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Results for “Reflex, Monosynaptic”

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PubMed1988

Segmental synaptic depression caused by diisopropylphosphorofluoridate and sarin is reversed by thyrotropin-releasing hormone in the neonatal rat spinal cord.

The organophosphorus compounds diisopropylphosphorofluoridate (DFP) and isopropylmethylphosphonofluoridate (sarin) depressed the monosynaptic reflex (MSR) in spinal cords from 7- to 9-day-old male rats. The concentrations of DFP and sarin which depressed the MSR by nearly 50% were 100 microM and 100 nM, respectively. Simultaneous superfusion of the cords with thyrotropin-releasing hormone (TRH) with either DFP or sarin resulted in a reversal of the depression. The depression caused by DFP was reversed to 95% of control by 100 nM TRH whereas similar reversal of sarin-induced depression required a 10-fold greater concentration of TRH. The potentiating effect of TRH was not affected by atropine even at a high concentration (1 microM) although atropine easily reversed organophosphorus-induced depression of the MSR. It appears that reversal of organophosphorus-induced depression by TRH might occur through a noncholinergic, TRH-sensitive receptor mechanism and may be unrelated to acetylcholinesterase activity. This action represents a possible utility of TRH as an adjunct in organophosphorus toxicity.

Animals↗

PubMed1989

Blocking effects of tetanus toxin and its fragment [A-B] on the excitatory and inhibitory synapses of the spinal motoneurone of the cat.

A highly purified fragment [A-B] preparation (5.5 micrograms of protein in 5 or 10 microliters which is far less than the minimal lethal dose), free from contamination with the whole toxin, was injected intraspinally into the neighbouring area of the gastrocnemius motoneurone pool (eight cats). Tetanus toxin (27 micrograms protein, about 100 LD50) in 5 or 10 microliters (four cats) and 10 microliters of Ringer's solution (four cats) were injected in the same way. Fragment [A-B] depressed both the monosynaptic reflex (MSR) of the gastrocnemius motoneurone pool and its inhibition by conditioning stimulus on the antagonistic peroneal nerve almost simultaneously in the individual cats, in contrast to the whole toxin which blocked first the inhibition of the MSR and later the MSR itself. The effects of fragment [A-B] appeared late, at about the time when the whole toxin blocked the MSR. The cats injected with fragment [A-B] did not die by intoxication. Fragment [A-B] at high doses (up to 120 micrograms) injected intramuscularly into the rat had no effect on neuromuscular transmission. The results clearly showed a blocking action of fragment [A-B] on inhibitory and excitatory synapses of the spinal motoneurones.

Animals↗

PubMed1992

Enzymatic inactivation of tachykinin neurotransmitters in the isolated spinal cord of the newborn rat.

A mixture of peptidase inhibitors increased the magnitude of the saphenous nerve-evoked slow depolarization of a lumbar ventral root and prolonged the similarly evoked inhibition of monosynaptic reflex (MSR) in the isolated spinal cord of the newborn rat in the presence of naloxone. The saphenous nerve-evoked MSR inhibition was curtailed by a tachykinin antagonist, GR71251, and after the treatment with GR71251, the peptidase inhibitor mixture no more prolonged the MSR inhibition. The present results suggest that enzymatic degradation plays a role in the termination of action of tachykinins released from primary afferents in the newborn rat spinal cord. The results provide a further support for the notion that tachykinins serve as neurotransmitters in the spinal cord of the newborn rat.

Animals↗

PubMed1984

Evidence for presynaptic inhibition of muscle spindle Ia afferents in man.

A new method for estimating presynaptic inhibition of soleus (Sol) Ia fibres in man is introduced based on the assessment of the amount of facilitation produced by a preceding homonymous Ia volley onto a Sol monosynaptic reflex. It was found in animal experiments that a reduction of such Ia facilitation reflects the amount of presynaptic inhibition exerted on these Ia fibres. Since, in man, a similar reduction of homonymous Ia facilitation was found after tibialis anterior vibration, this provides evidence for presynaptic inhibition of Sol Ia fibres, elicited here by the afferent discharge due to this flexor vibration.

Adult↗

PubMed1994

Short-latency excitation of hindlimb motoneurons induced by electrical stimulation of the pontomesencephalic tegmentum in the rat.

The monosynaptic reflex response evoked by stimulating the dorsal root L6 was greatly facilitated when a low intensity conditioning stimulus was applied to the pontomesencephalic tegmentum (PT) 1-2 ms in advance. When increasing the stimulus strength or the number of stimuli, motor discharges were recorded in the ventral roots and in nerves innervating hindlimb muscles. The lowest threshold site for reflex facilitation was found in a region just ventral to the superior colliculus. A descending volley was recorded from the medulla midline, in the region of the medial longitudinal fascicle (MLF) and from the spinal cord surface at thoracic and lumbar level. The latency of the descending volley and of the motor responses indicates that excitation of hindlimb motoneurons was due to activation of a disynaptic pathway having a relay in the lower brainstem. All spinal and peripheral responses evoked by PT stimulation disappeared when a small electrolytic lesion was placed in the MLF 1-2 mm rostral to the obex. The results show that in the rat the PT region may exert a powerful facilitatory action on hindlimb motoneurons.

Animals↗

PubMed1985

The systemic administration of local anaesthetics produces a selective depression of C-afferent fibre evoked activity in the spinal cord.

An electrophysiological analysis of the antinociceptive effects of systemic lidocaine and its longer acting primary amine congener, tocainide, has been performed in the decerebrate-spinal unanaesthetised rat. Neither of these local anaesthetic drugs when administered systemically in doses of up to 10 mg/kg (lidocaine) or 100 mg/kg (tocainide), produced any evidence of a block in the conduction of action potentials in A beta, A delta or C primary afferents. The local anaesthetics also failed to reduce mustard oil induced neurogenic extravasation, a test of cutaneous C-fibre terminal function. Lidocaine produced a transient (1-2 min) depression in monosynaptic reflexes at doses of greater than or equal to 1 mg/kg while tocainide had no effect on this reflex at any dose up to a 100 mg/kg. Both drugs, however, significantly suppressed the C-fibre evoked polysynaptic reflex generated by stimulating the sural nerve. The tocainide effect was longer lasting with less action on the short latency A beta-evoked reflex than lidocaine. The reflex activity in hamstring flexor alpha-motoneurones evoked by pinching the toes of the ipsilateral hind paw was reduced by both drugs but not abolished. Thermal and noxious chemical evoked reflexes were, however, completely suppressed by the local anaesthetic drugs, again with a longer action from tocainide. These results demonstrate that the systemic administration of drugs which increase the inactivation of sodium channels can produce a selective central block of certain types of afferent evoked activity in the spinal cord. There are resemblances between the selective C-fibre suppressing actions of systemically administered local anaesthetic and the pharmacological actions of narcotic opiates which may represent a similar mechanism for the analgesic action of these quite different classes of drugs.

Animals↗

PubMed1985

Modulation of spinal synaptic transmission by beta-melanocyte stimulating hormone (beta-MSH).

Synaptic modulation refers to altered excitability of a synapse by a substance that does not produce a spike potential at the synapse. Available evidence points to the conclusion that beta-melanocyte stimulating hormone (beta-MSH) modulates synaptic transmission through monosynaptic pathways in the cat spinal cord. Earlier evidence is reviewed, and new data are presented. In the first experiments populations of cells contributing to a knee jerk were studied using the Lloyd preparation, and MSH was found to increase the monosynaptic reflex. With intracellular single unit recording techniques, beta-MSH was found to facilitate recovery from synaptic transmission. With extracellular single unit recording techniques and iontophoretic methods for drug application, beta-MSH has been found to increase the probability of generation of single spike potentials by alpha-motoneurons in response to orthodromic stimulation. Administration of beta-MSH did not cause spontaneous discharge of alpha-motoneurons. The physiological and pharmacological importance of synaptic modulation is discussed.

Animals↗

PubMed2002

The special nature of human walking and its neural control.

Walking the way we do is inherently unstable. Sophisticated neurological control systems are required to ensure that we progress and maintain our balance at the same time. Most of what is known about the functional organization of these neurological control systems is inferred from studies on animals. Here, I compare selected studies on the neural control of human walking with similar studies in reduced animal preparations. The simple monosynaptic reflex appears to be controlled by comparable mechanisms in walking cats and humans. However, peripheral feedback mechanisms suggested to contribute to the switch from stance to swing on the basis of experiments in reduced cat preparations have little influence during human walking. A cat whose spinal cord has been completely transected can be made to walk on a treadmill by drug injections, but such an immediate effect of pharmacological intervention is not seen in humans. However, there have been reports that pharmacological intervention can improve the walking of patients with incomplete spinal cord injury, especially when pharmacological treatment is combined with training.

Animals↗

PubMed1997

Diisopropylfluorophosphate-induced depression of segmental monosynaptic transmission in neonatal rat spinal cord is also mediated by increased axonal activity.

Involvement of dorsal and ventral root activity for the depressant action of diisopropylfluorophosphate (DFP) on synaptic transmission was examined using in vitro spinal cord/root preparations. Superfusion of DFP produced a dose-dependent depression of monosynaptic reflex (MSR) and maximal depression of about 80% occurred at 1000 microM. The concentration to produce 50% of the maximal inhibition was about 100 microM of DFP. The DFP (100 microM)-induced depression of MSR was reversed by atropine (0.5 microM) but not by mecamylamine (0.5 microM). Contrary to the action on MSR, DFP potentiated the ventral root potential and 1st peak of dorsal root potential. The maximal potentiation was about 25% of control in both the root potentials at 100 microM of DFP. However, the second peak of dorsal root potential was slightly depressed (10-20% of control) by DFP (1-1000 microM). Further, the cords treated with DFP (100 microM) showed significant decrease in the cholinesterase (ChE) activity (27% of control). Results suggest that the DFP-induced depression was mediated at least by two different mechanisms, one through the inhibition of ChE activity and the other through the activation axonal activity having inhibitory inputs to the segmental synaptic transmission. These inputs mediate their action through muscarinic receptors.

Animals↗

PubMed1970

Early recovery of antidromic conduction through dendrites of spinal motoneurons in the normal, anoxic, and postanoxic states.

Penetration of two closely (3.2 Msec) spaced antidromic volleys in dendrites of spinal motoneurons is considered in the normal, anoxic, and postanoxic states. It is concluded that the value of the L-fraction (Lorente de N6) of membrane potential at the time of impulse conduction largely determines the extent of penetration or, in other words, the spatial decrement of dendritic conduction. The observations are pertinent to interpretations with respect to monosynaptic reflex transmission.

Dendrites↗

PubMed1989

Evidence for a contribution of the auditory cortex to audiospinal facilitation in man.

Facilitation of the spinal monosynaptic reflex by auditory stimulation has been demonstrated previously in animals and man. Analysis of the time course of audiospinal facilitation (ASF) in normal subjects is reported. The role of the cerebral cortex in the control of audiospinal facilitation was investigated in 32 patients with anatomically well-circumscribed lesions, the precise topography of which was determined stereotaxically. Lesions of the caudal part (Heschl's gyrus and temporal plane) of the superior temporal gyrus selectively depressed ASF evoked by contralateral auditory stimulation. In contrast, lesions in temporal, parietal and occipital lobes had no effect. Results obtained with frontal lobe lesions were not homogeneous. The specific involvement of auditory cortex in the gating of behavioral audiomotor reactions is discussed.

Acoustic Stimulation↗

PubMed1985

Dynamics of postural control in the child with Down syndrome.

We examined the development of neural control processes underlying stance balance in both developmentally normal children and children with Down syndrome to test the hypothesis that motor deficiencies in children with Down syndrome are associated with deficits within the automatic postural control system. We compared children with Down syndrome and developmentally normal children in two age groups (1-3 and 4-6 years) by using displacements of a platform and measuring electromyograms from leg muscles. The automatic muscle response pattern in both normal children and children with Down syndrome were directionally specific, although the pattern were more variable than in adults. Responses in children with Down syndrome showed no adaptive attenuation to changing task conditions. Onset latencies of responses in children with Down syndrome were significantly slower than in normal children. Presence of the monosynaptic reflex during platform perturbations at normal latencies suggests that balance problems in children with Down syndrome do not result from hypotonia, which researchers have defined as decreased segmental motoneuron pool excitability and pathology of stretch reflex mechanisms, but rather result from defects within higher level postural mechanisms.

Biomechanical Phenomena↗

PubMed1997

Characterization of adenosine receptors mediating spinal sensory transmission related to nociceptive information in the rat.

BACKGROUND: Adenosine analogs have been shown to produce antinociception after intrathecal administration. To determine the adenosine receptor subtype involved in spinal antinociception, the effects of selective agonists and an antagonist on the evoked potentials recorded from a neonatal rat spinal cord were studied. The measured potentials are a slow ventral root potential (slow VRP), which is the C-fiber-evoked excitatory response associated with nociceptive information; a monosynaptic reflex (MSR), which reflects a non-nociceptive transmission related to motor function; and a dorsal root potential (DRP), which reflects a gamma-aminobutyric acidA (GABA(A)) receptor-mediated presynaptic inhibition associated with analgesia. METHODS: The evoked potentials were recorded in response to electric stimulation of a lumbar dorsal root. Dose-response curves of agonists for these responses were obtained to determine their relative potency order. The antagonist dissociation constants (K(D) values) were estimated by Schild analysis. RESULTS: Adenosine agonists dose dependently inhibited the slow VRP and the MSR. However, the slow VRP was five to eight times more sensitive to them than was the MSR. The rank order of agonist potency was N6-cyclohexyladenosine (CHA) = N6-(R)-phenylisopropyladenosine (R-PIA) > 5'-N-ethylcarboxamidoadenosine (NECA) >> CGS 21680 in both responses. 8-Cyclopentyltheophylline produced dose-dependent parallel shifts to the right of NECA dose-response curves for these responses. Schild analysis gave linear plots with slopes near unity. The K(D) values of CPT for the MSR and the slow VRP were estimated to be 5.5 nM and 4.3 nM, respectively. The DRP was also depressed by adenosine agonists with potency order of CHA > NECA >> CGS 21680. 8-Cyclopentyltheophylline antagonized the inhibitory effects of CHA on the DRP. CONCLUSIONS: The results indicate that adenosine agonists inhibit spinal sensory transmission related to nociception by acting at the A1 receptors. The A1 receptor also seems to be involved in transmission related to the spinal motor system. Feedback inhibition mediated by GABA(A) receptors does not contribute to this antinociceptive action.

Adenosine↗

PubMed1994

GABA-B receptor-mediated spinal inhibition.

The intravenous administration to pentobarbitone-anaesthetized cats of the GABA-B antagonists CGP 46381 and CGP 35348 blocks the longer duration component of the inhibition of lumbar extensor monosynaptic reflexes by tetanic stimulation of low threshold flexor primary afferent fibres. GABA-B receptors thus appear to be associated with this inhibitory process, in addition to bicuculline-sensitive GABA-A receptors associated with shorter duration 'presynaptic' inhibition of reflexes and the depolarization of the terminals of primary afferent fibres.

Afferent Pathways↗

PubMed1995

Ketanserin-sensitive depressant actions of 5-HT receptor agonists in the neonatal rat spinal cord.

1. The monosynaptic reflex (MSR), recorded in vitro from the neonatal rat spinal cord, was depressed by 5-hydroxytryptamine (5-HT), 5-carboxamidotryptamine (5-CT), methysergide and R(+)-8-hydroxy-2-(di-n-propylamino) tetralin (8-OH-DPAT), and also by the selective 5-HT1D agonists, sumatriptan and N-methyl-3-(1-methyl-1-piperidinyl)-1H-indole-5-ethane sulphonamide (GR 85548). 2. Ketanserin (1 microM) and methiothepin (1 microM) reduced the duration of depressions elicited by 5-CT, but not those produced by 5-HT, sumatriptan, GR 85548, methysergide or 8-OH-DPAT. 3. The IC50 for MSR depression by 5-CT was 3.6, 2.1-6.2 nM (n = 4), by sumatriptan was 15.2, 12.9-18.0 nM (n = 32), by GR 85548 was 18.4, 11.7-29.1 nM (n = 12), by methysergide was 29.8, 10.2-87.1 nM (n = 4) and by 8-OH-DPAT was 0.21, 0.11-0.43 microM (n = 3) (geometric means and 95% confidence limits). 4. Ketanserin (0.1 or 1 microM) antagonized competitively responses to sumatriptan (apparent pA2 7.8 +/- 0.1, n = 5), GR 85548 (apparent pA2 7.6, unpaired data, n = 5), methysergide (apparent pA2 7.9 +/- 0.12, n = 4) and 8-OH-DPAT (apparent pA2 8.3 +/- 0.1, n = 3). Concentration-response curves to 5-CT showed a smaller, parallel shift to the right (apparent pA2 6.8 +/- 0.1, n = 4), but responses to 5-HT were unaffected by ketanserin (1 microM) (n = 4). 5. Methiothepin (1 microM) antagonized competitively responses to GR 85548 (apparent pA2 7.7, unpaired data, n = 5). 6. Mianserin (0.3 microM), a concentration sufficient to cause substantial block of 5-HT2C-mediated responses but have only a small effect on 5-HT1D-mediated actions, caused a small, non-parallel shift of the concentration-response curve to sumatriptan. 7. Depression of the MSR by sumatriptan was not blocked by (+/-)-cyanopindolol (0.1 microM), (+/-)-propranolol (0.5 or 1 microM) or spiroxatrine (0.1 microM), and depression of MSR by 8-OH-DPAT was not blocked by spiroxatrine (0.1 microM). (+/-)-Cyanopindolol (0.1 and 1 microM) itself induced a slow depression of the MSR. 8. The novel 5-HT1D antagonist, N-[4-methyl-1-piperazinyl) phenyl]2'-methyl-4'-(5-methyl-1,2,4-oxadiazol-3-yl) [1,1-biphenyl]-4-carboxamide (GR 127935, 30 nM to 1 microM) caused a concentration-related depression of the reflex (up to 50%) usually slow in onset. Neither with these concentrations nor with concentrations in the range 1-3 nM was there any unequivocal blockade of responses to sumatriptan. 9. It is concluded that sumatriptan, GR 85548, methysergide and 8-OH-DPAT depress the MSR in the neonate rat spinal cord via ketanserin-sensitive receptors, which have some similarities to 5-HT1D alpha receptors but which are not blocked by GR 127935. 5-HT released by tryptaminergic pathways may act via the same receptors to depress the MSR. 5-HT applied to the cord probably acts via a different, possibly novel 5-HT receptor to depress the MSR.

8-Hydroxy-2-(di-n-propylamino)tetralin↗

PubMed1988

Distribution of recurrent inhibition within a motor nucleus. I. Contribution from slow and fast motor units to the excitation of Renshaw cells.

The relation between the size of a monosynaptic reflex (MSR) to triceps surae and the resulting Renshaw cell discharge was used to evaluate the contribution from slow and fast motor units to the excitation of Renshaw cells. It is, however, difficult to interpret these results in terms of excitation contributed by slow and fast motor units because of the following reasons. First, the size of the MSR recorded in ventral roots is not linearly related to the number of recruited motor units, since larger motor axons contribute more to the size of the MSR than smaller ones. Second, the number of spikes evoked in a Renshaw cell burst is not linearly related to the excitatory input because Renshaw cell discharge saturates in the case of large responses. The contribution of small, early-recruited motoneurones to Renshaw cell excitation is consequently overestimated. Procedures were introduced to deal with these problems. It is concluded that the last-recruited motor units (probably 'fast twitch, fast fatiguing') on average contribute four times as much excitation to Renshaw cells as the first recruited ('slow twitch') motor units.

Animals↗

PubMed1969

Hind leg ataxia of cervical origin and cervico-lumbar spinal interactions with a supratentorial pathway.

1. Unilateral section of the nerves to an extensor muscle of the head, biventer cervicis, leads to an ataxia of the hind legs in cats.2. In chloralose anaesthetized cats, shocks to the central end of the cut biventer cervicis muscle nerves leads to direct discharges over lumbosacral ventral roots, to a facilitation of monosynaptic reflexes in flexor and extensor muscles and to a prolonged inhibition of spino-bulbo-spinal reflexes. Such effects are not unique, but follow stimulation of skin and muscle nerves of the forepaw.3. Supratentorial pathways are involved in descending spinal interactions in the chloralose anaesthetized cat, but are more critical for interactions taking origin in biventer cervicis nerve than in forepaw nerves.4. In non-anaesthetized spinal cats showing interactions from forepaw nerves, no interactions could be found taking origin in biventer cervicis nerves. Descending interactions from forepaw nerves could be reduced or abolished by anaesthetic doses of chloralose.5. The rich pathway from biventer cervicis nerve to the superior colliculus does not appear to be involved in the descending interactions reported here as neither stimulation nor ablation of the superior colliculi has any effect on descending interactions.

Anesthesia, Intravenous↗

PubMed1971

Spino-spinal mechanisms in the chloralose anaesthetized cat.

1. In chloralose anaesthetized cats the events in the lumbosacral cord that follow stimulation of a forepaw or neck nerve have been examined.2. Four events take place in the lumbosacral cord after forepaw or neck muscle nerve stimulation. These are: (1) a brief period of generalized enhanced motoneurone excitability, (2) a prolonged and as yet unexplained enhancement of monosynaptic reflexes, (3) a period of presynaptic inhibition in muscle and skin afferent fibres, and (4) a prolonged inhibition of spino-bulbo-spinal reflexes.3. A variable and sometimes selective reduction of one or another descending effects follows the placing of small lesions in the anterior portion of the suprasylvian gyrus.

Action Potentials↗