the flexor (posterior biceps-semitendinosus) MSR was not altered by fluoxetine. Cyproheptadine-HC1 (5 mg/kg) partially reversed the above blocking actions of 5-HTP and fluoxetine and a thoracic "cold block", which eliminates supraspinal inputs to the caudal spinal cord, also eliminated the blockade by fluoxetine on recurrent inhibition. Cyproheptadine (2.5-5 mg/kg) or phenoxybenzamine-HC1 (2.5-5 mg/kg), administered alone, enhanced recurrent inhibition of the extensor but not of the flexor MSR. Since a "cold block" increased recurrent inhibition of the extensor reflex in control animals but failed to alter the inhibition in animals pretreated with either DL-p-chlorophenylalanine (300 mg/kg i.p. for 2 consecutive days) or DL-a-methyl-p-tyrosine methyl ester-HC1 (125 mg/kg i.p. 16 and 4 h prior to experiment), the monoaminergic system would appear to be tonically active. In addition the neuronal uptake blocker, imipramine-HC1 (0.125-4 mg/kg), was more potent in antagonizing recurrent inhibition when injected intra-arterially to the spinal cord than when administered intra-arterially to the brain stem or intravenously, indicating that this agent acts in the spinal cord to block the inhibition. These results support our previous proposal (ref. 18) that a supraspinal system involving 5-HT and noradrenaline antagonizes recurrent inhibition of the quadriceps MSR. This monoaminergic system is tonically active with the 5-HT nerve terminals located in the spinal cord.

5-Hydroxytryptophan↗
PubMed1987

Posttetanic changes in the afferent and efferent activity of monosynaptic reflex in kittens.

Both the afferent volleys from the dorsal root and the monosynaptic reflex discharges from the corresponding ventral root were recorded with hook electrodes during stimulation of the nerves innervating the triceps surae muscles. The effects of conditioning high frequency tetanus on the magnitudes of these afferents and reflex volleys were examined in kittens of postnatal age 1-90 days and in adult cats. In young kittens under barbiturate anaesthesia, large-amplitude monosynaptic reflex discharge can be evoked without prior conditioning. The amplitude of this reflex discharge decreased with increasing age of the animal. Application of conditioning tetanic stimuli to the muscle nerves resulted in posttetanic depression followed by posttetanic potentiation of the monosynaptic reflex. The magnitude of posttetanic depression was much higher than that of potentiation in the first postnatal week. As the age increased, the magnitude of depression decreased while the magnitude of potentiation increased. The afferent volley showed a considerable posttetanic potentiation in older kittens and cats. No significant potentiation or depression was observed in the younger animals. Possible mechanisms contributing to posttetanic depression and potentiation are discussed.

Afferent Pathways↗
PubMed1988

Development of the monosynaptic reflex pathway in the human spinal cord.

Development of the monosynaptic reflex pathway of the spinal cord was investigated in 96 neurologically normal infants with ages ranging from 25 weeks in postconceptional age (PCA) to 24 months after full-term delivery (PDA) by examining H-reflexes from the triceps surae and hypothenar muscles in terms of their incidence, latency and maximal size in reference to the maximal M-wave. The triceps H-reflex was evoked in all cases, and the latency was longest (26 ms) in the youngest case of 25 weeks (PCA). It gradually shortened until full-term gestation, reaching the shortest value of 17 ms (mean). The H-reflex size initially increased until full-term gestation, reaching the maximum value of 70% and then reducing gradually to the plateau level of about 30% at 12 months (PDA). The hypothenar H-reflex could not be elicited until 32 weeks (PCA). The time course of changes in its latency and size was similar to those of the triceps H-reflex, except that it could not be elicited after 12 months (PDA). Thus, the monosynaptic reflex pathway is already functioning at the age of 25 weeks (PCA) in man. The significance of the systematic change in latency and excitability of the H-reflex with age is discussed.

Aging↗
PubMed1977

Tonic inhibitory influence of a supraspinal monoaminergic system on presynaptic inhibition of an extensor monosynaptic reflex.

Presynaptic inhibition of the extensor (quadriceps, QUAD) monosynaptic reflex (MSR) in unanaesthetized decerebrate cats was antagonized by imipramine hydrochloride (2-5 mg/kg), 5-hydroxytryptophan (75 mg/kg) and a specific 5-hydroxytryptamine (5-HT) neuronal uptake blocker, fluoxetine hydrochloride (Lilly 110140, 0.25-6 mg/kg). These effects of imipramine and fluoxetine were partially reversed by the 5-HT antagonist, cyproheptadine hydrochloride (5 mg/kg), and completely reversed by the application of a thoracic cold block which prevents supraspinal inputs to the caudal spinal cord. Imipramine, however, failed to antagonize this inhibition in animals pretreated with either DL-p-chlorophenylalanine (p-CPA, 300 mg/kg i.p. for 2 consecutive days) or DL-a-methyl-p-tyrosine methyl ester hydrochloride (a-MPt, 125 mg/kg i.p. 16 and 4 h prior to the experiment). Cyproheptadine (2.5--5 mg/kg); phenoxybenzamine hydrochloride (2.5-5 mg/kg) and a cold block enhanced the inhibition of this extensor MSR but a cold block failed to alter the inhibition in animals pretreated with p-CPA or a-MPT. Presynaptic inhibition of the flexor (posterior biceps-semitendinosus, PBST) MSR was however not blocked by imipramine, fluoxetine or a cold block nor enhanced by cyproheptadine or phenoxybenzamine. The effects of the drugs tested and a cold block on the excitability of the QUAD group Ia afferents were reciprocal to those on the MSR during presynaptic inhibition. The results of this study indicate that descending tonically active systems (1) involving 5-HT and noradrenaline, antagonize presynaptic inhibition of the QUAD but not the PBST-MSR, (2) decrease the excitability of the QUAD Ia afferents and (3) increase the excitability of QUAD motoneurones.

5-Hydroxytryptophan↗
PubMed1989

Interaction of reversible and irreversible cholinesterase inhibitors on the monosynaptic reflex in neonatal rats.

The ability of physostigmine (PHY) and pyridostigmine (PYR) to protect against the segmental synaptic depression caused by sarin was examined in isolated spinal cords from neonatal rats. The monosynaptic reflex was unaffected at concentrations up to 0.1 microM PHY or 0.3 microM PYR but raising the concentrations of either drug produced a concentration-dependent depression of the monosynaptic reflex which could be completely antagonized by atropine. The monosynaptic reflex was depressed by 50% at 0.45 microM PHY and 2 microM PYR with maximal depression occurring at 1 microM PHY (to about 10% of control) and 10 microM PYR (to about 35% of control). Pretreating the cords with 0.1 microM PHY and PYR for 30 min failed to protect against the depressant effects of sarin even though they inhibited total cholinesterase (ChE) by 27 and 21%, respectively. Both PHY and PYR depressed total ChE activity of the spinal cord in a concentration-dependent manner with 50% inhibition of ChE occurring at 0.8 microM. These results suggest that the carbamates affect segmental transmission by activation of a muscarinic receptor, that protective carbamylation of ChE is ineffective against organophosphorus-induced segmental depression, and that inhibition of ChE is unrelated to both carbamate- and organophosphorus-induced depression of the monosynaptic reflex.

Animals↗
PubMed1975

Studies on the receptor responsible for vibration induced inhibition of monosynaptic reflexes in man.

A further attempt has been made to define the receptor responsible for the inhibition of monosynaptic reflexes by vibration in man. Vibration of the tendo Achillis will produce inhibition of the H reflex even when the muscles of the anterior compartment of the leg are denervated or blocked with local anaesthetic, implying that there are receptors in the posterior compartment capable of producing this effect. However, there is evidence that vibration spreads through the limb. The inhibition is greater when the anterior compartment is innervated indicating that there is a contribution from receptors in this compartment. Stretching the muscles of the posterior compartment alone, or the muscles of the anterior and posterior compartments reciprocally does not influence the inhibition of the monosynaptic reflex by vibration. These observations support the contention that the reduction of the monosynaptic reflex by vibration in man is due to presynaptic inhibition resulting from activation of primary spindle endings.

Adult↗
PubMed1990

The pharmacology of the spinal monosynaptic reflex following conditioning of a cutaneous and muscle nerve.

Conditioning of the spinal monosynaptic reflex from cutaneous or muscle afferents results in facilitation followed by inhibition. We administered a series of agents which have been shown to alter the monosynaptic reflex by blocking specific inhibitory pathways. We found that administration of mecamylamine and atropine, agents which affect recurrent inhibition had no effect on the facilitation or inhibition of the MSR by conditioning the sural or medial gastrocnemius nerve. Similarly, bicuculline, an agent which blocks pre-synaptic inhibition, had no effect on the conditioning of the MSR. However, strychnine, a glycine antagonist which blocks post-synaptic inhibition, did alter both the facilitation and inhibition of the MSR by conditioning pulses. Strychnine enhanced the facilitation and partially blocked the inhibition of the MSR by both sural and medial gastrocnemius conditioning. These data show that the flexor reflex afferents and the larger diameter afferents alter the MSR solely through glycine-mediated post-synaptic inhibition.

Afferent Pathways↗
PubMed1990

[The spinal monosynaptic reflexes elicited from the tibialis anterior muscle--standardization of the reflexes and diagnostic use in L5 radiculopathy].

The spinal monosynaptic reflexes evoked in the tibialis anterior muscle were investigated to establish a practical method for assessing L5 radiculopathy. Voluntary contraction and averaging technique made it possible to consistently obtain the H-and T-reflexes from the muscle in which these reflexes are normally unelicitable at rest. Based on the study of fifty normal subjects, formulae were produced by an analysis of the simultaneous regression of the latencies of these reflexes on height and age, because these latencies were highly correlated with them. A side-to-side latency difference of the H-and T-waves greater than 1.5 msec. and 2.3 msec. respectively, and/or low amplitude less than 26% and 39% of the amplitude of the contralateral side respectively, could be considered abnormal. According to these criteria, eight out of twelve patients (67%) with unilateral compressive L5 radiculopathy showed abnormalities.

Electrophysiology↗
PubMed1985

Electroneurographic correlates of the monosynaptic reflex: experimental studies and normative data.

The neurographic concomitants of the monosynaptic reflex, evoked either by electrical stimulation of the tibial nerve at the popliteal fossa or by percussion of the Achilles tendon, have been recorded from the sciatic nerve in the lower and middle thigh. Neurographic recordings were characterised by two travelling waves (P1 and P2), respectively increasing and decreasing in latency in the proximal direction, that showed the same chronological trend of the propagated action potentials concurrently recorded in the dorsal and ventral spinal roots at the lumbar level. At variance with P2, the speed of propagation of the P1 volley was stimulus-related, being faster on mechanical than on electrical stimulation, probably because in the latter case the latency of the fastest afferents is overestimated. The P2 volley is subserved by alpha-efferent fibres in either case as suggested, inter alia, by the strict parallelism between the P2 volley and the monosynaptic reflex under appropriate experimental conditions. Simultaneous recordings of spinal root and sciatic nerve action potentials allowed the direct assessment of afferent and efferent conduction velocities, both in the proximal (that is from the middle thigh to the spinal recording site and vice-versa) and in the distal (that is from the lower to the middle thigh recording site and vice versa) segments of the reflex arc. As expected, the speed of propagation of impulses was significantly higher in the proximal than in the distal segments, as well as in the afferent than in efferent limb of the monosynaptic pathway. The P1-P2 time interval was longer on mechanical than on electrical stimulation, probably due to the increased spinal delay of the T versus the H reflex. The present study provides a reliable method for the direct assessment of alpha-efferent as well as of Ia afferent group fibres conduction velocity, provided that in the latter case mechanical stimuli be used.

Adult↗
PubMed1978

Mechanism of monosynaptic reflex reinforcement during Jendrassik manoeuvre in man.

The facilitating effect of the Jendrassik manoeuvre on monosynaptic reflexes in man has been studied by comparing H and T reflexes of the soleus and by blocking the effects of spindle activation by ischaemia of the leg. The Jendrassik manoeuvre equally enhances H and T reflexes provided that the test reflexes are small. The H reflex remains facilitated when the spindle activation cannot affect the soleus alpha-motoneurones--that is, when the Ia afferent nerve fibres from the soleus are blocked by ischaemia. It is concluded that the facilitating effect of the Jendrassik manoeuvre on the alpha-motoneurones is not predominantly routed via the gamma-loop.

Achilles Tendon↗
PubMed1987

Effects of acetaldehyde on the monosynaptic reflex pathway in the cat spinal cord.

The effects of acetaldehyde on monosynaptic reflexes were investigated in the cat spinal cord. Intravenous injection of lower doses of acetaldehyde (0.1-0.5 mg/kg) increased the amplitude of the ventral root monosynaptic reflex potentials elicited by the dorsal root stimulation; the amplitude was decreased at higher doses (1.0-10.0 mg/kg). Acetaldehyde hyperpolarized the motoneuron at lower and depolarized it at higher doses. In some cells, however, acetaldehyde induced an initial, brief depolarization and subsequent hyperpolarization. Depolarization increased with increasing the dose of acetaldehyde. Hyperpolarization was always associated with an increased amplitude of the monosynaptically-induced action potentials. Depolarization was accompanied by a decreased amplitude or block of the action potentials. During aldehyde-induced depolarization, antidromic action potentials were more severely depressed than orthodromic ones. The present results suggest that acetaldehyde acts predominantly on the motoneuron membrane resulting in hyperpolarization at relatively lower doses and in depolarization at higher doses.

Acetaldehyde↗