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At least 19 recordsLinked to original sources
PubMedDate not supplied

[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↗
PubMed1970

Reflex inhibition of monosynaptic reflexes by stimulation of type J pulmonary endings.

1. Monosynaptic reflexes, evoked from flexor and extensor hind limb muscle nerves in cats anaesthetized with pentobarbitone sodium, were depressed for several seconds after right intra-atrial injection of phenyl diguanide. Injection of the drug close to the aortic valves did not produce the same effect on the reflex. There was no obvious depression of polysynaptic reflexes on intra-atrial injection of phenyl diguanide.2. This depression of the monosynaptic reflex was present even after the administration of atropine, which lessened the hypotension due to phenyl diguanide. The blood gas tensions were also measured after the administration of phenyl diguanide, and were not altered to a degree where one would expect the depression to be secondary to a change in arterial gas tensions. The depression was also present in paralysed and artificially ventilated cats.3. The afferent pathway causing this depression of the monosynaptic reflex runs in the vagus nerve, as shown by experiments done before and after vagotomy. Intercollicular decerebration also abolished this inhibition of the monosynaptic reflex.4. Prior intravenous injection of strychnine (0.1 mg/kg) abolished the effect of intra-atrial administration of phenyl diguanide.5. It was concluded that stimulation of type J pulmonary endings causes a reflex inhibition of monosynaptic reflexes lasting for several seconds via regions of the brain cephalad to the intercollicular level.

Animals↗
PubMed1996

The influence of muscle spindle discharge on the human H reflex and the monosynaptic reflex in the cat.

1. Experiments were carried out to test the effect of changes in spindle resting discharge on the size of monosynaptic reflexes in the cat and on the H reflex in humans. Resting discharge was altered by contracting the triceps surae muscle at longer (hold-long) or shorter (hold-short) lengths than that at which the reflex was tested. 2. The reflex in the cat was larger after hold-long than after hold-short conditioning, and the difference, after an initial decline, was well maintained. For the human H reflex a similar pattern was observed except that 15 s after muscle conditioning the difference in reflex size had disappeared. 3. Monosynaptic reflex depression immediately after hold-long conditioning, when most of the muscle spindles are silent, was attributed to the high level of spindle discharge during the immediately preceding hold-long period. The time course of this inhibition was too long to be accounted for by presynaptic inhibition. 4. In the cat heteronymous muscle conditioning was used to test whether presynaptic inhibition could be responsible for reflex depression using the synergist muscle pair lateral gastrocnemius-soleus and medial gastrocnemius. Conditioning one of the pair did not affect the reflex in the other, the opposite result to that expected with presynaptic inhibition. A similar experiment in which the triceps H reflex in human subjects was facilitated by a quadriceps volley gave the same result. 5. Thus this study presents evidence that monosynaptic reflexes are depressed by the on-going discharge of muscle spindles in the homonymous muscle, but that this depression does not appear to involve "classical' presynaptic inhibition.

Adult↗
PubMed1957

Temporal summation in rhythmically active monosynaptic reflex pathways.

Monosynaptic reflex responses elicited by repetitive stimulation in the frequency range between 60 and 100 per second yield evidence of temporal summation. The relation between stimulus interval and mean monosynaptic reflex response in the steady state at the frequencies studied is described adequately by an exponential decaying to 1/e in 4 msec. Since the temporal course of spatial summation is described adequately by the same exponential it is concluded that the two phenomena, temporal and spatial, are expressions of the same fundamental process intrinsic to the workings of the monosynaptic reflex pathway, to wit the synaptic potential-residual facilitation mechanism of prior descriptions. Some discussion of implications is appended.

Reflex↗
PubMed1957

Reflex depression in rhythmically active monosynaptic reflex pathways.

A study has been made of the depression that occurs when a monosynaptic reflex pathway is subjected to repetitive stimulation. Reflex depression has a dual origin. High frequency or early depression is postsynaptic in origin and results from subnormality in the motoneurons. Low frequency, late, or enduring depression is presynaptic in origin. The conditioning volley-test volley technique and the frequency-mean monosynaptic reflex amplitude relation yield similar information concerning reflex depression. Each method has its advantages and for some purposes one or the other of the methods necessarily must be employed. The results of a variety of experiments are consistent with the proposition that reflex depression in the monosynaptic reflex pathway originates by action in the group IA afferent fibers of muscle origin that are responsible for monosynaptic reflex transmission. Depression is present at a frequency of 0.1 per second (6 per minute) and absent at a frequency of 0.05 per second (3 per minute). Thus it is impractical for most purposes to employ repetition rates that satisfy the requirement for designation as "single shock" stimulations. The temporal course of enduring depression has been determined. It is identical with that for a number of other phenomena observable in monosynaptic reflex pathways, which suggests a common origin. The mechanism of low frequency or enduring depression is discussed in the light of this suggestion.

Depression↗
PubMed2006

Acute muscle inflammation enhances the monosynaptic reflexes and c-fos expression in the feline spinal cord.

The aim of this research was to study the changes of the motor reflex activity (monosynaptic reflex (MSR) of the flexor and extensor muscles) and Fos immunoreactivity in lumbo-sacral spinal cord after acute induced myositis of m. gastrocnemius-soleus (GS). The experiments were carried out on ischaemic decerebrated, spinalized in C1 cats. After infiltration of the GS muscle with carrageenan (2%) MSRs of flexors and extensors showed a significant increase in amplitude +127+/-24.5% and +155+/-28.5%, respectively, p<0.05. The exposed effect was initiated within 30 min and achieved a maximum 2.8h after the intramuscular injections of carrageenan. After analysis of dynamics of the MSRs, animals were perfused and c-fos expression in the spinal segments L6-S1 was evaluated. In comparison to sham-operated animals, the number of Fos-immunoreactive (Fos-ir) cells was noticeably increased in the lumbar cord of cats with carrageenan-induced myositis. The labeled cells were concentrated in the ipsilateral laminae I/II, neck of the dorsal horn (V/VI) and intermediate zone (VII), however, clear predominance of their concentration was found in the deep laminae. The effect of muscle inflammation was also expressed as a significant decline in the number of NADPH-d-reactive cells (p<0.05) in ipsilateral laminae I/II of L6/L7. The results show that the input from acutely inflamed muscles may induce an increase of the reflex responsiveness of flexors and extensors which is not mediated via the gamma-spindle-loop and which coincides with a significant increase in c-fos expression in the deep laminae of the lumbar spinal cord.

Action Potentials↗
PubMed1959

Functional organization in the terminal segments of the spinal cord with a consideration of central excitatory and inhibitory latencies in monosynaptic reflex systems.

Prominent monosynaptic and disynaptic reflex discharges characterize ipsilateral reflex transmission in the third sacral segment. Convergence upon the motoneurons from the two sides of the body is inhibitory, that through disynaptic paths excitatory. The relative latencies of excitation and inhibition of reflex responses, of excitatory and inhibitory synaptic potentials, and of various aspects of impulse discharge in motoneurons are considered. It is concluded: (1) that a direct (i.e. monosynaptic) action of primary afferent collaterals upon motoneurons is responsible for inhibition of monosynaptic reflex discharge of antagonist motoneurons within a myotatic unit; (2) that the inhibitory postsynaptic potential as described is not the primary agency for monosynaptic reflex inhibition of monosynaptic reflex discharge; (3) that, however, a common causal agent may be responsible for inhibition of reflex discharge and for generation of an inhibitory postsynaptic potential; and (4) that the inhibitory post-synaptic potential may be linked with, or be the agent for, inhibition of soma response.

Motor Neurons↗
PubMed1994

A novel 5-HT receptor or a combination of 5-HT receptor subtypes may mediate depression of a spinal monosynaptic reflex in vitro.

The monosynaptic reflex (MSR), recorded in vitro from the neonatal rat spinal cord, was depressed by 5-hydroxytryptamine (5-HT) and 5-HT receptor agonists. The results, together with our previous findings, indicate an apparent rank order of potency: 5-carboxamidotryptamine (5-CT) > sumatriptan > methysergide > 5-HT >> 8-hydroxy-2-(di-n-propylamino) tetralin (8-OH-DPAT) > 5-methoxytryptamine (5-MeOT) = 1-[3-(trifluoromethyl)phenyl]-piperazine (TFMPP) > alpha-methyl-5-hydroxytryptamine (alpha-Me 5-HT) >> (+/-)-1-(2,5-dimethoxy-4-iodophenyl)-2-aminopropane (DOI). The equipotent molar ratios were 5-CT 0.12, sumatriptan 0.4, methysergide 0.72, 5-HT 1.0, 8-OH-DPAT 13.3, 5-MeOT 26.7, TFMPP 31, alpha-Me 5-HT 402 and DOI > 3333. Time for peak depression from start of agonist application was 3-4 min for 5-HT, 5 min for sumatriptan and 5-MeOT, 5-7 min for alpha-Me 5-HT and 12 min for 8-OH-DPAT. The half-time for recovery from peak depression was 1.5 +/- 0.3 min for 5-HT, 2.8 +/- 0.3 min for 5-MeOT, 5.3 +/- 1.5 min for sumatriptan, 13 +/- 2.9 min for 8-OH-DPAT and > 30 min for alpha-Me 5-HT. 8-OH-DPAT induced depression of the reflex (IC50 0.85, 0.7-1.0 microM, geometric mean and 95% confidence limits) was blocked by spiperone (1 microM, apparent pA2 6.3) suggesting mediation via 5-HT1A receptors.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed2006

[Excitation and inhibition in monosynaptic reflex arcs of white rats in conditions of spinal hyperreflexia].

The mechanisms of excitation and inhibition in monosynaptic reflex arcs of white rats in conditions of spinal superreflexion (a state, in which the amplitude of reflex monosynaptic discharges of a ventral root (MD VR) is close to a threshold of excitation of motoneurons axon) were investigated. The character of MD VR during recording of their reflex discharges from cut and uncut VR was studied. Previously established pattern MR VR generation as extremely high voltage and presence of its second component are observed in these conditions. In a state of superreflexion intersegmental interactions getting weaker and are particularly characterized by inhibitive influences from segment L4 on motoneurons of segment L5. It is shown that in animals with spinal superreflexion expression of the antidromic inhibition is weaker compare to intact ones. It was defined that reciprocal interrelations of flexor and extensor motoneurons are maintained and even strengthen.

Animals↗
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↗
PubMed1949

Post-tetanic potentiation of response in monosynaptic reflex pathways of the spinal cord.

Following tetanic afferent stimulation of a monosynaptic reflex pathway, the transmission through that pathway of isolated reflex volleys is enhanced for some minutes. Post-tetanic potentiation is comparable in the monosynaptic reflex arcs of flexor and extensor muscles. The facilitator and inhibitor actions of monosynaptic reflex afferent fibers, as well as the transmitter action, are potentiated following tetanization. Little post-tetanic change attends reflex transmission through plurisynaptic reflex arcs. Various tests for excitability change made independently of the tetanized afferent fibers reveal none or a slight depression. Hence the potentiating influence of a tetanus is limited to subsequent action on the part of the recently tetanized fibers themselves. Increase in the size of the individual impulses comprising an afferent volley such as might occur during positive after-potential, would accommodate the requirement for a limited process and provide for increased synaptic action. The proposed association between post-tetanic potentiation and positive after-potential (i.e. hyperpolarization) is supported by the following lines of evidence:- 1. Changes in intensity and duration of potentiation with change in frequency and duration of tetanic stimulation are characteristic of, and parallel to, the changes of positive after-potential in similar circumstances. 2. Afferent impulses are increased following a tetanus, and in a fashion that parallels the course of monosynaptic reflex potentiation. Post-tetanic potentiation, as here described, and after-discharge, whatever may be its mechanism, are unrelated phenomena.

Muscles↗
PubMed1982

Topical anesthesia: modulation of the monosynaptic reflexes by desensitization of the skin.

Skin desensitization by topical anesthesia was studied for its effect on the motoneuron excitability of the soleus muscle. Skin areas overlying calf, tibial, quadriceps and hamstrings muscles and skin dermatomes (L2, L3, L4, L5, S1 and S2) were studied separately. Motoneuron excitabilities were measured by the H-reflex and Achilles tendon reflex (for alpha and gamma motoneurons). It was shown that anesthesia applied to all skin areas and dermatomes, except those overlying the antagonist muscles, resulted in significant facilitation of the soleus H-reflex. In these cases, the ATR showed either slight inhibition or no significant changes. Anesthesia to the skin overlying the anterior tibial antagonistic muscle produced varied and inconsistent modifications in the amplitude of the H-reflex. In these cases the ATR was either slightly facilitated or showed no significant changes. These results appear to indicate the existence of on-going excitatory and inhibitory effects from the skin on the alpha and gamma motoneuron pool probably via segmental and suprasegmental levels. A possible clinical application of these results to modulate the motoneuron pool excitability is proposed.

Administration, Topical↗