Effects of some centrally acting muscle relaxants on spinal root potentials: A comparative study

Farkas, Sándor; Tarnawa, Istvàn; Berzsenyi, Pál

doi:10.1016/0028-3908(89)90053-1

Cited by 28 publications

(19 citation statements)

References 38 publications

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“…The results that the inhibitory effects of diazepam on the group II flexor reflex tended to be saturated at a dose of 2.5 mg/kg, a higher dose than that which caused a per fect inhibition of the flexor reflex recorded by the contrac tion of the flexor muscle (8), might indicate that the group II flexor reflex is a component of the polysynaptic reflexes which are resistant to the benzodiazepines as sug gested by Farkas et al (22) and Schlosser (23). The effects of diazepam in anesthetized spinal rats were reduced in comparison with those in intact rats, which is in agree ment with the results of other investigators (9,24), but di azepam did not affect the NA-induced facilitation of the group II flexor reflex.…”

Section: Discussionmentioning

confidence: 71%

The Effects of Centrally Acting Muscle Relaxants on the Intrathecal Noradrenaline-Induced Facilitation of the Flexor Reflex Mediated by Group II Afferent Fibers in Rats

Sakitama

1993

Japanese Journal of Pharmacology

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ABSTRACT-The effects of centrally acting muscle relaxants on the flexor reflex mediated by group II afferent fibers (group II flexor reflex) in anesthetized intact rats and on the intrathecal noradrenaline-HC1 induced facilitation of the group II flexor reflex in anesthetized spinal rats were investigated. In anesthetized intact rats, mephenesin, tolperisone-HCI, chlorpromazine-HC1 and baclofen inhibited the group II flexor reflex dose-dependently, whereas the inhibitory effect of tizanidine-HC1 was bell-shaped. The effect of diazepam tended to be saturated. In anesthetized spinal rats, mephenesin, tolperisone-HCI, chlorproma zine-HCI, diazepam and baclofen also depressed the group II flexor reflex, but tizanidine-HC1 slightly increased it. The intrathecal noradrenaline-HCI-induced facilitation of the group II flexor reflex was not affected by mephenesin or diazepam, but was inhibited by tizanidine-HCI, tolperisone-HCI, chlorproma zine-HCl and baclofen. These results suggest that compounds with centrally acting muscle relaxant activity depress the group II flexor reflex in different manners, and the inhibition of descending noradrenergic tonic facilitation within the spinal cord participates in the depressant action of the group II flexor reflex produced by tolperisone-HC1, tizanidine-HC1, chlorpromazine-HC1 and baclofen.

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Section: Discussionmentioning

confidence: 71%

The Effects of Centrally Acting Muscle Relaxants on the Intrathecal Noradrenaline-Induced Facilitation of the Flexor Reflex Mediated by Group II Afferent Fibers in Rats

Sakitama

1993

Japanese Journal of Pharmacology

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“…On the other hand, the flexor reflex evoked by non-nociceptive stimulation is not affected by morphine (4). Mephenesin, a centrally acting muscle relaxant, has been reported to depress PSRs (5,6) including the flexor reflex measured by the contractions of the flexor muscles (7,8), while the withdrawal response of the hindlimb is not affected by mephenesin (9). These re sults indicate that the flexor reflex mediated by group IV afferent fibers is depressed by morphine and not affected by mephenesin.…”

mentioning

confidence: 74%

The Flexor Reflex Mediated by Group II Afferent Fibers: Effects of Morphine-HCl and Mephenesin.

Sakitama

Ishikawa

1992

Jpn.J.Pharmacol

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ABSTRACT-The effects of morphine-HC1 and mephenesin on the flexor reflex mediated by group II afferent fibers were investigated. The flexor reflex was recorded by means of the electromyogram (EMG) evoked in the muscle tibialis anterior by stimulation of the ipsilateral tibial nerve in urethane a-chloralose anesthetized rats. Afferent volleys corresponding to the phasic EMG component of the flexor reflex with 7.6-msec latency (flexor EMG: fEMG) were also recorded using the double volley technique. The threshold of the afferent volleys mediating the fEMG was approximately twice as high as that of the most excitable afferent volleys, which were considered the spikes of group I afferent fibers, and the conduction velocity of the afferent volleys was 39.9 ± 3.2 m/sec. Morphine-HCI (5 mg/kg, i.v.) did not change the amplitude of the fEMG, but mephenesin (40 and 80 mg/kg, i.v.) de pressed it dose-dependently. These results suggest that the fEMG is a flexor reflex mediated by group II afferent fibers, which is not affected by morphine-HCI but depressed by mephenesin.Keywords: Morphine, Mephenesin, Flexor reflex, Group II afferent fiberThe flexor reflex, a polysynaptic reflex (PSR) whose afferent fibers consist of groups II, III and IV afferent fibers, has been recorded by the withdrawal response of the hindlimb, the contraction of the flexor muscle or the electromyogram (EMG) evoked in the flexor mus cles. These reflexes have been used to evaluate the effects of various drugs such as analgesics or centrally acting muscle relaxants; however, the effects of drugs are not always consistent. Morphine, a well-known analgesic, has been reported to depress the withdrawal response of the hindlimb (1-3), which is a flexor reflex induced by the nociceptive stimulation that is strong enough to activate group IV afferent fibers (4). On the other hand, the flexor reflex evoked by non-nociceptive stimulation is not affected by morphine (4). Mephenesin, a centrally acting muscle relaxant, has been reported to depress PSRs (5, 6) including the flexor reflex measured by the contractions of the flexor muscles (7,8), while the withdrawal response of the hindlimb is not affected by mephenesin (9). These re sults indicate that the flexor reflex mediated by group IV afferent fibers is depressed by morphine and not affected by mephenesin. Although the flexor reflex mediated by non-nociceptive group II afferent fibers seems to be depressed by mephenesin and not affected by morphine, little work has been performed on the flexor reflex mediated by these fibers. So, the aim of the present study was to investigate the effects of morphine-HCI and mephenesin on the flexor reflex mediated by group II afferent fibers.We attempted to use the phasic EMG component of the flexor reflex with a latency of 7.6 msec (flexor EMG: fEMG) as a flexor reflex mediated by group II afferent fibers because this component is thought to be evoked by non-nociceptive stimulation (10). As a first step, we recorded afferent volleys from the ipsilateral dorsal root simultane...

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“…Glycinergic and GABAergic synaptic potentials were blocked with strychnine (0.3 M) and bicuculline (3 M). Polysynaptic transmission was blocked or reduced by mephenesin (1 mM) (Farkas et al, 1989;Vinay et al, 1995). Locomotor-like activity was induced by perfusion of NMDA (3.5-10 M) and 5-hydroxytryptamine (5-HT; 3.5-15 M), occasionally in combination with dopamine (50 M; all from Sigma).…”

Section: Methodsmentioning

confidence: 99%

“…Of the excitatory responses, two were determined to be direct because they persisted in the presence of the barbiturate mephenesin (1 mM), which severely reduces the probability of disynaptic and polysynaptic neurotransmission (Farkas et al, 1989;Vinay et al, 1995;Butt and Kiehn, 2003). The remaining three excitatory responses were not tested in this way.…”

Section: Synaptic Connectivity Of Scinsmentioning

confidence: 99%

Segmental, Synaptic Actions of Commissural Interneurons in the Mouse Spinal Cord

Quinlan¹,

Kiehn²

2007

Journal of Neuroscience

121

148

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Left-right alternation depends on activity in commissural interneurons (CINs) that have axons crossing in the midline. In this study, we investigate the CIN connectivity to local motor neurons using a newly developed preparation of the in vitro neonatal mouse spinal cord that allows us to identify all classes of CINs. Nineteen of 29 short-range CINs with axonal projections Ͻ1.5 segments (sCINs) directly excited, directly inhibited, or indirectly inhibited contralateral motor neurons in the quiescent spinal cord. Excitation was glutamatergic and inhibition was mixed glycinergic and/or GABAergic. Long-range CINs were also found to have input to local, contralateral motor neurons. Thirteen of 29 descending CINs had similar synaptic connectivity to contralateral motor neurons as the sCINs, including direct excitation and direct and indirect inhibition. Some (9 of 23) rostrally projecting ascending CINs, and a few (2 of 10) CINs with bifurcating axons that both ascend and descend, indirectly inhibited local, contralateral motor neurons. Rhythmic firing during locomotor-like activity was observed in a number of CINs with segmental synaptic effects on contralateral motor neurons. This study outlines the basic connectivity pattern of CINs in the mouse spinal cord on a segmental level. Our study suggests that, based on observed synaptic connectivity, both short-and long-range CINs are likely involved in segmental left-right coordination and that the CIN system is organized into a dual-inhibitory and single-excitatory system. These systems are organized in a way that they could provide appropriate coordination during locomotion.

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Effects of some centrally acting muscle relaxants on spinal root potentials: A comparative study

Cited by 28 publications

References 38 publications

The Effects of Centrally Acting Muscle Relaxants on the Intrathecal Noradrenaline-Induced Facilitation of the Flexor Reflex Mediated by Group II Afferent Fibers in Rats

The Effects of Centrally Acting Muscle Relaxants on the Intrathecal Noradrenaline-Induced Facilitation of the Flexor Reflex Mediated by Group II Afferent Fibers in Rats

The Flexor Reflex Mediated by Group II Afferent Fibers: Effects of Morphine-HCl and Mephenesin.

Segmental, Synaptic Actions of Commissural Interneurons in the Mouse Spinal Cord

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