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Results for “Reflex, Monosynaptic”

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At least 37 records · Page 2Linked to original sources
PubMed1984

Orientation-induced artifacts in the measurement of monosynaptic reflexes.

Hoffmann and tendon jerk reflexes were tested in human subjects at various orientations between vertical, prone and supine. The data suggest that artifacts due to movement of soft tissue may explain the current disagreement in the literature on otolithic influences on these reflexes.

Electromyography↗
PubMed1984

Wiring diagrams of functional connectivity in monosynaptic reflex arcs of the spinal cord.

The direct functional connections between Ia and group II spindle afferent fibers from the cat medial gastrocnemius muscle and their homonymous motoneurons were examined in 10 acute experiments. Trains of stretch-evoked impulses from as many as 20 undivided sensory fibers were recorded simultaneously from 5 dorsal root filaments, as well as the corresponding excitatory postsynaptic potentials (EPSPs) they elicited in 10-20 motoneurons. Spike-triggered averaging [13] of these tape-recorded signals revealed the functional connections (or non-connections) between each Ia or group II afferent fiber and each motoneuron. Wiring diagrams constructed from these data indicate that the probability of a functional connection between an afferent fiber and a motoneuron decreases with the size of either and with the distance between the entry point of the afferent fiber and the motoneuron.

Afferent Pathways↗
PubMed1981

Facilitation of monosynaptic reflexes by voluntary contraction of muscle in remote parts of the body. Mechanisms involved in the Jendrassik Manoeuvre.

The facilitation of the tendon reflex of quadriceps, induced by voluntary contraction of a muscle group in the upper limb, evolves in the three phases and depends on several factos. These include the strength and type (ballistic or ramp) of the contraction. In the absence of any electromyographic activity in the conditioning muscle (from a lesion of its nerve trunk or by blockage of conduction by injection of xylocaine), a voluntary attempt to contract it causes only a moderate facilitation of the quadriceps motor nucleus; while reflex activation of the conditioning muscles, by vibration or sudden stretching. causes a more marked facilitation. Thus, it is concluded that at least two distinct mechanisms act sequentially. First, a general motor facilitation of supraspinal origin induces the first moderate phase of facilitations (phase I). This early facilitation precedes the onset of electromyographic activity in the conditioning muscle. Secondly, the more marked facilitation (phase II) is related to the stimulation of afferents originating from the conditioning muscles, either by fusimotor excitation in voluntary contraction or by manoeuvres which stimulate the spindle receptors mechanically. To investigate the transmission pathways of these facilitations, the latencies of these two phases were compared at two distant motor nuclei, the trigeminal motor nucleus and the quadriceps nucleus, following voluntary contractions of the tibialis anterior. Since the facilitations of the trigeminal motor nucleus precede those of the quadriceps motor nucleus, a slowly-travelling rostro-caudal facilitation is postulated during phase II when the facilitation is related to afferents coming from the contracting muscle. A long loop, therefore, is postulated to interpret the second phase of the facilitation curves.

Adolescent↗
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↗
PubMed2004

Endogenously released 5-hydroxytryptamine depresses the spinal monosynaptic reflex via 5-HT1D receptors.

In the spinal cord, various 5-hydroxytryptamine (5-HT) receptor subtypes are involved in the modulation of motor output. Previously, we have shown that 5-HT1B receptors mediate the monosynaptic reflex depression induced by exogenously applied 5-HT that was formed from the precursor L-5-hydroxytryptophan in spinalized rats. In this study, we determined the effects of endogenous 5-HT, which was released from serotonergic terminals by DL-p-chloroamphetamine, on spinal reflexes. DL-p-chloroamphetamine depressed the monosynaptic reflex and increased the polysynaptic reflex. The depletion of 5-HT abolished the monosynaptic reflex depression, but the increase in polysynaptic reflexes was maintained, suggesting that endogenous 5-HT released by DL-p-chloroamphetamine mediates depression of the monosynaptic reflex in the spinal cord. The depression of the monosynaptic reflex was antagonized by GR127935 (N-[methoxy-3-(4-methyl-l-piperazinyl)phenyl]-2'-methyl-4'-(5-methyl-1,2,4-oxadiazol-3-yl)[1,1-biphenyl]-4-carboxamide; 5-HT1B/1D receptor antagonist) and BRL15572 (3-[4-(4-chlorophenyl)piperazin-1-yl]-1,1-diphenyl-2-propanol; 5-HT1D receptor antagonist) but not by isamoltane (5-HT(1B) receptor antagonist). These results suggest that 5-HT released from serotonergic terminals depresses monosynaptic reflex transmission via 5-HT1D receptors.

Animals↗
PubMed2001

NO donor SIN-1 potentiates monosynaptic reflexes in the cat spinal cord.

The effect produced by the nitric oxide donor SIN-1 on monosynaptic reflexes was examined. Experiments were performed on anesthetized, paralyzed and spinalized cats. Lumbar monosynaptic reflexes were produced by stimulation of Ia afferents. I.v. application of SIN-1 (500 microg/kg) produced a mean marked potentiation of 704% of pre-drug control (100%) in the amplitude of monosynaptic reflexes. In addition, in other experiments a concentration-dependent effect on the amplitude of monosynaptic reflexes was observed after microinjections of SIN-1 into the ventral horn (1 microl; 10(-12) - 10(-3) M), with a mean facilitatory effect of 355%. In both cases, the potentiation was reversible 45 min after i.v. or local application of SIN-1. These results provide the first evidence that monosynaptic reflexes can be potentiated by nitric oxide.

Animals↗
PubMedDate not supplied

Effects and site of action of a single-breath of 100% CO2 on the monosynaptic reflexes in cats.

A single breath of 100% CO2 produces depression of the monosynaptic reflexes, recorded from L7 or S1 ventral root, after stimulation of the Posterior Biceps and Semitendinosus nerve (PBST) in anaesthetised cats. As the depression could not be attributed to the J-reflex(1), the possible site of action of the CO2 induced depression of monosynaptic reflexes was worked out. PBST nerve threshold did not change after CO2 introduction and the depression persisted in paralysed cats under controlled ventilation, thus eliminating the possibility of movement effect of the spinal cord due to tachypnoea. Spinal cord sections at the level of L1 and C1 abolished the depression, whereas the depression persisted in the decerebrate preparation. Thus it is concluded that a single-breath of 100% CO2 depresses the monosynaptic reflexes at the supraspinal level. Blood gas tensions (PO2 and pCO2) measured before and after CO2 introduction showed a shortlasting increase in pCO2 and not much significant change in pO2 compared to the long lasting depression of monosynaptic reflexes.

Action Potentials↗
PubMed1969

Presynaptic inhibition of the monosynaptic reflex by vibration.

In cats, the monosynaptic reflex (MSR) elicited from L7 or S1 dorsal roots, or from the tibial nerve (H reflex) was suppressed by vibration at 50-500 c/s of the hind limb with innervation intact. The MSR was not suppressed by selective vibration of cutaneous receptors, and suppression was still observed after the hind limb was skinned. In contrast, the phenomenon disappeared when all muscle nerves were crushed. SUPPRESSION OF THE MSR BY VIBRATION WAS SHOWN TO BE MEDIATED BY PRESYNAPTIC INHIBITION BY THE FOLLOWING METHODS: correlation with onset of the dorsal root potential (DRP) evoked by vibration, and abolition of both DRP and reflex suppression by picrotoxin; demonstration of primary afferent depolarization and normal excitability of motoneurones to direct stimulation. Reasons are given for deducing that the muscle afferent fibres responsible for the presynaptic inhibition induced by vibration are group Ia rather than groups Ib or II, or afferent fibres from Pacinian corpuscles.

Animals↗