32 results on '"Petrenko AB"'
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2. Spontaneous hyperactivity in mutant mice lacking the NMDA receptor GluRepsilon1 subunit is aggravated during exposure to 0.1 MAC sevoflurane and is preserved after emergence from sevoflurane anaesthesia.
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Petrenko AB, Kohno T, Wu J, Sakimura K, and Baba H
- Published
- 2008
3. Should we use psychostimulant drugs to boost the emergence from general anesthesia?
- Author
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Petrenko AB, Takamatsu M, and Baba H
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- 2012
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4. Intranasal Application of Xenon: A Shortcut to the Brain or Just a Longer Way to It through the Lungs?
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Petrenko AB and Baba H
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- 2012
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5. Free radical scavenger edaravone produces robust neuroprotection in a rat model of spinal cord injury.
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Ishii H, Petrenko AB, Sasaki M, Satoh Y, Kamiya Y, Tobita T, Furutani K, Matsuhashi M, Kohno T, and Baba H
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- 3,4-Methylenedioxyamphetamine metabolism, Analysis of Variance, Animals, Antipyrine therapeutic use, Cytokines metabolism, Disease Models, Animal, Dose-Response Relationship, Drug, Edaravone, Evoked Potentials, Motor drug effects, Evoked Potentials, Motor physiology, Lipid Peroxidation drug effects, Male, Phosphopyruvate Hydratase metabolism, Rats, Rats, Wistar, Recovery of Function drug effects, Severity of Illness Index, Spinal Cord drug effects, Spinal Cord physiopathology, Time Factors, Antipyrine analogs & derivatives, Neuroprotective Agents therapeutic use, Spinal Cord Injuries drug therapy
- Abstract
We used a multimodal approach to evaluate the effects of edaravone in a rat model of spinal cord injury (SCI). SCI was induced by extradural compression of thoracic spinal cord. In experiment 1, 30 min prior to compression, rats received a 3 mg/kg intravenous bolus of edaravone followed by a maintenance infusion of 1 (low-dose), 3 (moderate-dose), or 10 (high-dose) mg/kg/h edaravone. Although both moderate- and high-dose edaravone regimens promoted recovery of spinal motor-evoked potentials (MEPs) at 2 h post-SCI, the effect of the moderate dose was more pronounced. In experiment 2, moderate-dose edaravone was administered 30 min prior to compression, at the start of compression, or 10 min after decompression. Although both preemptive and coincident administration resulted in significantly improved spinal MEPs at 2 h post-SCI, the effect of preemptive administration was more pronounced. A moderate dose of edaravone resulted in significant attenuation of lipid peroxidation, as evidenced by lower concentrations of the free radical malonyldialdehyde in the spinal cord 3 h post-SCI. Malonyldialdehyde levels in the high-dose edaravone group were not reduced. Both moderate- and high-dose edaravone resulted in significant functional improvements, evidenced by better Basso-Beattie-Bresnahan (BBB) scores and better performance on an inclined plane during an 8 week period post-SCI. Both moderate- and high-dose edaravone significantly attenuated neuronal loss in the spinal cord at 8 weeks post-SCI, as evidenced by quantitative immunohistochemical analysis of NeuN-positive cells. In conclusion, early administration of a moderate dose of edaravone minimized the negative consequences of SCI and facilitated functional recovery., (Copyright © 2017 Elsevier B.V. All rights reserved.)
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- 2018
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6. Evaluation of the diagnostic accuracy of nonverbal signs used by medical staff to assess postoperative pain: A prospective study.
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Watanabe T, Okawa R, Sato T, Petrenko AB, and Baba H
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- Aged, Female, Humans, Male, Medical Staff psychology, Middle Aged, Pain Measurement methods, Pain Measurement psychology, Pain, Postoperative etiology, Pain, Postoperative psychology, Prospective Studies, Medical Staff standards, Nonverbal Communication psychology, Pain Measurement standards, Pain, Postoperative diagnosis
- Published
- 2017
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7. A Rising Tide Lifts All Boats: Increased Ventilation May Be Involved in Accelerated Recovery from Isoflurane Anesthesia after Flumazenil Administration.
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Petrenko AB and Baba H
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- Anesthesia Recovery Period, Anesthesia, Inhalation, Humans, Flumazenil, Isoflurane
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- 2017
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8. Risk factors for rescue analgesic use on the first postoperative day after upper limb surgery performed under single-injection brachial plexus block: a retrospective study of 930 cases.
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Watanabe T, Moriya K, Yoda T, Tsubokawa N, Petrenko AB, and Baba H
- Abstract
Background: Postoperative pain management after upper limb surgery is important for preventing adverse events that can prolong hospital stay and cause readmission. This study aimed to identify the risk factors associated with rescue analgesic use on the first postoperative day after upper limb surgery performed under single-injection brachial plexus block (BPB)., Findings: We retrospectively analyzed records from 930 patients who underwent upper limb surgery under a single-injection BPB. Postoperatively, patients were administered oral loxoprofen regularly and rescue analgesics when analgesia was insufficient. We assessed the association between patient, surgical information, and rescue analgesic use on the first day after surgery (from 7:00 PM on the day of surgery to 7:00 AM on the first postoperative day), using a logistic regression model. Multivariate analysis revealed a significant association between rescue analgesic use and bone surgery, in particular, osteotomy, ligament repair and reconstruction, osteosynthesis, treatment for an amputated digit, and surgical duration., Conclusion: Bone surgery (osteotomy, ligament repair and reconstruction, osteosynthesis, treatment for an amputated digit) and a longer operative time were risk factors for rescue analgesic use for treating postoperative pain after upper limb surgery performed under single-injection BPB., Competing Interests: This study was approved by the institutional ethics committee of the Niigata Hand Surgery Foundation Hospital (Seiro, Japan). The requirement for written informed consent was waived by the ethics committee.The authors declare no potential conflicts of interest with respect to the research, authorship, and/or publication of this article.Springer Nature remains neutral with regard to jurisdictional claims in published maps and institutional affiliations.
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- 2017
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9. Clinically relevant concentration of pregabalin has no acute inhibitory effect on excitation of dorsal horn neurons under normal or neuropathic pain conditions: An intracellular calcium-imaging study in spinal cord slices from adult rats.
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Baba H, Petrenko AB, and Fujiwara N
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- Animals, Blood Glucose metabolism, Diabetic Neuropathies chemically induced, Electric Stimulation, Male, Neuralgia complications, Neuralgia drug therapy, Pain Threshold drug effects, Posterior Horn Cells metabolism, Rats, Rats, Wistar, Spinal Cord metabolism, Spinal Nerve Roots physiopathology, Streptozocin, Analgesics administration & dosage, Calcium Signaling drug effects, Diabetic Neuropathies complications, Neuralgia metabolism, Posterior Horn Cells drug effects, Pregabalin administration & dosage, Spinal Cord drug effects
- Abstract
Pregabalin is thought to exert its therapeutic effect in neuropathic pain via binding to α2δ-1 subunits of voltage-gated calcium (Ca(2+)) channels. However, the exact analgesic mechanism after its binding to α2δ-1 subunits remains largely unknown. Whether a clinical concentration of pregabalin (≈10μM) can cause acute inhibition of dorsal horn neurons in the spinal cord is controversial. To address this issue, we undertook intracellular Ca(2+)-imaging studies using spinal cord slices with an intact attached L5 dorsal root, and examined if pregabalin acutely inhibits the primary afferent stimulation-evoked excitation of dorsal horn neurons in normal rats and in rats with streptozotocin-induced painful diabetic neuropathy. Under normal conditions, stimulation of a dorsal root evoked Ca(2+) signals predominantly in the superficial dorsal horn. Clinically relevant (10μM) and a very high concentration of pregabalin (100μM) did not affect the intensity or spread of dorsal root stimulation-evoked Ca(2+) signals, whereas an extremely high dose of pregabalin (300μM) slightly but significantly attenuated Ca(2+) signals in normal rats and in diabetic neuropathic (DN) rats. There was no difference between normal rats and DN rats with regard to the extent of signal attenuation at all concentrations tested. These results suggest that the activity of dorsal horn neurons in the spinal cord is not inhibited acutely by clinical doses of pregabalin under normal or DN conditions. It is very unlikely that an acute inhibitory action in the dorsal horn is the main analgesic mechanism of pregabalin in neuropathic pain states., (Copyright © 2016 Elsevier B.V. All rights reserved.)
- Published
- 2016
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10. Genetic inactivation and prolonged pharmacologic inhibition of monoacylglycerol lipase have opposite effects on anesthetic sensitivity to propofol.
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Petrenko AB, Yamazaki M, Sakimura K, Kano M, and Baba H
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- Animals, Behavior, Animal drug effects, Mice, Inbred C57BL, Mice, Knockout, Receptor, Cannabinoid, CB1 metabolism, Reflex, Righting drug effects, Anesthetics, Intravenous pharmacology, Arachidonic Acids metabolism, Drug Resistance drug effects, Drug Resistance genetics, Endocannabinoids metabolism, Glycerides metabolism, Monoacylglycerol Lipases antagonists & inhibitors, Monoacylglycerol Lipases genetics, Propofol pharmacology
- Abstract
Monoacylglycerol lipase (MGL) is a major enzyme involved in degradation of the endocannabinoid 2-arachidonoylglycerol (2-AG). Selective inhibitors of MGL are regarded as promising analgesics and anticancer agents. To gain insight into the possible consequences of their prolonged administration for anesthetic action, the effects of several inhalational and intravenous anesthetics were tested in knockout mice lacking the MGL gene in the loss of righting reflex (LORR) assay. Sensitivity to inhalational and most intravenous anesthetics was not altered in knockout mice. However, compared with wild-type littermates, they showed increased sensitivity to the intravenous anesthetic propofol. Permanently elevated levels of 2-AG after MGL knockout are known to cause desensitization of cannabinoid (CB1) receptors, which have been advocated as possible mediators of propofol anesthesia. Therefore, increased sensitivity to propofol in knockout mice at first suggested that 2-AG may potentiate CB1 receptors despite their hypofunction in these animals. Pharmacologic inhibition of MGL also causes desensitization of CB1 receptors, so sensitivity to propofol was tested further in C57BL/6N mice pretreated chronically with the selective MGL inhibitor JZL 184. Contrary to the results in knockout mice, these animals showed drastically reduced sensitivity to propofol. The reason for increased sensitivity to propofol after MGL knockout remains unclear, but may result from changes occurring in these animals during development. However, our results in C57BL/6N mice pretreated with JZL 184 confirmed the role of CB1 receptors in propofol anesthesia advocated previously, and also suggest that prolonged use of MGL inhibitors may be associated with the development of resistance to propofol., (Copyright © 2015 Elsevier B.V. All rights reserved.)
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- 2015
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11. Anaesthesia and orphan disease: marked attenuation of motor evoked potentials by high-dose dexmedetomidine in a child with Angelman syndrome undergoing scoliosis surgery: A case report with pharmacokinetic analysis.
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Ishii H, Petrenko AB, Tobita T, Furutani K, and Baba H
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- Adolescent, Angelman Syndrome complications, Angelman Syndrome diagnosis, Evoked Potentials, Motor physiology, Female, Humans, Monitoring, Intraoperative methods, Rare Diseases complications, Rare Diseases diagnosis, Scoliosis complications, Scoliosis diagnosis, Anesthesia methods, Angelman Syndrome surgery, Dexmedetomidine administration & dosage, Evoked Potentials, Motor drug effects, Rare Diseases surgery, Scoliosis surgery
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- 2015
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12. More solid evidence is required to validate a hypergravity-induced increase in sensitivity to propofol.
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Petrenko AB, Furutani K, and Baba H
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- Animals, Male, Anesthetics, Intravenous administration & dosage, Hypergravity, Propofol administration & dosage
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- 2014
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13. Augmented tonic pain-related behavior in knockout mice lacking monoacylglycerol lipase, a major degrading enzyme for the endocannabinoid 2-arachidonoylglycerol.
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Petrenko AB, Yamazaki M, Sakimura K, Kano M, and Baba H
- Subjects
- Animals, Benzodioxoles pharmacology, Inflammation chemically induced, Inflammation metabolism, Male, Mice, Mice, Inbred C57BL, Mice, Inbred CBA, Mice, Knockout, Neuralgia metabolism, Neuralgia physiopathology, Pain chemically induced, Piperidines pharmacology, Pyrazoles pharmacology, Receptor, Cannabinoid, CB1 agonists, Receptor, Cannabinoid, CB1 antagonists & inhibitors, Arachidonic Acids metabolism, Cannabinoid Receptor Modulators pharmacology, Endocannabinoids metabolism, Glycerides metabolism, Pain metabolism, Pain physiopathology, Pain Threshold drug effects, Phosphotransferases (Alcohol Group Acceptor) deficiency
- Abstract
Monoacylglycerol lipase (MGL) is the main enzyme responsible for degradation of the endocannabinoid 2-arachidonoylglycerol (2-AG). Selective inhibitors of MGL have antinociceptive effects upon acute administration and, therefore, hold promise as analgesics. To gain insight into the possible consequences of their prolonged administration, genetically modified mice with the knocked-out MGL gene were tested in several models of acute (phasic, tonic) and chronic (inflammatory, neuropathic) pain. MGL knockout mice showed normal acute phasic pain perception (pain thresholds) and no alleviation of pain perception in models of inflammatory and neuropathic pain. However, compared with wild-type controls, they showed significantly augmented nociceptive behavior in models of acute somatic and visceral tonic pain (formalin and acetic acid tests). The observed proalgesic changes in perception of tonic pain in MGL knockouts could have resulted from desensitization of cannabinoid receptors (known to occur after genetic inactivation of MGL). Supporting this notion, chronic pretreatment with the selective CB1 receptor antagonist AM 251 (employed to re-sensitize cannabinoid receptors in MGL knockouts) resulted in normalization of their tonic pain-related behaviors. Similar augmentation of tonic pain-related behaviors was replicated in C57BL/6N mice pretreated chronically with the selective MGL inhibitor JZL 184 (employed to pharmacologically desensitize CB1 receptors). These findings imply that prolonged use of MGL inhibitors, at doses causing close to complete inhibition of MGL enzymatic activity, not only have no beneficial analgesic effects, they may lead to exacerbation of some types of pain (particularly those with a tonic component)., (Copyright © 2014 Elsevier B.V. All rights reserved.)
- Published
- 2014
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14. Prolonged apnea, caused by remifentanil, during awakening from anesthesia for emergency ventriculoperitoneal shunt placement.
- Author
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Watanabe T, Watanabe Y, Takizawa D, Hiraoka H, Petrenko AB, and Baba H
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- Aged, Apnea drug therapy, Humans, Male, Naloxone therapeutic use, Narcotic Antagonists therapeutic use, Remifentanil, Ventriculoperitoneal Shunt, Anesthesia adverse effects, Anesthetics, Intravenous adverse effects, Apnea chemically induced, Piperidines adverse effects
- Published
- 2014
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15. Hypnotic effect of propofol and hypothalamic nuclei: are we barking up the right neurocircuitry?
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Petrenko AB, Watanabe T, and Baba H
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- Animals, Adrenergic Neurons drug effects, Anesthetics, Intravenous pharmacology, GABAergic Neurons drug effects, Hypnotics and Sedatives pharmacology, Neural Inhibition drug effects, Norepinephrine metabolism, Preoptic Area drug effects, Propofol pharmacology, gamma-Aminobutyric Acid metabolism
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- 2014
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16. Defining the role of NMDA receptors in anesthesia: are we there yet?
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Petrenko AB, Yamakura T, Sakimura K, and Baba H
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- Anesthetics therapeutic use, Animals, Humans, Protein Subunits, Receptors, N-Methyl-D-Aspartate chemistry, Anesthesia, Anesthetics pharmacology, Receptors, N-Methyl-D-Aspartate metabolism
- Abstract
N-methyl-d-aspartate (NMDA) receptors are important in mediating excitatory neurotransmission in the nervous system. They are preferentially inhibited by some general anesthetics and have, therefore, been implied in the mediation of their effects. This review summarizes the main research findings available related to NMDA receptors and their role in anesthesia. The contribution of NMDA receptors to the anesthetized state is discussed separately for each of its components: amnesia, analgesia, unconsciousness and immobility. Anesthetic-induced unconsciousness and immobility have received the most attention in the research community and are the main focus of this review. In the overall perspective, however, studies using pharmacological or electrophysiological approaches have failed to reach definitive conclusions regarding the contribution of NMDA receptors to these anesthetic endpoints. None of the studies have specifically addressed the role of NMDA receptors in the amnestic effect of general anesthetics, and the few available data are (at best) only indirect. NMDA receptor antagonism by general anesthetics may have a preventive anti-hyperalgesic effect. The only and most extensively used genetic tool to examine the role of NMDA receptors in anesthesia is global knockout of the GluN2A subunit of the NMDA receptor. These animals are resistant to many intravenous and inhalational anesthetics, but the interpretation of their phenotype is hindered by the secondary changes occurring in these animals after GluN2A knockout, which are themselves capable of altering anesthetic sensitivity. Generation of more sophisticated conditional knockout models targeting NMDA receptors is required to finally define their role in the mechanisms of anesthesia., (© 2013 Published by Elsevier B.V.)
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- 2014
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17. No evidence for the development of acute analgesic tolerance during and hyperalgesia after prolonged remifentanil administration in mice.
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Ishii H, Petrenko AB, Kohno T, and Baba H
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- Analgesics, Opioid adverse effects, Analgesics, Opioid pharmacology, Animals, Behavior, Animal, Hyperalgesia metabolism, Male, Mice, Mice, Inbred C57BL, Pain Threshold physiology, Piperidines adverse effects, Piperidines pharmacology, Remifentanil, Analgesics, Opioid administration & dosage, Drug Tolerance, Hyperalgesia chemically induced, Piperidines administration & dosage
- Abstract
Background: Acute opioid tolerance (AOT) and opioid-induced hyperalgesia (OIH) are undesirable effects of opioids that have been reported in both animals and humans. However, the development of AOT and OIH in cases of potent, short-acting μ-opioid receptor agonist remifentanil administration remains controversial. It has been suggested that the emergence of AOT and OIH by remifentanil could be dose and infusion duration dependent, i.e., low dose and short infusions may lead to negative results. In this study, we determined whether AOT and OIH could be elicited by prolonged, continuous administration of remifentanil at maximally tolerable doses in C57BL/6 mice., Results: The analgesic effects of continuously administered remifentanil [by short (1 h) and prolonged (4 h) intraperitoneal infusions] were studied. These experiments involved repeated measurements of thermal thresholds during remifentanil administration. Therefore, particular attention was paid to prevent cumulative tissue injury, which could mimic pronociceptive effects of remifentanil. To exclude the possibility of pseudoAOT during infusion, we used brief cooling of all ipsilateral hindpaws that exhibited analgesic response. Thermal thresholds remained steadily elevated over a 1-h period during continuous administration at infusion rates of 120, 180, and 240 mg/kg/h, which indicated no AOT development. To exclude the possibility of pseudoOIH after infusion, intact contralateral hindpaws were used for all postinfusion threshold measurements. Thermal thresholds at each infusion rate returned to the baseline values within 15 min after the termination of the administration. They did not decrease below the baseline values during 1 h following infusion, which indicated no OIH development. Similar threshold dynamics were also observed for thermal and mechanical testing modalities in animals infused at 120 mg/kg/h for 4 h as well as in animals with rapidly attained and maintained maximum analgesia for 3 h., Conclusions: These results suggest that neither intra-infusion AOT nor postinfusion OIH develops in mice receiving continuous remifentanil when the possibility of cumulative tissue injury mimicking AOT or OIH is carefully avoided.
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- 2013
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18. Increased brain monoaminergic tone after the NMDA receptor GluN2A subunit gene knockout is responsible for resistance to the hypnotic effect of nitrous oxide.
- Author
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Petrenko AB, Yamakura T, Kohno T, Sakimura K, and Baba H
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- Anesthetics chemistry, Anesthetics pharmacology, Animals, Biogenic Monoamines antagonists & inhibitors, Droperidol pharmacology, Gene Knockout Techniques, Halogenation, Hypnotics and Sedatives chemistry, Hypnotics and Sedatives pharmacology, Ketanserin pharmacology, Male, Mice, Mice, Inbred C57BL, Nitrous Oxide chemistry, Reflex, Righting drug effects, Unconsciousness chemically induced, Biogenic Monoamines metabolism, Brain drug effects, Brain metabolism, Drug Resistance genetics, Nitrous Oxide pharmacology, Receptors, N-Methyl-D-Aspartate deficiency, Receptors, N-Methyl-D-Aspartate genetics
- Abstract
N-methyl-d-aspartate (NMDA) receptors can be inhibited by inhalational anesthetics in vitro at clinically relevant concentrations. Here, to clarify the role of NMDA receptors in anesthetic-induced unconsciousness, we examined the hypnotic properties of isoflurane, sevoflurane and nitrous oxide in NMDA receptor GluN2A subunit knockout mice. The hypnotic properties of inhalational anesthetics were evaluated in mice in the loss of righting reflex (LORR) assay by measuring the 50% concentration for LORR (LORR ED(50)). Knockout mice displayed isoflurane and sevoflurane LORR ED(50) values similar to wild-type controls, indicating no significant contribution of these receptors to the hypnotic action of halogenated anesthetics. However, compared with wild-type controls, mutant mice displayed larger isoflurane LORR ED(50) values in the presence of nitrous oxide, indicating a resistance to this gaseous anesthetic. Knockout mice have enhanced brain monoaminergic activity which occurs secondary to NMDA receptor dysfunction, and the observed resistance to the isoflurane LORR ED(50)-sparing effect of nitrous oxide could be abolished by pretreatment with the dopamine D(2) receptor antagonist droperidol or with the serotonin 5-HT(2A) receptor antagonist ketanserin. Thus, resistance to nitrous oxide in knockout mice appears to be a secondary phenomenon of monoaminergic origin and not a direct result of impaired NMDA receptor function. Our results indicate that NMDA receptors are not critically involved in the hypnotic action of conventionally-used inhalational anesthetics. Also, they suggest that increased brain monoaminergic tone can diminish the effects of general anesthesia. Finally, they provide further evidence that changes secondary to genetic manipulation can explain the results obtained in global knockouts., (Copyright © 2012 Elsevier B.V. All rights reserved.)
- Published
- 2013
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19. When similar is not alike: decreased sensory thresholds after intravenous infusion of remifentanil may not be remifentanil-induced hyperalgesia.
- Author
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Petrenko AB, Ishii H, Kohno T, and Baba H
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- Animals, Male, Analgesics, Opioid administration & dosage, Analgesics, Opioid toxicity, Hyperalgesia chemically induced, Piperidines administration & dosage, Piperidines toxicity
- Published
- 2012
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20. Genetic reduction of GABA(A) receptor gamma2 subunit expression potentiates the immobilizing action of isoflurane.
- Author
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Seo K, Seino H, Yoshikawa H, Petrenko AB, Baba H, Fujiwara N, Someya G, Kawano Y, Maeda T, Matsuda M, Kanematsu T, and Hirata M
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- Adaptor Proteins, Signal Transducing genetics, Animals, Immobilization, Intracellular Signaling Peptides and Proteins genetics, Male, Mice, Mice, Inbred C57BL, Mice, Knockout, Receptors, GABA-A genetics, Spinal Cord drug effects, Spinal Cord metabolism, Anesthetics, Inhalation pharmacology, Isoflurane pharmacology, Receptors, GABA-A biosynthesis
- Abstract
Potentiation of inhibitory gamma-aminobutyric acid subtype A (GABA(A)) receptor function is involved in the mechanisms of anesthetic action. The present study examined the immobilizing action of the volatile anesthetic isoflurane in mice with double knockout (DKO) of phospholipase C-related inactive protein (PRIP)-1 and -2. Both of these proteins play important roles in the expression of GABA(A) receptors containing the gamma2 subunit on the neuronal cell surface. Immunohistochemistry for GABA(A) receptor subunits demonstrated reduced expression of gamma2 subunits in the spinal cord of the DKO mice. Immunohistochemistry also revealed up-regulation of the alpha1 and beta3 subunits even though there were no apparent differences in the immunoreactivities for the beta2 subunits between wild-type and DKO mice. The tail-clamp method was used to evaluate the anesthetic/immobilizing effect of isoflurane and the minimum alveolar concentration (MAC) was significantly lower in DKO mice compared with wild-type controls (1.07+/-0.01% versus 1.36+/-0.04% atm), indicating an increased sensitivity to isoflurane in DKO mice. These immunohistochemical and pharmacological findings suggest that reduced expression of the GABA(A) receptor gamma2 subunit affects the composition and function of spinal GABA(A) receptors and potentiates the immobilizing action of isoflurane., (Copyright 2010 Elsevier Ireland Ltd. All rights reserved.)
- Published
- 2010
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21. Reduced immobilizing properties of isoflurane and nitrous oxide in mutant mice lacking the N-methyl-D-aspartate receptor GluR(epsilon)1 subunit are caused by the secondary effects of gene knockout.
- Author
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Petrenko AB, Yamakura T, Kohno T, Sakimura K, and Baba H
- Subjects
- Animals, Dopamine Antagonists pharmacology, Dose-Response Relationship, Drug, Droperidol pharmacology, Isoflurane pharmacokinetics, Ketanserin pharmacology, Male, Mice, Mice, Inbred C57BL, Mice, Knockout, Pain Threshold, Pulmonary Alveoli chemistry, Serotonin Antagonists pharmacology, Anesthetics, Inhalation pharmacology, Gene Knockout Techniques, Isoflurane pharmacology, Movement drug effects, Nitrous Oxide pharmacology, Receptors, N-Methyl-D-Aspartate genetics
- Abstract
Background: Until recently, the N-methyl-D-aspartate (NMDA) receptor was considered to possibly mediate the immobility produced by inhaled anesthetics such as isoflurane and nitrous oxide. However, new evidence suggests that the role of this receptor in abolition of the movement response may be less important than previously thought. To provide further evidence supporting or challenging this view, we examined the anesthetic potencies of isoflurane and nitrous oxide in genetically modified animals with established NMDA receptor dysfunction caused by GluRepsilon1 subunit knockout., Methods: The immobilizing properties of inhaled anesthetics in mice quantitated by the minimum alveolar anesthetic concentration (MAC) were evaluated using the classic tail clamp method., Results: Compared with wild-type controls, NMDA receptor GluRepsilon1 subunit knockout mice displayed larger isoflurane MAC values indicating a resistance to the immobilizing action of isoflurane. Knockout mice were previously shown to have enhanced monoaminergic tone as a result of genetic manipulation, and this increase in MAC could be abolished in our experiments by pretreatment with the serotonin 5-hydroxytryptamine type 2A receptor antagonist ketanserin or with the dopamine D2 receptor antagonist droperidol at doses that did not affect MAC values in wild-type animals. Mutant mice also displayed resistance to the isoflurane MAC-sparing effect of nitrous oxide, but this resistance was similarly abolished by ketanserin and droperidol. Thus, resistance to the immobilizing action of inhaled anesthetics in knockout mice seems to be secondary to increased monoaminergic activation after knockout rather than a direct result of impaired NMDA receptor function., Conclusions: Our results confirm recent findings indicating no critical contribution of NMDA receptors to the immobility induced by isoflurane and nitrous oxide. In addition, they demonstrate the ability of changes secondary to genetic manipulation to affect the results obtained in global knockout studies.
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- 2010
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22. Taurine activates glycine and gamma-aminobutyric acid A receptors in rat substantia gelatinosa neurons.
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Wu J, Kohno T, Georgiev SK, Ikoma M, Ishii H, Petrenko AB, and Baba H
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- Animals, Bicuculline pharmacology, Data Interpretation, Statistical, GABA Antagonists pharmacology, Glycine Agents pharmacology, Male, Membrane Potentials drug effects, Neurons drug effects, Patch-Clamp Techniques, Rats, Rats, Wistar, Strychnine pharmacology, tau Proteins metabolism, GABA Agonists, Receptors, GABA-A drug effects, Receptors, Glycine administration & dosage, Substantia Gelatinosa drug effects, Taurine pharmacology
- Abstract
Taurine has been suggested to modulate nociceptive information at the spinal cord level. In this study, the pharmacological properties of taurine were investigated in adult rat substantia gelatinosa (SG) neurons using whole-cell patch-clamp method. We found that taurine seemed to have higher efficacy than glycine on glycine receptors in SG neurons. An increase in chloride conductance was responsible for taurine-induced currents. Taurine at 0.3 mM activated glycine receptors, whereas at 3 mM activated both glycine and gamma-aminobutyric acid A receptors. The currents activated by coapplication of taurine and glycine are cross inhibitive. Altogether these results show that taurine might represent another important neurotransmitter or modulator in SG neurons, which may be involved in antinociception.
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- 2008
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23. [New-onset pulmonary tuberculosis in women].
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Petrenko AB and Kononenko VG
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- Adolescent, Adult, Aged, Aged, 80 and over, Demography, Female, Humans, Incidence, Middle Aged, Prevalence, Russia epidemiology, Tuberculosis, Pulmonary microbiology, Tuberculosis, Pulmonary epidemiology
- Abstract
A clinical pattern, a social portrait, and the efficiency of inpatient treatment were studied in females with new-onset pulmonary tuberculosis. Four hundred and twenty-eight cases of new-onset pulmonary tuberculosis in 18-85-year-old women admitted to a specialized hospital (95, 178, and 155 patients in 1990, 2001, and 2005, respectively). The pattern of clinical forms was found to become much worse under the present conditions of epidemiological ill-being. There was a rise in the incidence of the disseminated form from 10.5 to 23.9% with a drop in that of the focal form from 23.2 to 7.1%. Pulmonary tuberculosis is characterized with the great extent of involvement, the high rate of destructive changes, abundant bacterial excretion, the increase of drug resistance (DR), and worsening of its pattern due to polyresistance and multiple DR. The efficiency of inpatient treatment for pulmonary tuberculosis significantly decreased: bacterial excretion ceased in 52.4-52.9%, destructive changes were eliminated in 30.4-34.3%. Under the present conditions in combination with biomedical and social factors, the detected specific features of pulmonary tuberculosis affected the results of inpatient treatment.
- Published
- 2008
24. Mutation of alpha1G T-type calcium channels in mice does not change anesthetic requirements for loss of the righting reflex and minimum alveolar concentration but delays the onset of anesthetic induction.
- Author
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Petrenko AB, Tsujita M, Kohno T, Sakimura K, and Baba H
- Subjects
- Anesthetics, Intravenous administration & dosage, Animals, Dose-Response Relationship, Drug, Mice, Mice, Knockout, Time Factors, Anesthetics, Intravenous pharmacology, Calcium Channels, T-Type genetics, Reflex drug effects
- Abstract
Background: T-type calcium channels regulate neuronal membrane excitability and participate in a number of physiologic and pathologic processes in the central nervous system, including sleep and epileptic activity. Volatile anesthetics inhibit native and recombinant T-type calcium channels at concentrations comparable to those required to produce anesthesia. To determine whether T-type calcium channels are involved in the mechanisms of anesthetic action, the authors examined the effects of general anesthetics in mutant mice lacking alpha1G T-type calcium channels., Methods: The hypnotic effects of volatile and intravenous anesthetics administered to mutant and C57BL/6 control mice were evaluated using the behavioral endpoint of loss of righting reflex. To investigate the immobilizing effects of volatile anesthetics in mice, the minimum alveolar concentration (MAC) values were determined using the tail-clamp method., Results: The 50% effective concentration for loss of righting reflex and MAC values for volatile anesthetics were not altered after alpha1G channel knockout. However, mutant mice required significantly more time to develop anesthesia/hypnosis after exposure to isoflurane, halothane, and sevoflurane and after intraperitoneal administration of pentobarbital., Conclusions: The 50% effective concentration for loss of righting reflex and MAC values for the volatile anesthetics were not altered after alpha1G calcium channel knockout, indicating that normal functioning of alpha1G calcium channels is not required for the maintenance of anesthetic hypnosis and immobility. However, the timely induction of anesthesia/hypnosis by volatile anesthetic agents and some intravenous anesthetic agents may require the normal functioning of these channel subunits.
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- 2007
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25. [Elucidation of anesthetic and analgesic effects of ketamine using NMDA receptor epsilon 1 subunit-deficient mice].
- Author
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Yamakura T, Petrenko AB, Baba Y, and Sakimura K
- Subjects
- Animals, Mice, Analgesics pharmacology, Anesthetics pharmacology, Ketamine pharmacology, Receptors, N-Methyl-D-Aspartate physiology
- Published
- 2006
26. Effects of ketamine on acute somatic nociception in wild-type and N-methyl-D-aspartate (NMDA) receptor epsilon1 subunit knockout mice.
- Author
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Petrenko AB, Yamakura T, Askalany AR, Kohno T, Sakimura K, and Baba H
- Subjects
- Animals, Behavior, Animal, Dose-Response Relationship, Drug, Drug Interactions, Formaldehyde pharmacology, Hot Temperature, Hyperalgesia drug therapy, Mice, Mice, Inbred C57BL, Mice, Knockout, Morphine administration & dosage, Pain psychology, Pain Measurement methods, Receptors, N-Methyl-D-Aspartate deficiency, Excitatory Amino Acid Antagonists administration & dosage, Ketamine administration & dosage, Nociceptors drug effects, Receptors, N-Methyl-D-Aspartate physiology
- Abstract
Although the properties of ketamine appear to be well characterized, there is a lot of ambiguity in the literature regarding its analgesic effects. After careful selection of proper experimental conditions and drug doses, we systematically characterized the effects of systemic ketamine on acute somatic nociception in mice and examined the role of the NMDA receptor epsilon1 subunit in mediating its analgesia. Intraperitoneal administration of ketamine was not analgesic in any of the phasic pain assays (thermal, mechanical, electrical) applied to C57BL/6 (wild-type) and NMDA receptor epsilon1 subunit knockout (mutant) mice. Surprisingly, rather than being analgesic for thermal nociception, ketamine showed pronociceptive properties in case of low-intensity heat stimulation in wild-type mice. In the formalin test (tonic pain), ketamine significantly reduced phase 2 nociceptive behavior in both wild-type and mutant mice. These data indicate that in wild-type mice ketamine has no analgesic effect on phasic pain in normal somatic tissues, but alleviates tonic pain after inflammation. Such analgesic spectrum of ketamine can be fully explained by its NMDA receptor antagonist properties. The results for the mutant mice suggest that the epsilon1 subunit of the NMDA receptor does not mediate the analgesic effects of ketamine in tonic pain.
- Published
- 2006
- Full Text
- View/download PDF
27. Effect of agmatine on heteromeric N-methyl-D-aspartate receptor channels.
- Author
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Askalany AR, Yamakura T, Petrenko AB, Kohno T, Sakimura K, and Baba H
- Subjects
- Aldehydes pharmacology, Animals, Cloning, Molecular, Dose-Response Relationship, Drug, Dose-Response Relationship, Radiation, Drug Interactions, Electric Stimulation methods, Epoxy Compounds pharmacology, Glutamic Acid pharmacology, Inhibitory Concentration 50, Membrane Potentials genetics, Membrane Potentials physiology, Microinjections methods, Oocytes drug effects, Oocytes physiology, Patch-Clamp Techniques methods, Receptors, N-Methyl-D-Aspartate genetics, Recombinant Proteins drug effects, Xenopus laevis, Agmatine pharmacology, Membrane Potentials drug effects, Receptors, N-Methyl-D-Aspartate chemistry, Receptors, N-Methyl-D-Aspartate drug effects
- Abstract
Endogenous polyamines like spermine are known to have four distinct effects on recombinant N-methyl-d-aspartate (NMDA) receptor channels: voltage-dependent inhibition, glycine-dependent stimulation, glycine-independent stimulation and decreased affinity to the agonist (l-glutamate). These effects are highly dependent on the constituting epsilon subunits (epsilon1-epsilon4) of the recombinant NMDA receptor channels. Agmatine reportedly inhibits native NMDA receptor channels in cultured hippocampal neurons. In the present investigation, the effects of agmatine on the epsilon/zeta heteromeric NMDA receptor channels expressed in Xenopus laevis oocytes were examined using the two-electrode voltage clamp method. Agmatine inhibited the four epsilon/zeta (epsilon1/zeta1, epsilon2/zeta1, epsilon3/zeta1 and epsilon4/zeta1) channels with similar sensitivity (an IC50 value of about 300microM at -70mV). This effect was dependent on the membrane potential and was more pronounced at hyperpolarized membrane potentials (voltage-dependent inhibition). Agmatine did not exhibit other stimulatory (glycine-dependent and -independent effects) or inhibitory (decreased affinity to l-glutamate) effects. These properties are similar to the pharmacological profile of well-characterized NMDA receptor channel blockers like phencyclidine and ketamine. Thus, regarding the effects on the NMDA receptor channels, agmatine is not like other endogenous polyamines rather it acts as a channel blocker.
- Published
- 2005
- Full Text
- View/download PDF
28. The NR3B subunit does not alter the anesthetic sensitivities of recombinant N-methyl-D-aspartate receptors.
- Author
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Yamakura T, Askalany AR, Petrenko AB, Kohno T, Baba H, and Sakimura K
- Subjects
- Amino Acid Sequence, Anesthetics, Dissociative pharmacology, Anesthetics, Inhalation pharmacology, Animals, Central Nervous System Depressants pharmacology, Ethanol pharmacology, Glutamic Acid pharmacology, Glycine pharmacology, Ketamine pharmacology, Mice, Mice, Inbred C57BL, Molecular Sequence Data, Nitrous Oxide pharmacology, Oocytes metabolism, RNA, Messenger biosynthesis, RNA, Messenger genetics, Receptors, N-Methyl-D-Aspartate agonists, Recombinant Proteins pharmacology, Xenopus, Anesthetics pharmacology, Receptors, N-Methyl-D-Aspartate drug effects
- Abstract
The N-methyl-D-aspartate (NMDA) receptor NR3B subunit co-assembles with NR1 and NR2 subunits to form a receptor complex with distinct channel properties. In the present study, we investigated the effects of co-expression of the NR3B subunit on the anesthetic sensitivities of NMDA receptors for NR1/NR2 channels expressed in Xenopus oocytes. Although the NR3B subunit prominently reduced the current amplitude of NR1/NR2A-B channels, the sensitivities of NR1/NR2A-B channels to Mg2+, ketamine, isoflurane, nitrous oxide, and ethanol were not altered by coexpression of the NR3B subunit. These results suggest that the anesthetic sensitivities of NMDA receptors do not depend on the presence or absence of the NR3 subunit. Mutations of two amino acid residues in the NR3B subunit at positions homologous to the N and N + 1 sites in the NR1 and NR2 subunits, which constitute the blocking sites for Mg2+ and ketamine, did not affect the sensitivities of NR1/NR2B/NR3B channels to Mg2+, ketamine and isoflurane. Thus, the amino acid residues at the N and N + 1 sites in NR3 subunits are unlikely to be involved in the formation of channel blocking sites in NR1/NR2/NR3 channels.
- Published
- 2005
- Full Text
- View/download PDF
29. Reduced sensitivity to ketamine and pentobarbital in mice lacking the N-methyl-D-aspartate receptor GluRepsilon1 subunit.
- Author
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Petrenko AB, Yamakura T, Fujiwara N, Askalany AR, Baba H, and Sakimura K
- Subjects
- Anesthetics, Dissociative pharmacokinetics, Animals, Biotransformation, Brain metabolism, Hypnotics and Sedatives pharmacokinetics, Injections, Intraperitoneal, Ketamine pharmacokinetics, Male, Mice, Mice, Inbred C57BL, Mice, Knockout, Mutation genetics, Mutation physiology, Pentobarbital pharmacokinetics, Reflex drug effects, Anesthetics, Dissociative pharmacology, Hypnotics and Sedatives pharmacology, Ketamine pharmacology, Pentobarbital pharmacology, Receptors, N-Methyl-D-Aspartate genetics
- Abstract
Ketamine is an IV anesthetic with N-methyl-d-aspartate receptor (NMDAR)-blocking properties. However, it is still unclear whether ketamine's general anesthetic actions are mediated primarily via blockade of NMDAR. Functional NMDARs are composed by the assembly of a GluRzeta1 (NR1) subunit with GluRepsilon (GluRepsilon1-4; NR2A-D) subunits, which confer unique properties on native NMDARs. We hypothesized that animals deficient in GluRepsilon1, an abundant and ubiquitously postnatally expressed NMDAR subunit, might be resistant to the effects of ketamine. Here, we evaluated a righting reflex to determine the general anesthetic/hypnotic potency of ketamine administered intraperitoneally to GluRepsilon1 knockout mice and compared these results with those for wild-type mice. Mutant mice were more resistant to ketamine than control mice. Unexpectedly, mutant mice were also more resistant to pentobarbital, which is thought not to interact with NMDAR at clinically relevant concentrations. Although these data in no way eliminate the possibility of the involvement of the NMDAR GluRepsilon1 subunit in mediation of ketamine anesthesia/hypnosis, they suggest the difficulties with interpretation of altered anesthetic sensitivity in knockout animal models.
- Published
- 2004
- Full Text
- View/download PDF
30. The role of N-methyl-D-aspartate (NMDA) receptors in pain: a review.
- Author
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Petrenko AB, Yamakura T, Baba H, and Shimoji K
- Subjects
- Animals, Central Nervous System drug effects, Chronic Disease, Excitatory Amino Acid Agonists administration & dosage, Excitatory Amino Acid Agonists pharmacology, Humans, Peripheral Nervous System drug effects, Receptors, N-Methyl-D-Aspartate drug effects, Receptors, N-Methyl-D-Aspartate metabolism, Pain physiopathology, Receptors, N-Methyl-D-Aspartate physiology
- Abstract
There is accumulating evidence to implicate the importance of N-methyl-D-aspartate (NMDA) receptors to the induction and maintenance of central sensitization during pain states. However, NMDA receptors may also mediate peripheral sensitization and visceral pain. NMDA receptors are composed of NR1, NR2 (A, B, C, and D), and NR3 (A and B) subunits, which determine the functional properties of native NMDA receptors. Among NMDA receptor subtypes, the NR2B subunit-containing receptors appear particularly important for nociception, thus leading to the possibility that NR2B-selective antagonists may be useful in the treatment of chronic pain.
- Published
- 2003
- Full Text
- View/download PDF
31. Unaltered pain-related behavior in mice lacking NMDA receptor GluRepsilon 1 subunit.
- Author
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Petrenko AB, Yamakura T, Baba H, and Sakimura K
- Subjects
- Animals, Axotomy, Blotting, Western, Formaldehyde pharmacology, Freund's Adjuvant pharmacology, Hindlimb drug effects, Hindlimb innervation, Hindlimb physiology, Irritants pharmacology, Male, Mice, Mice, Knockout, Nociceptors metabolism, Pain Measurement, Pain Threshold physiology, Physical Stimulation, Reaction Time genetics, Receptors, N-Methyl-D-Aspartate genetics, Receptors, N-Methyl-D-Aspartate metabolism, Behavior, Animal physiology, Pain genetics, Pain metabolism, Receptors, N-Methyl-D-Aspartate deficiency
- Abstract
Noxious afferent input following tissue damage and inflammation triggers a state of neuronal hyperexcitability-a phenomenon of central sensitization-which manifests behaviorally as allodynia and hyperalgesia. At the molecular level, maintenance of central sensitization is largely dependent on the N-methyl-D-aspartate receptor (NMDAR) activation. NMDARs are composed of GluRzeta1 (NR1) and one of four GluRepsilon (NR2) subunits, which determine the functional properties of native NMDARs. Although there is accumulating evidence to implicate GluRepsilon 2-containing NMDARs in pain mechanisms, the functional significance of GluRepsilon 1-containing NMDARs in this setting has not been examined in detail. Here, we used hind paw injection of formalin, complete Freund's adjuvant and a nerve injury model to investigate the effects of GluRepsilon 1 subunit gene deletion on pain-related behavior in mice. In all of the models tested, GluRepsilon 1-deficient mice exhibited responses similar to wild-type controls. These results suggest that GluRepsilon 1 disruption does not result in altered nociceptive behavior in mice. Although the contribution of other nociceptive pathways cannot be ruled out, we speculate that the preserved function of GluRepsilon 2-containing NMDARs could explain unaltered nociceptive behavior in mutant mice.
- Published
- 2003
- Full Text
- View/download PDF
32. A possible role for glutamate receptor-mediated excitotoxicity in chronic pain.
- Author
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Petrenko AB and Shimoji K
- Published
- 2001
- Full Text
- View/download PDF
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