WordNet
- relating to or occurring in a term or fixed period of time; "terminal examinations"; "terminal payments"
- a contact on an electrical device (such as a battery) at which electric current enters or leaves (同)pole
- station where transport vehicles load or unload passengers or goods (同)terminus, depot
- electronic equipment consisting of a device providing access to a computer; has a keyboard and display
- being or situated at an end; "the endmost pillar"; "terminal buds on a branch"; "a terminal station"; "the terminal syllable"
- causing or ending in or approaching death; "a terminal patient"; "terminal cancer"
- of or relating to or situated at the ends of a delivery route; "freight pickup is a terminal service"; "terminal charges"
- any bundle of nerve fibers running to various organs and tissues of the body (同)nervus
- control of your emotions; "this kind of tension is not good for my nerves"
PrepTutorEJDIC
- 『終りの』,末端の / 毎期の,定期の;学期末の / 『死に至る』, / 末端 / (電池の)端子 / (町の中心に近い)空港バス発着場;(一般に,鉄道・バスの)終点,終着駅
- 〈C〉『神経』 / 〈C〉《複数形で》『神経過敏』,いらだち / 〈U〉『勇気』,度胸(courage) / 〈U〉《時にa ~》厚かましさ,ずぶとさ;無礼 / 〈C〉葉脈;(昆虫の)翅脈(しみゃく) / 〈人,特に自分〉‘に'力を与える,‘を'元気づける
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出典(authority):フリー百科事典『ウィキペディア（Wikipedia）』「2013/12/20 13:19:02」(JST)
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- 1. 神経伝導検査の概要 overview of nerve conduction studies
- 2. Lower extremity nerve blocks: Techniques
- 3. 外傷性単神経障害 traumatic mononeuropathies
- 4. 肘および手首の尺骨神経障害 ulnar neuropathy at the elbow and wrist
- 5. 骨盤手術に関連する神経損傷 nerve injury associated with pelvic surgery
English Journal
- M2 receptors exert analgesic action on DRG sensory neurons by negatively modulating VR1 activity.
- De Angelis F1, Marinelli S, Fioretti B, Catacuzzeno L, Franciolini F, Pavone F, Tata AM.Author information 1Department of Biology and Biotechnologies C. Darwin, "Sapienza" University of Rome, Rome, Italy.AbstractThe peripheral application of the M2 cholinergic agonist arecaidine on sensory nerve endings shows anti-nociceptive properties. In this work, we analyze in vitro, the mechanisms downstream M2 receptor activation causing the analgesic effects, and in vivo the effects produced by M2 agonist arecaidine administration on nociceptive responses in a murine model of nerve growth factor (NGF)-induced pain. Cultured DRG neurons treated with arecaidine showed a decreased level of VR1 and SP transcripts. Conversely, we found an increased expression of VR1 and SP transcripts in DRG from M2/M4(-/-) mice compared to WT and M1(-/-) mice, confirming the inhibitory effect in particular of M2 receptors on SP and VR1 expression. Patch-clamp experiments in the whole-cell configuration showed that arecaidine treatment caused a reduction of the fraction of capsaicin-responsive cells, without altering the mean capsaicin-activated current in responsive cells. We also demonstrated that arecaidine prevents PKCϵ translocation to the plasma membrane after inflammatory agent stimulation, mainly in medium-small sensory neurons. Finally, in mice, we have observed that intraperitoneal injection of arecaidine reduces VR1 expression blocking hyperalgesia and allodynia caused by NGF intraplantar administration. In conclusion, our data demonstrate that in vivo M2 receptor activation induces desensitization to mechanical and heat stimuli by a down-regulation of VR1 expression and by the inhibition of PKCϵ activity hindering its translocation to the plasma membrane, as suggested by in vitro experiments.
- Journal of cellular physiology.J Cell Physiol.2014 Jun;229(6):783-90. doi: 10.1002/jcp.24499.
- The peripheral application of the M2 cholinergic agonist arecaidine on sensory nerve endings shows anti-nociceptive properties. In this work, we analyze in vitro, the mechanisms downstream M2 receptor activation causing the analgesic effects, and in vivo the effects produced by M2 agonist arecaidine
- PMID 24166293
- Sensory Nerve Terminal Mitochondrial Dysfunction Induces Hyperexcitability in Airway Nociceptors via Protein Kinase C.
- Hadley SH1, Bahia PK, Taylor-Clark TE.Author information 1Department of Molecular Pharmacology and Physiology, Morsani College of Medicine, University of South Florida, Tampa, Florida.AbstractAirway sensory nerve excitability is a key determinant of respiratory disease-associated reflexes and sensations such as cough and dyspnea. Inflammatory signaling modulates mitochondrial function and produces reactive oxygen species (ROS). Peripheral terminals of sensory nerves are densely packed with mitochondria; thus, we hypothesized that mitochondrial modulation would alter neuronal excitability. We recorded action potential firing from the terminals of individual bronchopulmonary C-fibers using a mouse ex vivo lung-vagal ganglia preparation. C-fibers were characterized as nociceptors or non-nociceptors based upon conduction velocity and response to transient receptor potential (TRP) channel agonists. Antimycin A (mitochondrial complex III Qi site inhibitor) had no effect on the excitability of non-nociceptors. However, antimycin A increased excitability in nociceptive C-fibers, decreasing the mechanical threshold by 50% and increasing the action potential firing elicited by a P2X2/3 agonist to 270% of control. Antimycin A-induced nociceptor hyperexcitability was independent of TRP ankyrin 1 or TRP vanilloid 1 channels. Blocking mitochondrial ATP production with oligomycin or myxothiazol had no effect on excitability. Antimycin A-induced hyperexcitability was dependent on mitochondrial ROS and was blocked by intracellular antioxidants. ROS are known to activate protein kinase C (PKC). Antimycin A-induced hyperexcitability was inhibited by the PKC inhibitor bisindolylmaleimide (BIM) I, but not by its inactive analog BIM V. In dissociated vagal neurons, antimycin A caused ROS-dependent PKC translocation to the membrane. Finally, H2O2 also induced PKC-dependent nociceptive C-fiber hyperexcitability and PKC translocation. In conclusion, ROS evoked by mitochondrial dysfunction caused nociceptor hyperexcitability via the translocation and activation of PKC.
- Molecular pharmacology.Mol Pharmacol.2014 Jun;85(6):839-48. doi: 10.1124/mol.113.091272. Epub 2014 Mar 18.
- Airway sensory nerve excitability is a key determinant of respiratory disease-associated reflexes and sensations such as cough and dyspnea. Inflammatory signaling modulates mitochondrial function and produces reactive oxygen species (ROS). Peripheral terminals of sensory nerves are densely packed wi
- PMID 24642367
- Expression of transient receptor potential channels TRPC1 and TRPV4 in venoatrial endocardium of the rat heart.
- Shenton FC1, Pyner S2.Author information 1School of Biological & Biomedical Sciences, Durham University, Durham DH1 3LE, UK.2School of Biological & Biomedical Sciences, Durham University, Durham DH1 3LE, UK. Electronic address: susan.pyner@durham.ac.uk.AbstractThe atrial volume receptor reflex arc serves to regulate plasma volume. Atrial volume receptors located in the endocardium of the atrial wall undergo mechanical deformation as blood is returned to the atria of the heart. The mechanosensitive channel(s) responsible for regulating plasma volume remain to be determined. Here we report that the TRP channel family members TRPC1 and TRPV4 were expressed in sensory nerve endings in the atrial endocardium. Furthermore, TRPC1 and TRPV4 were coincident with the nerve ending vesicle marker synaptophysin. Calcitonin gene-related peptide was exclusively confined to the myo- and epicardium of the atria. The small conductance Ca(2+)-activated K(+) channels (SK2 and SK4) were also present, however there was no relationship between SK and TRP channels. SK2 channels were expressed in nerves in the epicardium, while SK4 channels were in some regions of the endocardium but appeared to be present in epithelial cells rather than sensory endings. In conclusion, we have provided the first evidence for TRPC1 and TRPV4 channels as potential contributors to mechanosensation in the atrial volume receptors.
- Neuroscience.Neuroscience.2014 May 16;267:195-204. doi: 10.1016/j.neuroscience.2014.02.047. Epub 2014 Mar 12.
- The atrial volume receptor reflex arc serves to regulate plasma volume. Atrial volume receptors located in the endocardium of the atrial wall undergo mechanical deformation as blood is returned to the atria of the heart. The mechanosensitive channel(s) responsible for regulating plasma volume remain
- PMID 24631674
Japanese Journal
- 早期診断と重症度診断のための新しいアプローチ法 : PINT試験と神経伝導検査馬場基準について (特集 糖尿病神経障害の最近の進歩)
- 馬場 正之,鈴木 千恵子
- 糖尿病 57(8), 595-597, 2014-08
- NAID 40020197884
- 筋損傷にともなう神経筋接合部の変化
- 辻本 尚弥,春日 規克,西沢 富江,山下 晋
- 久留米大学健康・スポーツ科学センター研究紀要 = Kurume journal of health and sports science 21, 1-7, 2014-03
- … Regarding the neuromuscular junction, the nerve ending and the area of the motor end plate degenerated gradually, reaching a maximum on day 4 and day 6, respectively.The terminal arborization was reduced to a minimum on day 4. …
- NAID 120005448747
- 2. 早期診断と重症度診断のための新しいアプローチ法：PINT試験と神経伝導検査馬場基準について
- 馬場 正之,鈴木 千恵子
- 糖尿病 57(8), 595-597, 2014
- NAID 130004688048
Related Links
- terminal nerve n. Any of the plexiform nerve strands passing parallel and medial to the olfactory tracts, distributing with the olfactory nerves and passing centrally into the anterior perforated substance. terminal nerve, a small nerve ...
- Medical Dictionary terminal nerve n. Any of the plexiform nerve strands passing parallel and medial to the olfactory tracts, distributing with the olfactory nerves and passing centrally into the anterior perforated substance. The ...
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| 関連記事 | 「terminal」「nerve」 |
「terminal」
- n.
- adj.
- 終端の、終末の、末期の
- 関
- distal、end、end stage、ending、extremity、full-blown、terminal region、terminal stage、terminally、termini、terminus
「nerve」
- n.