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Hormone
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For other uses, see Hormone (disambiguation).
Different types of hormones are secreted in the body, with different biological roles and functions.
A hormone (from the Greek participle “ὁρμῶ”, "to set in motion, urge on") is any member of a class of signaling molecules produced by glands in multicellular organisms that are transported by the circulatory system to target distant organs to regulate physiology and behaviour. Hormones have diverse chemical structures, mainly of 3 classes: eicosanoids, steroids, and amino acid/protein derivatives (amines, peptides, and proteins). The glands that secrete hormones comprise the endocrine signaling system. The term hormone is sometimes extended to include chemicals produced by cells that affect the same cell (autocrine or intracrine signalling) or nearby cells (paracrine signalling).
Hormones are used to communicate between organs and tissues for physiological regulation and behavioral activities, such as digestion, metabolism, respiration, tissue function, sensory perception, sleep, excretion, lactation, stress, growth and development, movement, reproduction, and mood.[1][2] Hormones affect distant cells by binding to specific receptor proteins in the target cell resulting in a change in cell function. When a hormone binds to the receptor, it results in the activation of a signal transduction pathway that typically activates gene transcription resulting in increased expression of target proteins; non-genomic effects are more rapid, and can be synergistic with genomic effects.[3] Amino acid–based hormones (amines and peptide or protein hormones) are water-soluble and act on the surface of target cells via second messengers; steroid hormones, being lipid-soluble, move through the plasma membranes of target cells (both cytoplasmic and nuclear) to act within their nuclei.
Hormone secretion may occur in many tissues. Endocrine glands are the cardinal example, but specialized cells in various other organs also secrete hormones. Hormone secretion occurs in response to specific biochemical signals from a wide range of regulatory systems. For instance, serum calcium concentration affects parathyroid hormone synthesis; blood sugar (serum glucose concentration) affects insulin synthesis; and because the outputs of the stomach and exocrine pancreas (the amounts of gastric juice and pancreatic juice) become the input of the small intestine, the small intestine secretes hormones to stimulate or inhibit the stomach and pancreas based on how busy it is. Regulation of hormone synthesis of gonadal hormones, adrenocortical hormones, and thyroid hormones is often dependent on complex sets of direct influence and feedback interactions involving the hypothalamic-pituitary-adrenal (HPA), -gonadal (HPG), and -thyroid (HPT) axes.
Upon secretion, certain hormones, including protein hormones and catecholamines, are water-soluble and are thus readily transported through the circulatory system. Other hormones, including steroid and thyroid hormones, are lipid-soluble; to allow for their widespread distribution, these hormones must bond to carrier plasma glycoproteins (e.g., thyroxine-binding globulin (TBG)) to form ligand-protein complexes. Some hormones are completely active when released into the bloodstream (as is the case for insulin and growth hormones), while others are prohormones that must be activated in specific cells through a series of activation steps that are commonly highly regulated. The endocrine system secretes hormones directly into the bloodstream typically into fenestrated capillaries, whereas the exocrine system secretes its hormones indirectly using ducts. Hormones with paracrine function diffuse through the interstitial spaces to nearby target tissue.
Contents
[hide]
1 Introduction/Overview
2 Regulation
3 Receptors
4 Effects
5 Chemical classes
5.1 Animal
5.2 Plant
6 Therapeutic use
7 Hormone-behavior interactions
8 Comparison with neurotransmitters
9 Binding proteins
10 Discovery
11 See also
12 References
13 External links
Introduction/Overview[edit]
Further information: Signal transduction
Hormonal signaling involves the following steps:[4]
Biosynthesis of a particular hormone in a particular tissue
Storage and secretion of the hormone
Transport of the hormone to the target cell(s)
Recognition of the hormone by an associated cell membrane or intracellular receptor protein
Relay and amplification of the received hormonal signal via a signal transduction process: This then leads to a cellular response. The reaction of the target cells may then be recognized by the original hormone-producing cells, leading to a down-regulation in hormone production. This is an example of a homeostatic negative feedback loop.
Breakdown of the hormone.
Hormone producing cells are typically of a specialized cell type, residing within a particular endocrine gland, such as the thyroid gland, ovaries, and testes. Hormones exit their cell of origin via exocytosis or another means of membrane transport. The hierarchical model is an oversimplification of the hormonal signaling process. Cellular recipients of a particular hormonal signal may be one of several cell types that reside within a number of different tissues, as is the case for insulin, which triggers a diverse range of systemic physiological effects. Different tissue types may also respond differently to the same hormonal signal.
Regulation[edit]
The rate of hormone biosynthesis and secretion is often regulated by a homeostatic negative feedback control mechanism. Such a mechanism depends on factors that influence the metabolism and excretion of hormones. Thus, higher hormone concentration alone cannot trigger the negative feedback mechanism. Negative feedback must be triggered by overproduction of an "effect" of the hormone.
Hormone secretion can be stimulated and inhibited by:
Other hormones (stimulating- or releasing -hormones)
Plasma concentrations of ions or nutrients, as well as binding globulins
Neurons and mental activity
Environmental changes, e.g., of light or temperature
One special group of hormones is the tropic hormones that stimulate the hormone production of other endocrine glands. For example, thyroid-stimulating hormone (TSH) causes growth and increased activity of another endocrine gland, the thyroid, which increases output of thyroid hormones.
To release active hormones quickly into the circulation, hormone biosynthetic cells may produce and store biologically inactive hormones in the form of pre- or prohormones. These can then be quickly converted into their active hormone form in response to a particular stimulus.
Eicosanoids are considered to act as local hormones. They are considered to be "local" because they possess specific effects on target cells close to their site of formation. They also have a rapid degradation cycle, making sure they do not reach distal sites within the body.[5]
Receptors[edit]
The left diagram shows a steroid (lipid) hormone (1) entering a cell and (2) binding to a receptor protein in the nucleus, causing (3) mRNA synthesis which is the first step of protein synthesis. The right side shows protein hormones (1) binding with receptors which (2) begins a transduction pathway. The transduction pathway ends (3) with transcription factors being activated in the nucleus, and protein synthesis beginning. In both diagrams, a is the hormone, b is the cell membrane, c is the cytoplasm, and d is the nucleus.
Most hormones initiate a cellular response by initially binding to either cell membrane associated or intracellular receptors. A cell may have several different receptor types that recognize the same hormone but activate different signal transduction pathways, or a cell may have several different receptors that recognize different hormones and activate the same biochemical pathway.
Receptors for most peptide as well as many eicosanoid hormones are embedded in the plasma membrane at the surface of the cell and the majority of these receptors belong to the G protein-coupled receptor (GPCR) class of seven alpha helix transmembrane proteins. The interaction of hormone and receptor typically triggers a cascade of secondary effects within the cytoplasm of the cell, often involving phosphorylation or dephosphorylation of various other cytoplasmic proteins, changes in ion channel permeability, or increased concentrations of intracellular molecules that may act as secondary messengers (e.g., cyclic AMP). Some protein hormones also interact with intracellular receptors located in the cytoplasm or nucleus by an intracrine mechanism.
For steroid or thyroid hormones, their receptors are located inside the cell within the cytoplasm of the target cell. These receptors belong to the nuclear receptor family of ligand-activated transcription factors. To bind their receptors, these hormones must first cross the cell membrane. They can do so because they are lipid-soluble. The combined hormone-receptor complex then moves across the nuclear membrane into the nucleus of the cell, where it binds to specific DNA sequences, regulating the expression of certain genes, and thereby increasing the levels of the proteins encoded by these genes.[6] However, it has been shown that not all steroid receptors are located inside the cell. Some are associated with the plasma membrane.[7]
Effects[edit]
Hormones have the following effects on the body:
stimulation or inhibition of growth
wake-sleep cycle and other circadian rhythms
mood swings
induction or suppression of apoptosis (programmed cell death)
activation or inhibition of the immune system
regulation of metabolism
preparation of the body for mating, fighting, fleeing, and other activity
preparation of the body for a new phase of life, such as puberty, parenting, and menopause
control of the reproductive cycle
hunger cravings
A hormone may also regulate the production and release of other hormones. Hormone signals control the internal environment of the body through homeostasis.
Chemical classes[edit]
As hormones are defined functionally, not structurally, they may have diverse chemical structures. Hormones occur in multicellular organisms (plants, animals, fungi, brown algae and red algae). These compounds occur also in unicellular organisms, and may act as signaling molecules,[8][9] but there is no consensus if, in this case, they can be called hormones.
Animal[edit]
Further information: List of human hormones
Vertebrate hormones fall into three main chemical classes:
Amino acid derived – Examples include melatonin and thyroxine.
Peptides, polypeptides and proteins. – Small peptide hormones include TRH and vasopressin. Peptides composed of scores or hundreds of amino acids are referred to as proteins. Examples of protein hormones include insulin and growth hormone. More complex protein hormones bear carbohydrate side-chains and are called glycoprotein hormones. Luteinizing hormone, follicle-stimulating hormone and thyroid-stimulating hormone are examples of glycoprotein hormones.
Eicosanoids – hormones derive from lipids such as arachidonic acid, lipoxins and prostaglandins. These hormones are produced by cyclooxygenases and lipoxygenases and there are many drugs that include the NSAIDs like ibuprofen and naproxen which effect the activity of the cyclooxygenases and inhibit the formation of these eicosanoid hormones.[10]
Steroid – Hormones derived from cholesterol. Examples of steroid hormones include the sex hormones estradiol and testosterone as well as the stress hormone cortisol.[11]
Compared with vertebrates, insects and crustaceans possess a number of structurally unusual hormones such as the juvenile hormone, a sesquiterpenoid.[12]
Plant[edit]
Further information: Plant hormone § Classes of plant hormones
Plant hormones include abscisic acid, auxin, cytokinin, ethylene, and gibberellin.
Therapeutic use[edit]
Many hormones and their structural and functional analogs are used as medication. The most commonly prescribed hormones are estrogens and progestogens (as methods of hormonal contraception and as HRT),[13] thyroxine (as levothyroxine, for hypothyroidism) and steroids (for autoimmune diseases and several respiratory disorders). Insulin is used by many diabetics. Local preparations for use in otolaryngology often contain pharmacologic equivalents of adrenaline, while steroid and vitamin D creams are used extensively in dermatological practice.
A "pharmacologic dose" or "supraphysiological dose" of a hormone is a medical usage referring to an amount of a hormone far greater than naturally occurs in a healthy body. The effects of pharmacologic doses of hormones may be different from responses to naturally occurring amounts and may be therapeutically useful, though not without potentially adverse side effects. An example is the ability of pharmacologic doses of glucocorticoids to suppress inflammation.
Hormone-behavior interactions[edit]
This section does not cite any sources. Please help improve this section by adding citations to reliable sources. Unsourced material may be challenged and removed. (May 2014) (Learn how and when to remove this template message)
At the neurological level, behavior can be inferred based on: hormone concentrations; hormone-release patterns; the numbers and locations of hormone receptors; and the efficiency of hormone receptors for those involved in gene transcription. Not only do hormones influence behavior, but also behavior and the environment influence hormones. Thus, a feedback loop is formed. For example, behavior can affect hormones, which in turn can affect behavior, which in turn can affect hormones, and so on.
Three broad stages of reasoning may be used when determining hormone-behavior interactions:
The frequency of occurrence of a hormonally dependent behavior should correspond to that of its hormonal source
A hormonally dependent behavior is not expected if the hormonal source (or its types of action) is non-existent
The reintroduction of a missing behaviorally dependent hormonal source (or its types of action) is expected to bring back the absent behavior
Comparison with neurotransmitters[edit]
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There are various clear distinctions between hormones and neurotransmitters:
A hormone can perform functions over a larger spatial and temporal scale than can a neurotransmitter.
Hormonal signals can travel virtually anywhere in the circulatory system, whereas neural signals are restricted to pre-existing nerve tracts
Assuming the travel distance is equivalent, neural signals can be transmitted much more quickly (in the range of milliseconds) than can hormonal signals (in the range of seconds, minutes, or hours). Neural signals can be sent at speeds up to 100 meters per second.
Neural signalling is an all-or-nothing (digital) action, whereas hormonal signalling is an action that can be continuously variable as dependent upon hormone concentration.
Binding proteins[edit]
Hormone transport and the involvement of binding proteins is an essential aspect when considering the function of hormones. There are several benefits with the formation of a complex with a binding protein: the effective half-life of the bound hormone is increased; a reservoir of bound hormones is created, which evens the variations in concentration of unbound hormones (bound hormones will replace the unbound hormones when these are eliminated).[14]
Discovery[edit]
The discovery of hormones and endocrine signaling occurred during studies of how the digestive system regulates its activities, as explained at Secretin § Discovery.
See also[edit]
Autocrine signaling
Cytokine
Endocrine system
Endocrinology
Environmental hormones
Growth factor
Hormone disruptor
Intracrine
List of investigational hormonal agents
Metabolomics
Neuroendocrinology
Paracrine signaling
Plant hormones or plant growth regulators
Semiochemical
Sex-hormonal agent
Sexual motivation and hormones
References[edit]
Jump up ^ Neave N (2008). Hormones and behaviour: a psychological approach. Cambridge: Cambridge Univ. Press. ISBN 978-0521692014. Lay summary – Project Muse.
Jump up ^ "Hormones". MedlinePlus. U.S. National Library of Medicine.
Jump up ^ Ruhs, Stefanie; Nolze, Alexander; Hübschmann, Ralf; Grossmann, Claudia (July 2017). "30 YEARS OF THE MINERALOCORTICOID RECEPTOR: Nongenomic effects via the mineralocorticoid receptor". The Journal of Endocrinology. 234 (1): T107–T124. doi:10.1530/JOE-16-0659. ISSN 1479-6805. PMID 28348113.
Jump up ^ Nussey S, Whitehead S (2001). Endocrinology: an integrated approach. Oxford: Bios Scientific Publ. ISBN 978-1-85996-252-7.
Jump up ^ "Eicosanoids". www.rpi.edu. Retrieved 2017-02-08.
Jump up ^ Beato M, Chavez S, Truss M (1996). "Transcriptional regulation by steroid hormones". Steroids. 61 (4): 240–251. doi:10.1016/0039-128X(96)00030-X. PMID 8733009.
Jump up ^ Hammes SR (2003). "The further redefining of steroid-mediated signaling". Proc Natl Acad Sci USA. 100 (5): 21680–2170. doi:10.1073/pnas.0530224100. PMC 151311  . PMID 12606724.
Jump up ^ Lenard J (1992). "Mammalian hormones in microbial cells". Trends Biochem. Sci. 17 (4): 147–50. doi:10.1016/0968-0004(92)90323-2. PMID 1585458.
Jump up ^ Janssens PM. "Did vertebrate signal transduction mechanisms originate in eukaryotic microbes?". Trends in Biochemical Sciences. 12: 456–459. doi:10.1016/0968-0004(87)90223-4.
Jump up ^ "Eicosanoid Synthesis and Metabolism: Prostaglandins, Thromboxanes, Leukotrienes, Lipoxins". themedicalbiochemistrypage.org. Retrieved 2017-02-07.
Jump up ^ Marieb, Elaine (2014). Anatomy & physiology. Glenview, IL: Pearson Education, Inc. ISBN 978-0321861580.
Jump up ^ Heyland A, Hodin J, Reitzel AM (2005). "Hormone signaling in evolution and development: a non-model system approach". BioEssays. 27 (1): 64–75. doi:10.1002/bies.20136. PMID 15612033.
Jump up ^ "Hormone Therapy". Cleveland Clinic.
Jump up ^ Boron WF, Boulpaep EL. Medical physiology : a cellular and molecular approach. Updated 2. Philadelphia, Pa: Saunders Elsevier; 2012.
External links[edit]
HMRbase: A database of hormones and their receptors
Hormones at the US National Library of Medicine Medical Subject Headings (MeSH)
[show]
v
t
e
Hormones
Endocrine
glands
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text:
Sciatic nerve
From Wikipedia, the free encyclopedia
Jump to: navigation, search
Sciatic Nerve
Right gluteal region, showing surface markings for arteries and sciatic nerve
Details
From
Lumbar and sacral plexus (L4-S3)
To
Tibial and common fibular nerve
Innervates
Lateral rotator group (except piriformis and quadratus femoris) and the posterior compartment of thigh
Identifiers
Latin
Nervus ischiadicus
Dorlands
/Elsevier
n_05/12566006
TA
A14.2.07.046
FMA
19034
Anatomical terms of neuroanatomy
[edit on Wikidata]
The sciatic nerve (/saɪˈætɪk/; also called ischiadic nerve, ischiatic nerve, "butt nerve") is a large nerve in humans and other animals. It begins in the lower back and runs through the buttock and down the lower limb. It is the longest and widest single nerve in the human body, going from the top of the leg to the foot on the posterior aspect.[1] The sciatic nerve provides the connection to the nervous system for nearly the whole of the skin of the leg, the muscles of the back of the thigh, and those of the leg and foot. It is derived from spinal nerves L4 to S3. It contains fibers from both the anterior and posterior divisions of the lumbosacral plexus.
Contents
[hide]
1 Structure
1.1 Development
2 Function
3 Clinical significance
3.1 Sciatica
3.2 Injury
3.3 Other disease
3.4 Anesthetic
4 Society and culture
5 See also
6 Additional images
7 See also
8 Notes
9 References
10 External links
Structure[edit]
The sciatic nerve is formed from the L4 to S3 segments of the sacral plexus, a collection of nerve fibres that emerge from the sacral part of the spinal cord. The fibres unite to form a single nerve in front of the piriformis muscle. The nerve passes beneath piriformis and through the greater sciatic foramen, exiting the pelvis.[2]:422–4 From here, it travels down the posterior thigh to the popliteal fossa. The nerve travels in the posterior compartment of the thigh behind (superficial to) the adductor magnus muscle, and is itself in front of (deep to) one head of the biceps femoris muscle. At the popliteal fossa, the nerve divides into its two branches:[2]:532
The tibial nerve, which travels down the posterior compartment of the leg into the foot
The common peroneal nerve (also called the common fibular nerve), which travels down the anterior and lateral compartments of the leg into the foot
The sciatic nerve is the largest nerve in the human body.[2]:422–4
Tibial and common peroneal nerve (aka common fibular nerve)
Development[edit]
This section needs expansion. You can help by adding to it. (March 2014)
Function[edit]
The sciatic nerve supplies sensation to the skin of the foot, as well as the entire lower leg (except for its inner side). Sensation to skin to the sole of the foot is provided by the tibial nerve, and the lower leg and upper surface of the foot via the common fibular nerve.[2]:422–4
The sciatic nerve also innervates muscles. In particular:[2]:422–4
Via the tibial nerve, the muscles in the posterior compartment of the leg and sole of the foot (plantar aspect).[a]
Via the common peroneal nerve (also called the common fibular nerve), the muscles in the anterior and lateral compartments of the leg.[b]
Clinical significance[edit]
Sciatica[edit]
Main article: Sciatica
Pain caused by a compression or irritation of the sciatic nerve by a problem in the lower back is called sciatica. Common causes of sciatica include the following lower back and hip conditions: spinal disc herniation, degenerative disc disease, lumbar spinal stenosis, spondylolisthesis, and piriformis syndrome.[3] Other acute causes of sciatica include coughing, muscular hypertension, and sneezing.[4]
Injury[edit]
Sciatic nerve injury occurs between 0.5% and 2.0% of the time during total hip arthroplasty.[5] Sciatic nerve palsy is a complication of total hip arthroplasty with an incidence of 0.2% to 2.8% of the time, or with an incidence of 1.7% to 7.6% following revision.[6] Following the procedure, in rare cases, a screw, broken piece of trochanteric wire, fragment of methyl methacrylate bone cement, or Burch-Schneider metal cage can impinge on the nerve; this can cause sciatic nerve palsy which may resolve after the fragment is removed and the nerve freed. The nerve can be surrounded in oxidized regenerated cellulose to prevent further scarring. Sciatic nerve palsy can also result from severe spinal stenosis following the procedure, which can be addressed by spinal decompression surgery.[5][7] It is unclear if inversion therapy is able to decompress the sacral vertebrae, it may only work on the lumbar aspects of the sciatic nerves.
Sciatic nerve injury may also occur from improperly performed injections into the buttock, and may result in sensory loss.[8]:66
Other disease[edit]
Bernese periacetabular osteotomy resulted in major nerve deficits in the sciatic or femoral nerves in 2.1% of 1760 patients, of whom approximately half experienced complete recovery within a mean of 5.5 months.[9]
Sciatic nerve exploration can be done by endoscopy in a minimally invasive procedure to assess lesions of the nerve.[10] Endoscopic treatment for sciatic nerve entrapment has been investigated in deep gluteal syndrome; "Patients were treated with sciatic nerve decompression by resection of fibrovascular scar bands, piriformis tendon release, obturator internus, or quadratus femoris or by hamstring tendon scarring."[11]
Anesthetic[edit]
Signals from the sciatic nerve and it branches can be blocked, in order to interrupted transmission of pain signal from the innervation area, by performing a regional nerve blockade called a sciatic nerve block.
Society and culture[edit]
According to Jewish law, the sciatic nerve (Hebrew: Gid hanasheh) cannot be eaten, to commemorate Jacob's hurt in his struggle with an Angel.[12]
See also[edit]
Lesser sciatic notch
Greater sciatic notch
Additional images[edit]
Sciatic nerve.
Structures surrounding left hip-joint.
Nerves of the right lower extremity. Posterior view.
Sciatic nerve.
Sciatic nerve.
Sciatic nerve.
See also[edit]
This article uses anatomical terminology; for an overview, see Anatomical terminology.
Notes[edit]
Jump up ^ Namely the flexor hallicus longus, flexor digitorum longus, tibialis posterior and popliteus of the deep part of the compartment, and the gastrocnemius, soleus and plantaris of the superficial part of the compartment.
Jump up ^ Namely the tibialis anterior, extensor hallucis longus, extensor digitorum longus, and fibularis tertius (peroneus tertius) of the anterior compartment, and the Fibularis longus and brevis of the lateral compartment.
References[edit]
This article incorporates text in the public domain from the 20th edition of Gray's Anatomy (1918)
Jump up ^ "sciatic nerve (anatomy)". Britannica Online Encyclopedia. Retrieved 23 April 2012.
^ Jump up to: a b c d e Drake, Richard L.; Vogl, Wayne; Tibbitts, Adam W.M. Mitchell; illustrations by Richard; Richardson, Paul (2005). Gray's anatomy for students. Philadelphia: Elsevier/Churchill Livingstone. ISBN 978-0-8089-2306-0.
Jump up ^ "Sciatica - Topic Overview". WebMD. 21 July 2010. Retrieved 23 April 2012.
Jump up ^ "What is sciatica: What causes sciatica?". MedicalBug. 11 April 2012. Retrieved 23 April 2012.
^ Jump up to: a b Stiehl JB, Stewart WA (1998). "Late sciatic nerve entrapment following pelvic plate reconstruction in total hip arthroplasty". J Arthroplasty. 13 (5): 586–8. doi:10.1016/s0883-5403(98)90060-2. PMID 9726326.
Jump up ^ Alessandro Bistolfi; et al. (2011). "Operative Management of Sciatic Nerve Palsy due to Impingement on the Metal Cage after Total Hip Revision: Case Report". Case Rep Med. 2011: 830296. doi:10.1155/2011/830296. PMC 3163138  . PMID 21876701.
Jump up ^ Abitbol JJ, Gendron D, Laurin CA, Beaulieu MA (1990). "Gluteal nerve damage following total hip arthroplasty. A prospective analysis". J Arthroplasty. 5 (4): 319–22. doi:10.1016/s0883-5403(08)80090-3. PMID 2290087. is cited by Stiehl and Stewart for the 0.5-2.0% figure.
Jump up ^ James, William D.; Berger, Timothy G.; et al. (2006). Andrews' Diseases of the Skin: clinical Dermatology. Saunders Elsevier. ISBN 0-7216-2921-0.
Jump up ^ Sierra RJ, Beaule P, Zaltz I, Millis MB, Clohisy JC, Trousdale RT (2012). "Prevention of nerve injury after periacetabular osteotomy". Clin. Orthop. Relat. Res. 470 (8): 2209–19. doi:10.1007/s11999-012-2409-1. PMC 3392380  . PMID 22684336.
Jump up ^ Mobbs RJ, Teo C (2004). "Endoscopic-assisted sciatic nerve exploration". Minim Invasive Neurosurg. 47 (3): 178–80. doi:10.1055/s-2004-818488. PMID 15343436.
Jump up ^ Martin HD, Shears SA, Johnson JC, Smathers AM, Palmer IJ (2011). "The endoscopic treatment of sciatic nerve entrapment/deep gluteal syndrome". Arthroscopy. 27 (2): 172–81. doi:10.1016/j.arthro.2010.07.008. PMID 21071168.
Jump up ^ Goldberger, Moshe. "1: Not to Eat the Gid HaNasheh". The First Prohibitions. Retrieved 10 March 2014.
External links[edit]
Sciatic_nerve at the Duke University Health System's Orthopedics program
MedlinePlus Image 19503
pelvis at The Anatomy Lesson by Wesley Norman (Georgetown University) (pelvicnerves)
glutealregion at The Anatomy Lesson by Wesley Norman (Georgetown University) (glutealner)
Sciatica and the Sciatic Nerve
[hide]
v
t
e
Nerves of the lumbosacral plexus
Lumbar plexus
iliohypogastric
lateral cutaneous branch
anterior cutaneous branch
ilioinguinal
anterior scrotal ♂/labial ♀
genitofemoral
femoral branch
genital branch
Lateral cutaneous
patellar
obturator
anterior
cutaneous
posterior
accessory
femoral
anterior cutaneous branches
saphenous
(infrapatellar
medial crural cutaneous
sacral plexus
sciatic
common peroneal
lateral sural cutaneous
communicating branch
deep peroneal
lateral terminal branch
medial terminal branch
dorsal digital
superficial peroneal
medial dorsal cutaneous
intermediate dorsal cutaneous
dorsal digital
tibial
medial sural cutaneous
medial calcaneal
medial plantar (common plantar digital nerves
proper plantar digital)
lateral plantar (deep branch
superficial branch
common plantar digital
proper plantar digital)
sural
lateral dorsal cutaneous
lateral calcaneal
other
Muscular
superior gluteal
inferior gluteal
lateral rotator group (to quadratus femoris
to obturator internus
to the piriformis)
cutaneous: posterior cutaneous of thigh (inferior cluneal
perineal branches)
perforating cutaneous
coccygeal plexus
pudendal
inferior anal
perineal
deep
posterior scrotal ♂/labial ♀
dorsal of the penis ♂/clitoris ♀
anococcygeal
Related
cutaneous innervation of the lower limbs
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Gauhati High Court
From Wikipedia, the free encyclopedia
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Gauhati High Court
গুৱাহাটী উচ্চ ন্যায়ালয়
High Court Building
Established
5 April 1948
Country
India
Location
Principal Seat: Guwahati, Assam
Circuit Benches: Kohima, Aizawl & Itanagar
Composition method
Presidential with confirmation of Chief Justice of India and Governor of respective state.
Authorized by
Constitution of India
Decisions are appealed to
Supreme Court of India
Judge term length
mandatory retirement by age of 62
No. of positions
24 (17+7)
Website
www.ghconline.gov.in
Chief Justice
Currently
Ajit Singh
Since
5 March 2016
The Gauhati High Court (Assamese: গুৱাহাটী উচ্চ ন্যায়ালয়) was established on 1 March 1948 after the Government of India Act 1935 was passed. It was originally known as the High Court of Assam and Nagaland, but renamed as Gauhati High Court in 1971 by the North East Areas (Reorganisation) Act, 1971.
It has largest jurisdiction in terms of states, with its area covering the states of Assam, Arunachal Pradesh, Nagaland, and Mizoram.
Contents
[hide]
1 History
2 Principal Seat & Benches[1]
2.1 The Kohima Bench for Nagaland state
2.2 The Itanagar bench for Arunachal Pradesh state
2.3 The Aizawl bench for Mizoram state
3 Judges from the High Court currently serving in the Supreme Court of India
4 See also
5 References
6 External links
History[edit]
After Indian independence, the Assam Legislative Assembly adopted a resolution on 9 September 1947 that a High Court be established for the Province of Assam. In exercise of power conferred by the Government of India Act 1935, the Governor General of India on 1 March 1948 promulgated the Assam High Court Order, 1948, establishing the High Court of Assam. It was inaugurated on 5 April 1948 by H. J. Kania, the Chief Justice of India. Sir R.F. Lodge was sworn in as the first Chief Justice of the Assam High Court on the same day. The Assam High Court initially had its sittings at Shillong but shifted to Guwahati on 14 August 1948.
Later, when Nagaland state was created on 1 December 1963, the Assam High Court was renamed as the High Court of Assam and Nagaland. On re-organization of the northeastern region of India by the North Eastern Area (Re-organization) Act, 1971, a common High Court was established for the five northeastern states: Assam, Manipur, Meghalaya, Nagaland and Tripura and the two Union Territories: Arunachal Pradesh and Mizoram. It was again renamed as the Gauhati High Court.
After Meghalaya, Manipur and Tripura got its High Court, the Gauhati High Court ceased its jurisdiction in these three states.
Principal Seat & Benches[1][edit]
The principal seat of the Gauhati High Court is at Guwahati in Assam. The court has 3 outlying benches. These are:
The Kohima bench for Nagaland state (established on 1 December 1972)
The Aizawl bench for Mizoram state (established on 5 July 1990)
The Itanagar bench for Arunachal Pradesh state (established on 12 August 2000)
Former benches, now full-fledged high courts:
The Imphal bench (established on 21 January 1972) (Converted to a High Court in March 2013)
The Agartala bench established on 24 January 1972) (Converted to a High Court in March 2013)
The Shillong bench established on 4 September 1974)(Converted to a High Court in March 2013)
The Kohima Bench for Nagaland state[edit]
The Kohima Bench is located on the eastern slope of the Ministers’ Hill in the capital city of Nagaland, Kohima. The building where the Kohima Bench is, was earlier a Hostel which was renovated for the Kohima Bench. The inauguration of the Bench at the capital Kohima, was on 1 December 1972, by the Hon’ble Mr. Justice M.C.Pathak.
Permanent Judge for the State of Nagaland
Mr. Justice Lanusungkum Jamir (Portfolio Judge)[2]
Elevated as Additional Judge on 22 May 2013.
The Itanagar bench for Arunachal Pradesh state[edit]
The Permanent Bench at Itanagar was inaugurated on 12 August 2000 by Hon'ble Chief Justice of the Supreme Court of India, Dr. A.S. Anand at Naharlagun which is located about 13 km. from the capital town, Itanagar.
Permanent Judge for the State of Arunachal Pradesh
Pranoy Kumar Musahary (01/07/2008 - Till Date)retired now
The Aizawl bench for Mizoram state[edit]
The Aizawl Permanent Bench is situated at the capital city of Mizoram, Aizawl. On 5 July 1990, the Aizawl Permanent Bench of the Gauhati High Court was established and inaugurated by the then Chief Justice of India, Mr. Justice S.B.Mukherjee
Permanent Judge for the State of Mizoram
Mr. Justice M. R. Pathak (Portfolio Judge)[3]
Elevated as Additional Judge of the Gauhati High Court on 22 May 2013
Mr. Justice Michael Zothankhuma (Station Judge)[4]
Elevated as Additional Judge, Gauhati High Court on 7 January 2015
Judges from the High Court currently serving in the Supreme Court of India[edit]
Hon'ble Mr. Justice Ananga Kumar Patnaik(Former Chief Justice of Gauhati High Court)
Hon'ble Mr. Justice Jasti Chelameswar (Former Chief Justice of Gauhati High Court)
Hon'ble Mr. Justice Ranjan Gogoi (Former Judge, Gauhati High Court)
Hon'ble Mr. Justice Madan B. Lokur (Former Chief Justice of Gauhati High Court)
Hon'ble Mr. Justice A.K. Goel (Former Chief Justice of Gauhati High Court)
Hon'ble Mr. Justice Abhay Manohar Sapre (Former Chief Justice of Gauhati High Court)
Hon'ble Mr. Justice Amitava Roy (Former Judge, Gauhati High Court)
See also[edit]
Assam portal
High Courts of India
References[edit]
Jump up ^ http://www.ghconline.gov.in
Jump up ^ http://kohimahighcourt.gov.in/Judges%20profile.html
Jump up ^ http://ghcazlbench.nic.in/Profile.htm
Jump up ^ http://ghcazlbench.nic.in/Profile.htm
Jurisdiction and Seats of Indian High Courts
Judge strength in High Courts increased
External links[edit]
Gauhati High Court - Legal Directory
High Court website
[hide]
v
t
e
High courts of India
Allahabad High Court
Bombay High Court
Calcutta High Court
Chhattisgarh High Court
Delhi High Court
Gujarat High Court
Gauhati High Court
Himachal Pradesh High Court
Hyderabad High Court
Jammu and Kashmir High Court
Jharkhand High Court
Karnataka High Court
Kerala High Court
Madhya Pradesh High Court
Madras High Court
Manipur High Court
Meghalaya High Court
Odisha High Court
Patna High Court
Punjab and Haryana High Court
Rajasthan High Court
Sikkim High Court
Tripura High Court
Uttarakhand High Court
Retrieved from "https://en.wikipedia.org/w/index.php?title=Gauhati_High_Court&oldid=803749662"
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This page was last edited on 4 October 2017, at 11:24.
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