The Experts below are selected from a list of 231 Experts worldwide ranked by ideXlab platform
Hideki Ono - One of the best experts on this subject based on the ideXlab platform.
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GABAB receptors do not mediate the inhibitory actions of gabapentin on the Spinal Reflex in rats.
Journal of pharmacological sciences, 2004Co-Authors: Shinobu Shimizu, Motoko Honda, Mitsuo Tanabe, Hideki OnoAbstract:Abstract The clinical effectiveness of gabapentin for the treatment of epilepsy, spasticity, and neuropathic pain has been established. The mechanisms responsible for those actions, however, are still not clearly understood. We have recently demonstrated that gabapentin reduces the Spinal Reflex in rats via mechanisms that do not involve γ-aminobutyric acid (GABA)A receptors. In the study, we attempted to explore the involvement of GABAB receptors in gabapentin-induced inhibition of the Spinal Reflexes in Spinalized rats. Stimulation of the dorsal root at L5 elicited the segmental mono- (MSR) and polysynaptic Reflex (PSR) in the ipsilateral ventral root. The microinjection of gabapentin (1.5 and 5 nmol) into the ventral horn reduced both MSR and PSR, whereas the injection into the dorsal horn only inhibited the PSR, indicating that systemic gabapentin inhibits the MSR at the ventral horn and it inhibits the PSR at both the ventral and dorsal horns. The GABAB-receptor antagonist CGP35348 (0.5 nmol) injected into the ventral horn antagonized the inhibition of the Spinal Reflexes by the GABAB-receptor agonist baclofen (i.v.) but not by gabapentin (i.v.). Thus, GABAB receptors do not appear to contribute to the gabapentin-induced inhibition of the Spinal Reflex.
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Tricyclic analogs cyclobenzaprine, amitriptyline and cyproheptadine inhibit the Spinal Reflex transmission through 5-HT2 receptors
European Journal of Pharmacology, 2002Co-Authors: Motoko Honda, Takashi Nishida, Hideki OnoAbstract:The centrally acting muscle relaxant cyclobenzaprine decreases the amplitude of monosynaptic Reflex potentials by inhibiting the facilitatory descending serotonergic influences in the Spinal cord. Interestingly, the structure of cyclobenzaprine is much similar to those of amitriptyline and cyproheptadine. In the present study, we attempted to elucidate the relationship between 5-HT(2) receptor antagonistic and inhibitory effects of cyclobenzaprine, amitriptyline, cyproheptadine and ketanserin on the Spinal Reflexes. Cyclobenzaprine, amitriptyline, cyproheptadine, and ketanserin significantly inhibited facilitatory effects of 1-(2,5-dimethoxy-4-iodophenyl)-2-aminopropane (DOI) on flexor Reflexes and mono- and polysynaptic Spinal Reflex potentials in Spinalized rats. In intact rats, these drugs significantly reduced the mono- and polysynaptic Reflex potentials. 5-HT depletion significantly prevented the depression of the Spinal Reflex potentials induced by these drugs. These results suggest that the inhibitory effects of cyclobenzaprine, amitriptyline, and cyproheptadine on mono- and polysynaptic Reflex potentials are due to the inhibition of descending serotonergic systems through 5-HT(2) receptors in the Spinal cord.
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Method for recording Spinal Reflexes in mice: effects of thyrotropin-releasing hormone, DOI, tolperisone and baclofen on monosynaptic Spinal Reflex potentials.
Japanese journal of pharmacology, 2001Co-Authors: H Okada, M Honda, Hideki OnoAbstract:Mice were used to record the Spinal Reflex potentials and to examine the effects of some drugs upon them. In anesthetized mice, laminectomy was performed in the lumbo-sacral region, and monosynaptic Reflex potential (MSR) and polysynaptic Reflex potential were recorded from the L5 ventral root after stimulation of the L5 dorsal root. Thyrotropin-releasing hormone (TRH) and 1-(4-iodo-2,5-dimethoxyphenyl)-2-aminopropane hydrochloride (DOI) produced transient and long-lasting increases in the MSR amplitude, respectively. Tolperisone hydrochloride and baclofen produced transient and long-lasting MSR depressions, respectively. These results show that mice can be used to record Spinal Reflex potentials, and that it may be possible to study the Spinal cord function of mutant and knockout mice using this method.
Motoko Honda - One of the best experts on this subject based on the ideXlab platform.
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GABAB receptors do not mediate the inhibitory actions of gabapentin on the Spinal Reflex in rats.
Journal of pharmacological sciences, 2004Co-Authors: Shinobu Shimizu, Motoko Honda, Mitsuo Tanabe, Hideki OnoAbstract:Abstract The clinical effectiveness of gabapentin for the treatment of epilepsy, spasticity, and neuropathic pain has been established. The mechanisms responsible for those actions, however, are still not clearly understood. We have recently demonstrated that gabapentin reduces the Spinal Reflex in rats via mechanisms that do not involve γ-aminobutyric acid (GABA)A receptors. In the study, we attempted to explore the involvement of GABAB receptors in gabapentin-induced inhibition of the Spinal Reflexes in Spinalized rats. Stimulation of the dorsal root at L5 elicited the segmental mono- (MSR) and polysynaptic Reflex (PSR) in the ipsilateral ventral root. The microinjection of gabapentin (1.5 and 5 nmol) into the ventral horn reduced both MSR and PSR, whereas the injection into the dorsal horn only inhibited the PSR, indicating that systemic gabapentin inhibits the MSR at the ventral horn and it inhibits the PSR at both the ventral and dorsal horns. The GABAB-receptor antagonist CGP35348 (0.5 nmol) injected into the ventral horn antagonized the inhibition of the Spinal Reflexes by the GABAB-receptor agonist baclofen (i.v.) but not by gabapentin (i.v.). Thus, GABAB receptors do not appear to contribute to the gabapentin-induced inhibition of the Spinal Reflex.
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Tricyclic analogs cyclobenzaprine, amitriptyline and cyproheptadine inhibit the Spinal Reflex transmission through 5-HT(2) receptors.
European journal of pharmacology, 2003Co-Authors: Motoko Honda, Takashi NishidaAbstract:The centrally acting muscle relaxant cyclobenzaprine decreases the amplitude of monosynaptic Reflex potentials by inhibiting the facilitatory descending serotonergic influences in the Spinal cord. Interestingly, the structure of cyclobenzaprine is much similar to those of amitriptyline and cyproheptadine. In the present study, we attempted to elucidate the relationship between 5-HT(2) receptor antagonistic and inhibitory effects of cyclobenzaprine, amitriptyline, cyproheptadine and ketanserin on the Spinal Reflexes. Cyclobenzaprine, amitriptyline, cyproheptadine, and ketanserin significantly inhibited facilitatory effects of 1-(2,5-dimethoxy-4-iodophenyl)-2-aminopropane (DOI) on flexor Reflexes and mono- and polysynaptic Spinal Reflex potentials in Spinalized rats. In intact rats, these drugs significantly reduced the mono- and polysynaptic Reflex potentials. 5-HT depletion significantly prevented the depression of the Spinal Reflex potentials induced by these drugs. These results suggest that the inhibitory effects of cyclobenzaprine, amitriptyline, and cyproheptadine on mono- and polysynaptic Reflex potentials are due to the inhibition of descending serotonergic systems through 5-HT(2) receptors in the Spinal cord.
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Tricyclic analogs cyclobenzaprine, amitriptyline and cyproheptadine inhibit the Spinal Reflex transmission through 5-HT2 receptors
European Journal of Pharmacology, 2002Co-Authors: Motoko Honda, Takashi Nishida, Hideki OnoAbstract:The centrally acting muscle relaxant cyclobenzaprine decreases the amplitude of monosynaptic Reflex potentials by inhibiting the facilitatory descending serotonergic influences in the Spinal cord. Interestingly, the structure of cyclobenzaprine is much similar to those of amitriptyline and cyproheptadine. In the present study, we attempted to elucidate the relationship between 5-HT(2) receptor antagonistic and inhibitory effects of cyclobenzaprine, amitriptyline, cyproheptadine and ketanserin on the Spinal Reflexes. Cyclobenzaprine, amitriptyline, cyproheptadine, and ketanserin significantly inhibited facilitatory effects of 1-(2,5-dimethoxy-4-iodophenyl)-2-aminopropane (DOI) on flexor Reflexes and mono- and polysynaptic Spinal Reflex potentials in Spinalized rats. In intact rats, these drugs significantly reduced the mono- and polysynaptic Reflex potentials. 5-HT depletion significantly prevented the depression of the Spinal Reflex potentials induced by these drugs. These results suggest that the inhibitory effects of cyclobenzaprine, amitriptyline, and cyproheptadine on mono- and polysynaptic Reflex potentials are due to the inhibition of descending serotonergic systems through 5-HT(2) receptors in the Spinal cord.
Takashi Nishida - One of the best experts on this subject based on the ideXlab platform.
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Tricyclic analogs cyclobenzaprine, amitriptyline and cyproheptadine inhibit the Spinal Reflex transmission through 5-HT(2) receptors.
European journal of pharmacology, 2003Co-Authors: Motoko Honda, Takashi NishidaAbstract:The centrally acting muscle relaxant cyclobenzaprine decreases the amplitude of monosynaptic Reflex potentials by inhibiting the facilitatory descending serotonergic influences in the Spinal cord. Interestingly, the structure of cyclobenzaprine is much similar to those of amitriptyline and cyproheptadine. In the present study, we attempted to elucidate the relationship between 5-HT(2) receptor antagonistic and inhibitory effects of cyclobenzaprine, amitriptyline, cyproheptadine and ketanserin on the Spinal Reflexes. Cyclobenzaprine, amitriptyline, cyproheptadine, and ketanserin significantly inhibited facilitatory effects of 1-(2,5-dimethoxy-4-iodophenyl)-2-aminopropane (DOI) on flexor Reflexes and mono- and polysynaptic Spinal Reflex potentials in Spinalized rats. In intact rats, these drugs significantly reduced the mono- and polysynaptic Reflex potentials. 5-HT depletion significantly prevented the depression of the Spinal Reflex potentials induced by these drugs. These results suggest that the inhibitory effects of cyclobenzaprine, amitriptyline, and cyproheptadine on mono- and polysynaptic Reflex potentials are due to the inhibition of descending serotonergic systems through 5-HT(2) receptors in the Spinal cord.
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Tricyclic analogs cyclobenzaprine, amitriptyline and cyproheptadine inhibit the Spinal Reflex transmission through 5-HT2 receptors
European Journal of Pharmacology, 2002Co-Authors: Motoko Honda, Takashi Nishida, Hideki OnoAbstract:The centrally acting muscle relaxant cyclobenzaprine decreases the amplitude of monosynaptic Reflex potentials by inhibiting the facilitatory descending serotonergic influences in the Spinal cord. Interestingly, the structure of cyclobenzaprine is much similar to those of amitriptyline and cyproheptadine. In the present study, we attempted to elucidate the relationship between 5-HT(2) receptor antagonistic and inhibitory effects of cyclobenzaprine, amitriptyline, cyproheptadine and ketanserin on the Spinal Reflexes. Cyclobenzaprine, amitriptyline, cyproheptadine, and ketanserin significantly inhibited facilitatory effects of 1-(2,5-dimethoxy-4-iodophenyl)-2-aminopropane (DOI) on flexor Reflexes and mono- and polysynaptic Spinal Reflex potentials in Spinalized rats. In intact rats, these drugs significantly reduced the mono- and polysynaptic Reflex potentials. 5-HT depletion significantly prevented the depression of the Spinal Reflex potentials induced by these drugs. These results suggest that the inhibitory effects of cyclobenzaprine, amitriptyline, and cyproheptadine on mono- and polysynaptic Reflex potentials are due to the inhibition of descending serotonergic systems through 5-HT(2) receptors in the Spinal cord.
Jason C. Siegler - One of the best experts on this subject based on the ideXlab platform.
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Changes in the quadriceps Spinal Reflex pathway after repeated sprint cycling are not influenced by ischemic preconditioning
European Journal of Applied Physiology, 2020Co-Authors: Paul W. Marshall, Stine Brock Rasmussen, Malene Krogh, Samuel Halley, Jason C. SieglerAbstract:Purpose We examined the effect of ischemic preconditioning (IPC) on changes in muscle force, activation, and the Spinal Reflex pathway during and after repeated sprint cycling. Methods Eight recreationally active men (high-intensity cardiorespiratory training > 3 times per week, > 6 months) completed two exercise sessions (5 sets of 5 cycling sprints, 150% max W), preceded by either IPC (3 × 5 min leg occlusions at 220 mmHg) or SHAM (3 × 5 min at 20 mmHg). Knee extensor maximal force and rate of force were measured before (PRE), immediately post (POST), 1H, and 24H after cycling. Twitch interpolation and resting potentiated twitches were applied to estimate voluntary activation and muscle contractility, respectively. Quadriceps H-Reflex recruitment curves were collected at all time-points using 10 Hz doublet stimulation to allow estimation of H-Reflex post-activation depression. Surface electromyograms and tissue oxygenation (via near-infrared spectroscopy) were continuously recorded during cycling. Results IPC did not affect any measure of neuromuscular function or performance during cycling. Maximal force and muscle contractility were significantly lower at POST and 1H compared to PRE and 24H by up to 50% ( p
Gérard Amarenco - One of the best experts on this subject based on the ideXlab platform.
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External anal sphincter contraction during cough: not a simple Spinal Reflex.
Neurourology and Urodynamics, 2006Co-Authors: Xavier Deffieux, Patrick Raibaut, Patrick Rene-corail, Rose Katz, Michel Perrigot, Samer Sheikh Ismael, Philippe Thoumie, Gérard AmarencoAbstract:AIMS: To assess whether the anal contraction during voluntary coughing is a simple Spinal Reflex-mediated activity or not. To address this question we studied the external intercostal (EIC) muscle activity and external anal sphincter (EAS) response to cough. MATERIALS AND METHODS: Electromyographic recordings were made from pre-gelled disposable surface electrodes. EAS electromyographic recordings were made from the EAS of the pelvic floor in 15 continent women all suffering from urgency and/or frequency without urge or stress urinary incontinence, and referred for urodynamic investigation. Electromyographic signal was immediately integrated (EMGi). The abdominal pressure was recorded with bladder and rectal pressure. EAS EMGi was recorded during successive voluntary cough. In three women, we have also recorded EIC EMGi activity since it is synchronous with diaphragmatic EMG activity during cough initiation. RESULTS: In all subjects, EAS EMGi activity precedes the onset of the abdominal pressure increase. The mean latency of EAS EMGi was 615 msec (+/-278). In the three subjects whose EMGi activity was recorded both on EAS and EIC, the onset of EAS EMGi activity occurred before the EIC EMGi activity (latency ranging from 40 to 780 msec) and before the increase in the abdominal pressure. CONCLUSIONS: The present study suggests that during coughing, EAS EMG activity increases before external intercostal muscle EMGi activity. The contraction of the EAS preceding the activation of muscles involved in coughing indicates that this response is not a result of a simple Spinal Reflex, but more likely the result of a more intricate Reflex involving complex integrative centers.
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external anal sphincter contraction during cough not a simple Spinal Reflex
Neurourology and Urodynamics, 2006Co-Authors: Xavier Deffieux, Patrick Raibaut, Rose Katz, Michel Perrigot, Samer Sheikh Ismael, Philippe Thoumie, Patrick Renecorail, Gérard AmarencoAbstract:Aims: To assess whether the anal contraction during voluntary coughing is a simple Spinal Reflex-mediated activity or not. To address this question we studied the external intercostal (EIC) muscle activity and external anal sphincter (EAS) response to cough. Materials and Methods: Electromyographic recordings were made from pre-gelled disposable surface electrodes. EAS electromyographic recordings were made from the EAS of the pelvic floor in 15 continent women all suffering from urgency and/or frequency without urge or stress urinary incontinence, and referred for urodynamic investigation. Electromyographic signal was immediately integrated (EMGi). The abdominal pressure was recorded with bladder and rectal pressure. EAS EMGi was recorded during successive voluntary cough. In three women, we have also recorded EIC EMGi activity since it is synchronous with diaphragmatic EMG activity during cough initiation. Results: In all subjects, EAS EMGi activity precedes the onset of the abdominal pressure increase. The mean latency of EAS EMGi was 615 msec (±278). In the three subjects whose EMGi activity was recorded both on EAS and EIC, the onset of EAS EMGi activity occurred before the EIC EMGi activity (latency ranging from 40 to 780 msec) and before the increase in the abdominal pressure. Conclusions: The present study suggests that during coughing, EAS EMG activity increases before external intercostal muscle EMGi activity. The contraction of the EAS preceding the activation of muscles involved in coughing indicates that this response is not a result of a simple Spinal Reflex, but more likely the result of a more intricate Reflex involving complex integrative centers. Neurourol. Urodynam. 25:782–787, 2006. © 2006 Wiley-Liss, Inc.
