関: nerve ending

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）』「2012/09/04 17:21:29」(JST)

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This article is about the part of the human nervous system. For other uses, see Nerve (disambiguation). For nerves in other species, see Nervous system.

Nerves (yellow)

A nerve is an enclosed, cable-like bundle of axons (the long, slender projections of neurons) in the peripheral nervous system. A nerve provides a common pathway for the electrochemical nerve impulses that are transmitted along each of the axons to peripheral organs.

In the central nervous system, the analogous structures are known as tracts.^[1]^[2] Neurons are sometimes called nerve cells, though this term is potentially misleading since many neurons do not form nerves, and nerves also include non-neuronal Schwann cells that coat the axons in myelin.

Each nerve is a cordlike structure that contains many axons. These axons are often referred to as "fibres". Within a nerve, each axon is surrounded by a layer of connective tissue called the endoneurium. The axons are bundled together into groups called fascicles, and each fascicle is wrapped in a layer of connective tissue called the perineurium. Finally, the entire nerve is wrapped in a layer of connective tissue called the epineurium.

Anatomy

Nerves are categorized into three groups based on the direction that signals are conducted:

Afferent nerves conduct signals from sensory neurons to the central nervous system, for example from the mechanoreceptors in skin.
Efferent nerves conduct signals from the central nervous system along motor neurons to their target muscles and glands.
Mixed nerves contain both afferent and efferent axons, and thus conduct both incoming sensory information and outgoing muscle commands in the same bundle.

Nerves can be categorized into two groups based on where they connect to the central nervous system:

Spinal nerves innervate much of the body, and connect through the spinal column to the spinal cord. They are given letter-number designations according to the vertebra through which they connect to the spinal column.
Cranial nerves innervate parts of the head, and connect directly to the brain (especially to the brainstem). They are typically assigned Roman numerals from 1 to 12, although cranial nerve zero is sometimes included. In addition, cranial nerves have descriptive names.

Cross-section of a nerve

Each nerve is covered externally by a dense sheath of connective tissue, the epineurium. Underlying this is a layer of flat cells, the perineurium, which forms a complete sleeve around a bundle of axons. Perineurial septae extend into the nerve and subdivide it into several bundles of fibers. Surrounding each such fiber is the endoneurium. This forms an unbroken tube which extends from the surface of the spinal cord to the level at which the axon synapses with its muscle fibers, or ends in sensory receptors. The endoneurium consists of an inner sleeve of material called the glycocalyx and an outer, delicate, meshwork of collagen fibers. Nerves are bundled along with blood vessels, since the neurons of a nerve have fairly high energy requirements. Within the endoneurium, the individual nerve fibers are surrounded by a low protein liquid called endoneurial fluid. The endoneurium has properties analogous to the blood–brain barrier, in that it prevents certain molecules from crossing from the blood into the endoneurial fluid. In this respect, endoneurial fluid is similar to cerebro-spinal fluid in the central nervous system. During the development of nerve edema from nerve irritation or (injury), the amount of endoneurial fluid may increase at the site of irritation. This increase in fluid can be visualized using magnetic resonance neurography, and thus MR neurography can identify nerve irritation and/or injury.

Physiology

A nerve conveys information in the form of electrochemical impulses (known as nerve impulses or action potentials) carried by the individual neurons that make up the nerve. These impulses are extremely fast, with some myelinated neurons conducting at speeds up to 120 m/s. The impulses travel from one neuron to another by crossing a synapse, the message is converted from electrical to chemical and then back to electrical.^[1]^[2]

Nerves can be categorized into two groups based on function:

Sensory nerves conduct sensory information from their receptors to the central nervous system, where the information is then processed. Thus they are synonymous with afferent nerves.
Motor nerves conduct signals from the central nervous system to muscles. Thus they are synonymous with efferent nerves.^[1]^[2]

Clinical importance

Micrograph demonstrating perineural spread of prostate cancer. H&E stain.

Damage to nerves can be caused by physical injury or swelling (e.g. carpal tunnel syndrome), autoimmune diseases (e.g. Guillain-Barré syndrome), infection (neuritis), diabetes or failure of the blood vessels surrounding the nerve. A pinched nerve occurs when pressure is placed on a nerve, usually from swelling due to an injury or pregnancy. Nerve damage or pinched nerves are usually accompanied by pain, numbness, weakness, or paralysis. Patients may feel these symptoms in areas far from the actual site of damage, a phenomenon called referred pain. Referred pain occurs because when a nerve is damaged, signalling is altered for all parts of the area from which the nerve receives input, not just the site of the damage. Neurologists usually diagnose disorders of the nerves by a physical examination, including the testing of reflexes, walking and other directed movements, muscle weakness, proprioception, and the sense of touch. This initial exam can be followed with tests such as nerve conduction study and electromyography (EMG).

Cancer

Cancer can spread along nerves; this is known as perineural spread and often is associated with a worse prognosis.

Growth and stimulation

Nerve growth normally ends in adolescence, but can be re-stimulated with a molecular mechanism known as "Notch signaling."^[3]

References

Wikimedia Commons has media related to: Nerves

^ ^a ^b ^c Purves D, Augustine GJ, Fitzppatrick D et al. (2008). Neuroscience (4th ed.). Sinauer Associates. pp. 11–20. ISBN 978-0-87893-697-7.
^ ^a ^b ^c Marieb EN, Hoehn K (2007). Human Anatomy & Physiology (7th ed.). Pearson. pp. 388–602. ISBN 0-8053-5909-5.
^ Yale Study Shows Way To Re-Stimulate Brain Cell Growth ScienceDaily (Oct. 22, 1999) — Results Could Boost Understanding Of Alzheimer's, Other Brain Disorders

UpToDate Contents

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1. 神経伝導検査の概要 overview of nerve conduction studies
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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
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English Journal

The JNK inhibitor, SP600125, potentiates the glial response and cell death induced by methamphetamine in the mouse striatum.

Urrutia A1, Granado N1, Gutierrez-Lopez MD1, Moratalla R2, O'Shea E1, Colado MI1.Author information 1Departamento de Farmacologia, Facultad de Medicina, Universidad Complutense, Madrid, Spain.2Instituto Cajal, Consejo Superior de Investigaciones Científicas, CSIC, Madrid, Spain.AbstractThis study investigates the effect of the selective Jun NH2-terminal kinase 1/2 (JNK1/2) inhibitor, (SP600125) on the striatal dopamine nerve terminal loss and on the increased interleukin-15 (IL-15) expression and glial response induced by methamphetamine (METH). Mice were given repeated low doses of METH (4 mg/kg, i.p., three times separated by 3 h) and killed 24 h or 7 d after the last dose. SP600125 (30 mg/kg, i.p) was administered 30 min before the last METH injection. Results indicate that METH produced dopaminergic axonal neurotoxicity reflected as a marked decrease in the striatal density of tyrosine hydroxylase-immunoreactive (TH-ir) fibres and dopamine transporter-immunoreactivity (DAT-ir) 24 h after dosing. These effects were not modified by SP600125. This compound also failed to prevent the long-term loss of dopamine levels and DAT observed 7 d following METH injection. Nevertheless, SP600125 potentiated METH-induced striatal cell loss reflected by an increase in Fluoro-Jade immunostaining, cleaved capase-3 immunoreactivity and the number of terminal deoxyncleotidyl transferase-mediated dUTP nick end labelling (TUNEL) positive cells. In line with a deleterious effect of JNK1/2 inhibition, SP600125 increased the astroglial and microglial response induced by METH and interfered with drug-induced IL-15 expression. Together these data indicate that, not only does SP600125 fail to protect against the dopaminergic damage induced by METH but also, in fact, it potentiates the glial response and the non-dopaminergic striatal cell loss caused by the drug.
The international journal of neuropsychopharmacology / official scientific journal of the Collegium Internationale Neuropsychopharmacologicum (CINP).Int J Neuropsychopharmacol.2014 Feb;17(2):235-46. doi: 10.1017/S1461145713000850. Epub 2013 Oct 8.
This study investigates the effect of the selective Jun NH2-terminal kinase 1/2 (JNK1/2) inhibitor, (SP600125) on the striatal dopamine nerve terminal loss and on the increased interleukin-15 (IL-15) expression and glial response induced by methamphetamine (METH). Mice were given repeated low doses
PMID 24103647

Is there a role for nitric oxide in methamphetamine-induced dopamine terminal degeneration?

Friend DM, Fricks-Gleason AN, Keefe KA.Author information Interdepartmental Program in Neuroscience, University of Utah, 401 MREB, 20 North 1900 East, Salt Lake City, UT, 84132, USA, da.friend@utah.edu.AbstractMethamphetamine (METH) abuse results in long-term damage to the dopaminergic system, manifesting as decreases in dopamine (DA) tissue content, DA transporter binding, as well as tyrosine hydroxylase and vesicular monoamine transporter immunostaining. However, the exact cascade of events that ultimately result in this damage has not been clearly elucidated. One factor that has been heavily implicated in METH-induced DA terminal degeneration is the production of nitric oxide (NO). Unfortunately, many of the studies attempting to clarify the role of NO in METH-induced neurotoxicity have been confounded by issues such as the disruption of METH-induced hyperthermia, preventing the formation of strong conclusions. As a result, there is a body of work suggesting that NO is sufficient for METH-induced neurotoxicity, while other studies suggest that NO does not play a role in METH-induced degeneration of DA nerve terminals. This review summarizes the existing studies investigating the role of NO in METH-induced neurotoxicity, and argues that while NO may be necessary for METH-induced neurotoxicity, it is not sufficient. Finally, important areas of future investigation are highlighted and discussed.
Neurotoxicity research.Neurotox Res.2014 Feb;25(2):153-60. doi: 10.1007/s12640-013-9415-2. Epub 2013 Aug 6.
Methamphetamine (METH) abuse results in long-term damage to the dopaminergic system, manifesting as decreases in dopamine (DA) tissue content, DA transporter binding, as well as tyrosine hydroxylase and vesicular monoamine transporter immunostaining. However, the exact cascade of events that ultimat
PMID 23918001

Glycidol induces axonopathy and aberrations of hippocampal neurogenesis affecting late-stage differentiation by exposure to rats in a framework of 28-day toxicity study.

Akane H1, Shiraki A2, Imatanaka N3, Akahori Y3, Itahashi M2, Abe H2, Shibutani M4.Author information 1Laboratory of Veterinary Pathology, Tokyo University of Agriculture and Technology, 3-5-8 Saiwai-cho, Fuchu-shi, Tokyo 183-8509, Japan.2Laboratory of Veterinary Pathology, Tokyo University of Agriculture and Technology, 3-5-8 Saiwai-cho, Fuchu-shi, Tokyo 183-8509, Japan; Pathogenetic Veterinary Science, United Graduate School of Veterinary Sciences, Gifu University, 1-1 Yanagido, Gifu-shi, Gifu 501-1193, Japan.3Chemicals Evaluation and Research Institute, 1-4-25 Koraku, Bunkyo-ku, Tokyo 112-0004, Japan.4Laboratory of Veterinary Pathology, Tokyo University of Agriculture and Technology, 3-5-8 Saiwai-cho, Fuchu-shi, Tokyo 183-8509, Japan. Electronic address: mshibuta@cc.tuat.ac.jp.AbstractDevelopmental exposure to glycidol induces aberrations of late-stage neurogenesis in the hippocampal dentate gyrus of rat offspring, whereas maternal animals develop axonopathy. To investigate the possibility whether similar effects on adult neurogenesis could be induced by exposure in a framework of 28-day toxicity study, glycidol was orally administered to 5-week-old male Sprague-Dawley rats by gavage at 0, 30 or 200mg/kg for 28 days. At 200mg/kg, animals revealed progressively worsening gait abnormalities as well as histopathological and immunohistochemical changes suggestive of axonal injury as evidenced by generation of neurofilament-L(+) spheroids in the cerebellar granule layer and dorsal funiculus of the medulla oblongata, central chromatolysis in the trigeminal nerve ganglion cells and axonal degeneration in the sciatic nerves. At the same dose, animals revealed aberrations in neurogenesis at late-stage differentiation as evidenced by decreases of both doublecortin(+) and dihydropyrimidinase-like 3(+) cells in the subgranular zone (SGZ) and increased reelin(+) or calbindin-2(+) γ-aminobutyric acid-ergic interneurons and neuron-specific nuclear protein(+) mature neurons in the dentate hilus. These effects were essentially similar to that observed in offspring after maternal exposure to glycidol. These results suggest that glycidol causes aberrations in adult neurogenesis in the SGZ at the late stage involving the process of neurite extension similar to the developmental exposure study in a standard 28-day toxicity study.
Toxicology letters.Toxicol Lett.2014 Jan 30;224(3):424-32. doi: 10.1016/j.toxlet.2013.10.026. Epub 2013 Nov 1.
Developmental exposure to glycidol induces aberrations of late-stage neurogenesis in the hippocampal dentate gyrus of rat offspring, whereas maternal animals develop axonopathy. To investigate the possibility whether similar effects on adult neurogenesis could be induced by exposure in a framework o
PMID 24185127