WordNet

plant by the roots
(botany) the usually underground organ that lacks buds or leaves or nodes; absorbs water and mineral salts; usually it anchors the plant to the ground
a number that, when multiplied by itself some number of times, equals a given number
cause to take roots
take root and begin to grow; "this plant roots quickly"
(linguistics) the form of a word after all affixes are removed; "thematic vowels are part of the stem" (同)root word, base, stem, theme, radical
the part of a tooth that is embedded in the jaw and serves as support (同)tooth_root
come into existence, originate; "The problem roots in her depression"
belonging to or on or near the back or upper surface of an animal or organ or part; "the dorsal fin is the vertical fin on the back of a fish and certain marine mammals"
an encapsulated neural structure consisting of a collection of cell bodies or neurons
the condition of belonging to a particular place or group by virtue of social or ethnic or cultural lineage; "his roots in Texas go back a long way"; "he went back to Sweden to search for his roots"; "his music has African roots"

PrepTutorEJDIC

《しばしば複数形で》『根』 / 『根元』 / 《the~》『根源』,根本;根底 / 《複数形で》(その人の根底にある)ある場所との根源的なつながり / (数学で)根,ルート / (派生語の)語根(例えばrootlessの中のroot) / 〈植物〉‘を'『根づかせる』 / 《しばしば受動態で》(根をおろしたように)(…に)…‘を'『定着させる』『+『名』+『to』(『in』)+『名』》 / (…に)『根を下ろす』,定着する《+『in』(『on』,『to』)+『名』》
〈豚などが〉(…をあさって)鼻で地面を掘る《+『about』(『around』)『for』+『名』》 / (…を捜して)〈人が〉かき回す《+『about for』+『名』》
(…を)声援する,(…の)成功を願う《+『for』+『名』》
(植物の)背部の,背の
神経節・ガングリオン，結節腫《主に手首にできる良性の嚢腫(のうしゆ)》・〔知的･産業的活動の〕中心，中枢〔of〕
《補語にのみ用いて》(植物が)根づいた / (考えなどが)定着した

Wikipedia preview

出典(authority):フリー百科事典『ウィキペディア（Wikipedia）』「2016/09/25 01:33:12」(JST)

wiki en

A dorsal root ganglion (or spinal ganglion) (also known as a posterior root ganglion), is a cluster of nerve cell bodies (a ganglion) in a posterior root of a spinal nerve. The dorsal root ganglia contain the cell bodies of sensory neurons (afferent).

Structure

The axons of dorsal root ganglion neurons are known as afferents. In the peripheral nervous system, afferents refer to the axons that relay sensory information into the central nervous system (i.e. the brain and the spinal cord). These neurons are of the pseudo-unipolar type, meaning they have an axon with two branches that act as a single axon, often referred to as a distal process and a proximal process.

Note: the neuron can consist of three parts:

Dendrite that receives the information and relays it to the Soma, or cell body.
Soma—the cell body of the neuron
Axon: which relays information from the soma.

In a neuron, the dendrite receives information from another neuron's axon at the synapse, and the axon sends information to the next neuron's dendrites, even though the dendrite may be covered with myelin.

Unlike the majority of neurons found in the central nervous system, an action potential in posterior root ganglion neuron may initiate in the distal process in the periphery, bypass the cell body, and continue to propagate along the proximal process until reaching the synaptic terminal in the posterior horn of spinal cord.

Distal section

The distal section of the axon may either be a bare nerve ending or encapsulated by a structure that helps relay specific information to nerve. Two examples where the nerve ending of the distal process is encapsulated as such are, Meissner's corpuscles, which render the distal processes of mechanosensory neurons sensitive to stroking only, and Pacinian corpuscles, which make neurons more sensitive to vibration.^[1]

Location

The dorsal root ganglia lie in the intervertebral foramina.

Development

The dorsal root ganglia develop in the embryo from neural crest cells, not neural tube. Hence, the spinal ganglia can be regarded as gray matter of the spinal cord that became translocated to the periphery.

Function

Nociception

Proton-sensing G protein-coupled receptors are expressed by DRG sensory neurons and might play a role in acid-induced nociception.^[2]

Mechanosensitive channels

The nerve endings of dorsal root ganglion neurons have a variety of sensory receptors that are activated by mechanical, thermal, chemical, and noxious stimuli.^[3] In these sensory neurons, a group of ion channels thought to be responsible for somatosensory transduction have been identified. Compression of the dorsal root ganglion by a mechanical stimulus lowers the voltage threshold needed to evoke a response and causes action potentials to be fired.^[4] This firing may even persist after the removal of the stimulus.^[4]

Two distinct types of mechanosensitive ion channels have been found in the posterior root ganglion neurons. The two channels are broadly classified as either high-threshold (HT) or low threshold (LT).^[3] As their names suggest, they have different thresholds as well as different sensitivities to pressure. These are cationic channels whose activity appears to be regulated by the proper functioning of the cytoskeleton and cytoskeleton associated proteins.^[3] The presence of these channels in the posterior root ganglion gives reason to believe that other sensory neurons may contain them as well.

High-threshold mechanosensitive channels

High-threshold channels have a possible role in nociception. These channels are found predominantly in smaller sensory neurons in the dorsal root ganglion cells and are activated by higher pressures, two attributes that are characteristic of nociceptors.^[3] Also, the threshold of HT channels was lowered in the presence of PGE2 (a compound that sensitizes neurons to mechanical stimuli and mechanical hyperalgesia) which further supports a role for HT channels in the transduction of mechanical stimuli into nociceptive neuronal signals.^[3]^[4]^[5]

Presynaptic control

The presynaptic regulation of the dorsal nerve ending discharge in the spinal cord can occur through certain types of GABA_A receptors but not through the activation of glycine receptors which are absent from these types of terminals. Thus GABA_A receptors but not glycine receptors can presynaptically control nociception and pain transmission.^[6]

References

^ Kandel ER, Schwartz JH, Jessell TM. Principles of Neural Science, 4th ed., p.431–433. McGraw-Hill, New York (2000). ISBN 0-8385-7701-6
^ Huang CW, Tzeng JN, Chen YJ, Tsai WF, Chen CC, Sun WH (2007). "Nociceptors of dorsal root ganglion express proton-sensing G-protein-coupled receptors". Mol. Cell. Neurosci. 36 (2): 195–210. doi:10.1016/j.mcn.2007.06.010. PMID 17720533.
^ ^a ^b ^c ^d ^e Cho, H.; Shin, J.; Shin, C. Y.; Lee, S. Y.; Oh, U. (2002). "Mechanosensitive ion channels in cultured sensory neurons of neonatal rats". The Journal of neuroscience : the official journal of the Society for Neuroscience. 22 (4): 1238–1247. PMID 11850451.
^ ^a ^b ^c Sugawara, O.; Atsuta, Y.; Iwahara, T.; Muramoto, T.; Watakabe, M.; Takemitsu, Y. (1996). "The effects of mechanical compression and hypoxia on nerve root and dorsal root ganglia. An analysis of ectopic firing using an in vitro model". Spine. 21 (18): 2089–2094. doi:10.1097/00007632-199609150-00006. PMID 8893432.
^ Syriatowicz, J. P.; Hu, D.; Walker, J. S.; Tracey, D. J. (1999). "Hyperalgesia due to nerve injury: Role of prostaglandins". Neuroscience. 94 (2): 587–594. doi:10.1016/S0306-4522(99)00365-6. PMID 10579219.
^ Lorenzo LE, Godin AG, Wang F, St-Louis M, Carbonetto S, Wiseman PW, Ribeiro-da-Silva A, De Koninck Y (June 2014). "Gephyrin Clusters Are Absent from Small Diameter Primary Afferent Terminals Despite the Presence of GABA_A Receptors". J. Neurosci. 34 (24): 8300–17. doi:10.1523/JNEUROSCI.0159-14.2014. PMID 24920633.

Additional images

Medulla spinalis
Scheme showing structure of a typical spinal nerve.

External links

Anatomy figure: 02:04-09 at Human Anatomy Online, SUNY Downstate Medical Center
Histology image: 04401loa – Histology Learning System at Boston University
Photo of model at Ohio State University
Diagram at webanatomy.net
Photo at uwlax.edu

UpToDate Contents

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1. 脊髄および後根神経節に影響を与える腫瘍随伴性症候群 paraneoplastic syndromes affecting the spinal cord and dorsal root ganglia
2. ガングリオンと結節 ganglia and nodules
3. 脊髄障害の解剖学および局在性 anatomy and localization of spinal cord disorders
4. 臨床神経生理学 clinical neurophysiology
5. 進行性核上性麻痺（PSP） progressive supranuclear palsy psp

English Journal

Cortistatin attenuates inflammatory pain via spinal and peripheral actions.

Morell M1, Camprubí-Robles M2, Culler MD3, de Lecea L4, Delgado M5.Author information 1Institute of Parasitology and Biomedicine Lopez-Neyra, IPBLN-CSIC, 18016 Granada, Spain.2Institute of Molecular and Cell Biology, Miguel Hernandez University, 03202 Alicante, Spain.3IPSEN Group, Milford, MA 01757, USA.4Department of Psychiatry and Behavioral Sciences, Stanford University, Stanford, CA 94305, USA.5Institute of Parasitology and Biomedicine Lopez-Neyra, IPBLN-CSIC, 18016 Granada, Spain. Electronic address: mdelgado@ipb.csic.es.AbstractClinical pain, as a consequence of inflammation or injury of peripheral organs (inflammatory pain) or nerve injury (neuropathic pain), represents a serious public health issue. Treatment of pain-related suffering requires knowledge of how pain signals are initially interpreted and subsequently transmitted and perpetuated. To limit duration and intensity of pain, inhibitory signals participate in pain perception. Cortistatin is a cyclic-neuropeptide that exerts potent inhibitory actions on cortical neurons and immune cells. Here, we found that cortistatin is a natural analgesic component of the peripheral nociceptive system produced by peptidergic nociceptive neurons of the dorsal root ganglia in response to inflammatory and noxious stimuli. Moreover, cortistatin is produced by GABAergic interneurons of deep layers of dorsal horn of spinal cord. By using cortistatin-deficient mice, we demonstrated that endogenous cortistatin critically tunes pain perception in physiological and pathological states. Furthermore, peripheral and spinal injection of cortistatin potently reduced nocifensive behavior, heat hyperalgesia and tactile allodynia in experimental models of clinical pain evoked by chronic inflammation, surgery and arthritis. The analgesic effects of cortistatin were independent of its anti-inflammatory activity and directly exerted on peripheral and central nociceptive terminals via Gαi-coupled somatostatin-receptors (mainly sstr2) and blocking intracellular signaling that drives neuronal plasticity including protein kinase A-, calcium- and Akt/ERK-mediated release of nociceptive peptides. Moreover, cortistatin could modulate, through its binding to ghrelin-receptor (GHSR1), pain-induced sensitization of secondary neurons in spinal cord. Therefore, cortistatin emerges as an anti-inflammatory factor with potent analgesic effects that offers a new approach to clinical pain therapy, especially in inflammatory states.
Neurobiology of disease.Neurobiol Dis.2014 Mar;63:141-54. doi: 10.1016/j.nbd.2013.11.022. Epub 2013 Dec 9.
Clinical pain, as a consequence of inflammation or injury of peripheral organs (inflammatory pain) or nerve injury (neuropathic pain), represents a serious public health issue. Treatment of pain-related suffering requires knowledge of how pain signals are initially interpreted and subsequently trans
PMID 24333694

The chemokine CCL5 induces CCR1-mediated hyperalgesia in mice inoculated with NCTC 2472 tumoral cells.

Pevida M1, Lastra A2, Meana A3, Hidalgo A4, Baamonde A5, Menéndez L6.Author information 1Laboratorio de Farmacología, Facultad de Medicina, Instituto Universitario de Oncología del Principado de Asturias (IUOPA), Universidad de Oviedo, c/ Julián Clavería 6, 33006 Oviedo, Asturias, Spain. Electronic address: pevidamarta@uniovi.es.2Laboratorio de Farmacología, Facultad de Medicina, Instituto Universitario de Oncología del Principado de Asturias (IUOPA), Universidad de Oviedo, c/ Julián Clavería 6, 33006 Oviedo, Asturias, Spain. Electronic address: lastraana@uniovi.es.3Centro Comunitario de Sangre y Tejidos del Principado de Asturias, CIBER de Enfermedades Raras (CIBERER), U714, Oviedo, Asturias, Spain. Electronic address: investigacion.ccst@telefonica.net.4Laboratorio de Farmacología, Facultad de Medicina, Instituto Universitario de Oncología del Principado de Asturias (IUOPA), Universidad de Oviedo, c/ Julián Clavería 6, 33006 Oviedo, Asturias, Spain. Electronic address: hidalgo@uniovi.es.5Laboratorio de Farmacología, Facultad de Medicina, Instituto Universitario de Oncología del Principado de Asturias (IUOPA), Universidad de Oviedo, c/ Julián Clavería 6, 33006 Oviedo, Asturias, Spain. Electronic address: arbaiza@uniovi.es.6Laboratorio de Farmacología, Facultad de Medicina, Instituto Universitario de Oncología del Principado de Asturias (IUOPA), Universidad de Oviedo, c/ Julián Clavería 6, 33006 Oviedo, Asturias, Spain. Electronic address: luismen@uniovi.es.AbstractAlthough the expression of the chemokine receptor CCR1 has been demonstrated in several structures related to nociception, supporting the nociceptive role of chemokines able to activate it, the involvement of CCR1 in neoplastic pain has not been previously assessed. We have assayed the effects of a CCR1 antagonist, J113863, in two murine models of neoplastic hyperalgesia based on the intratibial injection of either NCTC 2472 fibrosarcoma cells, able to induce osteolytic bone injury, or B16-F10 melanoma cells, associated to mixed osteolytic/osteoblastic bone pathological features. The systemic administration of J113863 inhibited thermal and mechanical hyperalgesia but not mechanical allodynia in mice inoculated with NCTC 2472 cells. Moreover, in these mice, thermal hyperalgesia was counteracted following the peritumoral (10-30μg) but not spinal (3-5μg) administration of J113863. In contrast, hyperalgesia and allodynia measured in mice inoculated with B16-F10 cells remained unaffected after the administration of J113863. The inoculation of tumoral cells did not modify the levels of CCL3 at tumor or spinal cord. In contrast, although the concentration of CCL5 remained unmodified in mice inoculated with B16-F10 cells, increased levels of this chemokine were measured in tumor-bearing limbs, but not the spinal cord, of mice inoculated with NCTC 2472 cells. Increased levels of CCL5 were also found following the incubation of NCTC 2472, but not B16-F10, cells in the corresponding culture medium. The intraplantar injection of CCL5 (0.5ng) to naïve mice evoked thermal hyperalgesia prevented by the coadministration of J113863 or the CCR5 antagonist, d-Ala-peptide T-amide (DAPTA), demonstrating that CCL5 can induce thermal hyperalgesia in mice through the activation of CCR1 or CCR5. However, contrasting with the inhibitory effect evoked by J113863, the systemic administration of DAPTA did not prevent tumoral hyperalgesia. Finally, the peritumoral administration of an anti-CCL5 antibody completely inhibited thermal hyperalgesia evoked by the inoculation of NCTC 2472 cells.
Neuroscience.Neuroscience.2014 Feb 14;259:113-25. doi: 10.1016/j.neuroscience.2013.11.055. Epub 2013 Dec 4.
Although the expression of the chemokine receptor CCR1 has been demonstrated in several structures related to nociception, supporting the nociceptive role of chemokines able to activate it, the involvement of CCR1 in neoplastic pain has not been previously assessed. We have assayed the effects of a
PMID 24316469

The role of miR-146a in dorsal root ganglia neurons of experimental diabetic peripheral neuropathy.

Wang L1, Chopp M2, Szalad A1, Zhang Y1, Wang X1, Zhang RL1, Liu XS1, Jia L1, Zhang ZG3.Author information 1Department of Neurology, Henry Ford Hospital, 2799 W. Grand Boulevard, Detroit, MI 48202, United States.2Department of Neurology, Henry Ford Hospital, 2799 W. Grand Boulevard, Detroit, MI 48202, United States; Department of Physics, Oakland University, Rochester, MI 48309, United States.3Department of Neurology, Henry Ford Hospital, 2799 W. Grand Boulevard, Detroit, MI 48202, United States. Electronic address: zhazh@neuro.hfh.edu.AbstractSensory neurons mediate diabetic peripheral neuropathy. Using a mouse model of diabetic peripheral neuropathy (BKS.Cg-m+/+Lepr(db)/J (db/db) mice) and cultured dorsal root ganglion (DRG) neurons, the present study showed that hyperglycemia downregulated miR-146a expression and elevated interleukin-1 receptor-activated kinase (IRAK1) and tumor necrosis factor receptor-associated factor 6 (TRAF6) levels in DRG neurons. In vitro, elevation of miR-146a by miR-146a mimics in DRG neurons increased neuronal survival under high-glucose conditions. Downregulation and elevation of miR-146a in DRG neurons, respectively, were inversely related to IRAK1 and TRAF6 levels. Treatment of diabetic peripheral neuropathy with sildenafil, a phosphodiesterase type 5 inhibitor, augmented miR-146a expression and decreased levels of IRAK1 and TRAF6 in the DRG neurons. In vitro, blockage of miR-146a in DRG neurons abolished the effect of sildenafil on DRG neuron protection and downregulation of IRAK1 and TRAF6 proteins under hyperglycemia. Our data provide the first evidence showing that miR-146a plays an important role in mediating DRG neuron apoptosis under hyperglycemic conditions.
Neuroscience.Neuroscience.2014 Feb 14;259:155-63. doi: 10.1016/j.neuroscience.2013.11.057. Epub 2013 Dec 6.
Sensory neurons mediate diabetic peripheral neuropathy. Using a mouse model of diabetic peripheral neuropathy (BKS.Cg-m+/+Lepr(db)/J (db/db) mice) and cultured dorsal root ganglion (DRG) neurons, the present study showed that hyperglycemia downregulated miR-146a expression and elevated interleukin-1
PMID 24316060

Japanese Journal

Biodistribution of gold nanoparticles in mice and investigation of their possible translocation by nerve uptake around the alveolus

, , [他],
The Journal of Toxicological Sciences 40(2), 243-249, 2015
… Furthermore, the possibility of migration of nanoparticles through the nerves that project around the alveolus, including the nodose ganglion and dorsal root ganglion (DRG), was investigated. …
NAID 130004904038

Diethyldithiocarbamate, a superoxide dismutase inhibitor, inhibits axonal transport in cultured mouse dorsal root ganglion neurons

Isonaka Risa
The Kitasato medical journal 44(2), 183-188, 2014-09
NAID 40020211075

Up-regulation of brain-derived neurotrophic factor in the dorsal root ganglion of the rat bone cancer pain model

Tomotsuka Naoto,Kaku Ryuji,Obata Norihiko,Matsuoka Yoshikazu,Kanzaki Hirotaka,Taniguchi Arata,Muto Noriko,Omiya Hiroki,Itano Yoshitaro,Sato Tadasu,Ichikawa Hiroyuki,Mizobuchi Satoshi,Morimatsu Hiroshi
Journal of Pain Research 7, 415-423, 2014-07-11
… in this study, we investigated changes of BDNF expression in dorsal root ganglia in a rat bone cancer pain model. … As we expected, BDNF mRNA (messenger ribonucleic acid) and protein were significantly increased in L3 dorsal root ganglia after intra-tibial inoculation of MRMT-1 rat breast cancer cells. …
NAID 120005517857

Related Pictures

★リンクテーブル★

リンク元	「脊髄神経節」「背根神経節」「脊髄知覚神経節」「spinal ganglia」「後根神経節」
拡張検索	「dorsal root ganglion neuron」
関連記事	「root」「dorsal」

「脊髄神経節」

Dorsal root ganglion
	A dorsal root ganglion (DRG) from a chicken embryo (around stage of day 7) after incubation overnight in NGF growth medium stained with anti-neurofilament antibody. Axons growing out of the ganglion are visible.
	A spinal nerve with its ventral and dorsal roots. The dorsal root ganglion is the "spinal ganglion", following the dorsal root.
Details
Precursor	neural crest
Identifiers
Latin	ganglion sensorium nervi spinalis
MeSH	A08.340.390.340
TA	A14.2.00.006
FMA	5888
	Anatomical terminology [edit on Wikidata]