WordNet

regulate housing in; of certain areas of towns (同)district
any of the regions of the surface of the Earth loosely divided according to latitude or longitude (同)geographical zone
(anatomy) any encircling or beltlike structure (同)zona
a locally circumscribed place characterized by some distinctive features
an area or region distinguished from adjacent parts by a distinctive feature or characteristic
release or pull the trigger on; "Trigger a gun"
an act that sets in motion some course of events (同)induction, initiation
a device that activates or releases or causes something to happen
dividing an area into zones or sections reserved for different purposes such as residence and business and manufacturing etc
a sensory receptor that responds to chemical stimuli

PrepTutorEJDIC

(何らかの目的・特徴などによって他の地域と区別された)『地帯』,地域,地区(belt, area) / (気候によって地球を大別した)帯(たい) / 《米》(交通・郵便などの)同一料金区域;(郵便番号で分けた)郵便区 / (環状の)ベルト,輪,帯 / …‘を'地帯(地区)に分ける / (…の目的に)〈地域〉‘を'区画規制する《+名+as(for)+名》 / …‘を'帯で巻く,‘に'帯印をつける
(銃砲の)引き金 / 《話》敏しような,抜け目のない / 〈一連の事件・反応など〉‘を'起こす,誘発する《+off+名,+名+off》
(都市計画の)区画制,地区制

Wikipedia preview

出典(authority):フリー百科事典『ウィキペディア（Wikipedia）』「2015/06/24 07:15:54」(JST)

wiki en

The chemoreceptor trigger zone (CTZ) is an area of the medulla oblongata that receives inputs from blood-borne drugs or hormones, and communicates with other structures in the vomiting center to initiate vomiting. The CTZ is located within the area postrema, which is on the floor of the fourth ventricle and is outside of the blood–brain barrier.^[1] It is also part of the vomiting center itself.^[2]The neurotransmitters implicated in the control of nausea and vomiting include acetylcholine, dopamine, histamine (H-1 receptor), substance P (NK-1 receptor), and serotonin (5-HT3 receptor). There are also opioid receptors present, which may be involved in the mechanism by which opiates cause nausea and vomiting. The blood brain barrier is not as developed here, and drugs such as dopamine which can normally not enter the CNS may still stimulate the CTZ.^[3]

Evolutionary significance

The CTZ is in the medulla oblongata, which is phylogenetically the oldest part of the nervous system.^{[citation needed]} Early lifeforms developed a brainstem, or inner brain, and nothing more. This part of the brain is responsible for basic survival instincts and reactions, for example to make an organism turn its head and look where an auditory stimulus was heard. The brainstem is where the medulla is located, and therefore also the area postrema and the CTZ. Then later lifeforms developed another segment of the brain, which includes the limbic system. This area of the brain is responsible for producing emotion and emotional responses to external stimuli, and also is significantly involved in memory and reward systems. Evolutionarily, the cerebral cortex is the most recent development. This area of the brain is responsible for critical thinking and reasoning, and is actively involved in decision making. It has been discovered that a major cause of increased intelligence in species including humans is the increase in cortical neurons in the brain.^[4] The emetic response was selected for protective purposes, and serves as a safeguard against poisoning of the body. This response gets toxins and drugs out of the body by summoning control over motor neurons which stimulate muscles in the chest and thoracic diaphragm to expel contents from the stomach.

Chemoreception

Since the CTZ is located in the medulla oblongata, it therefore does not have a specific Blood–brain barrier.^[3] This means that large polar molecules, such as emetic toxins, can diffuse through to and reach the CTZ quite easily. This is because the medulla oblongata is located in the area of the brain, the most inferior portion, which does not have a robust and highly developed blood-brain barrier. Without this barrier, emetic drugs and toxins are free to interact with a receptor (biochemistry), or multiple receptors located in the CTZ. These receptors in the CTZ are called chemoreceptors because they interact with different types of chemicals which are usually referred to as neurotransmitters. These neurotransmitters implement their effects on the CTZ receptors by binding to them which sets off a chain of events which produces an action potential. Studies have shown that neurons in the CTZ increase their rate of firing when exposed to emetic substances.^[3] The CTZ has many different types of receptors, which are specific to different types of toxins or drugs that might be present in the bloodstream and thus that can affect the CTZ. Types of CTZ receptors include dopamine, serotonin, histamine, substance P, opioid, and acetylcholine receptors. It has been discovered that the cholinergic neurons are actually nicotinic.^[5] These receptors are meant to monitor the amount of associated neurotransmitter of these receptors in the blood. For instance, the CTZ has opioid receptors that monitor the level of opioids in the blood, and when the amount of opioids in the blood reach a certain level, the opioid receptors in the CTZ will signal to the rest of the vomiting center to initiate vomiting. This is because the CTZ sends the "vomit" command through action potentials, and these specific action potentials that trigger emesis are only produced when a certain amount of opioids bind to a certain amount of opioid receptors in the CTZ. Neurons in the CTZ, and area postrema in general, actually have two types of receptors: those at the surface of the neuron and those that are located deeper down in the dendrites.^[5] The receptors on the surface of the neuron are chemoreceptors that are activated from direct contact of emetic substances in the blood, whereas the receptors that are deeper down on the dendrites are receptors that are activated in response to the activated chemoreceptors on the surface.^[5]

Communication

The vomiting center of the brain refers to the groups of loosely organized neurons in the medulla that include the CTZ within the area postrema and the nucleus tractus solitarii.^[2] One of the ways the chemoreceptor trigger zone implements its effects on the vomiting center is by activation of the opioid mu receptors and delta receptors.^[6] The activation of these opioid receptors in the CTZ are especially important for patients who take opioid based pain medications on a regular basis. However, opioids do not play a role in communication to the vomiting center of the brain, they only induce communication.^[6] Dopamine and serotonin have been found to play the biggest role in communication from the CTZ to the remainder of the vomiting center, as well as histamine.^[6] Chemoreceptors in the CTZ relay information about there being emetic agents in the blood to the adjacent nucleus tractus solitarii (NTS).^[7] The relaying happens by the initiation of an action potential, which is caused by the chemoreceptor causing a change in electric potential in the neuron it is embedded in, which then subsequently causes an action potential. This happens constantly, so the chemoreceptors in the CTZ are continually sending information about how much emetic agents are in the blood, even when emesis is not signaled for. The NTS is organized into subnuclei that direct many different functions relating to swallowing, gastric sensation, laryngeal and pharyngeal sensation, baroreceptor function, and respiration.^[7] The NTS directs signals about these functions to a central pattern generator (CPG). This CPG actually coordinates the sequences of physical movements during emesis. The main neurotransmitters involved in communication between the CTZ and remaining vomiting center are serotonin, dopamine, histamine, and endogenous opioids which include endorphins, enkephalins, dynorphin.

The CTZ communicates with the other parts of the vomiting center through neurons that contain 5-HT₃, D₂, H₁ and H₂ receptors.^[6] It has been seen that intraventricular administration of histamine in dogs causes an emetic response.^[8] This shows that histamine plays a significant role in signaling for emetic action in the CTZ. Some classes of molecules have been shown to inhibit the emetic response due to histamine, these include mepyramine, burimamide and metiamide.^[8]

Phosphodiesterases

Recent studies have found that phosphodiesterase 4 (PDE4) inhibitors, such as Rolipram, cause emesis as one of their side effects.^[9] It has been found that these PDE4 isoforms are expressed in the CTZ and in the brainstem in general.^[9] The mRNA products from genes that code for these PDE4 isoforms are plentiful in the CTZ, and not only located in CTZ neurons, but also in glial cells and blood vessels associated with the CTZ neurons.^[9] PDE4 mRNAs are transcribed more in the area postrema and the CTZ than anywhere else in the brainstem.^[9] The PDE4 degrades the phosphodiester bonds in the second messenger molecule cyclic adenosine monophosphate (cAMP), which is one of the ways the brain relays information. By modifying cAMP signaling in the CTZ, it is thought that this could mediate the emetic effects of PDE4 inhibitors in the CTZ.^[9]

H-Channels

Most of the neurons located in the CTZ express hyperpolarization-activated cation channels (H-channels).^[10] Since the neurons in the CTZ convey information relating to emesis to the other parts of the vomiting center, it was thought that these H-channels might play a role in nausea and the emetic response. Recently, evidence of this notion that H-channels in CTZ neurons play a role in emesis has come to light. It has been found that ZD7288, which is a H-channel inhibitor, inhibited the acquisition of conditioned taste aversion (CTA) in rats and reduced apomorphine-induced c-Fos expression in the area postrema where the CTZ is located.^[10] This suggests that the neurons that express H-channels in the CTZ and area postrema are involved in nausea and the emetic response.^[10]

The vomiting center of the brain

This integrates the emetic response. This is the area in which "a final decision is made" about whether to evoke an emetic response or not. This decision is based heavily on the information which the CTZ relays to the rest of the vomiting center, but also the chemoreceptors in the GI tract, the information sent to the vomiting center by the vestibular system, and higher order centers located in the cortex.^[6] The vomiting center is not a discrete or specific place in the brain, but rather an area consisting of many nuclei, axons, and receptors that together cause the physical changes necessary to induce vomiting.^[6] Also, emesis can occur by direct neural stimulation of the vomiting center.^[11]

Damage to the CTZ

Damage to the CTZ can either benefit or severely hurt someone. Damage can come via stroke, physical injury, or over-excitation resulting in neuron death. Once the damage has occurred, the effects can cause the emetic response to disappear, or cause the emetic response to heighten, in some cases causing intractable vomiting that leave patients in severe distress. In cases such as these, if the damage is severe enough, little can be done to inhibit an intractable vomiting response because the chemoreceptors in the CTZ are physically damaged or hindered in some way. Recently, it has been discovered that physical changes in the area postrema and CTZ do in fact cause emesis or inhibit it.^[12] Specifically, compression of blood vessels which are physically located near in or around the CTZ, and that result in physical compression of the area postrema as a whole, have been found to be the cause of chronic medically intractable emesis and weight loss.^[12] Surgical microvascular decompression resulted in postoperative and long-term resolution of emesis.^[12]

Antiemetic medications

Antiemetic medications often target the CTZ to completely inhibit or greatly reduce vomiting. Most of these work by not allowing certain blood-borne drugs (usually pain killers or stimulants) to bind to their respective receptors located in the CTZ. The antiemetic medications can block the binding site on a chemoreceptor in the CTZ, so that the emetic agent cannot bind to it to cause its emetic effects.^[6] Another way that antiemetic medications can work is by binding to a chemoreceptor in the CTZ, but instead of initiate vomiting, the medication can cause the receptors to send signals to the other parts of the vomiting center that inhibit emesis.^[6] Also, some anti-emetic medications work by lowering the amount of dopamine levels in the brain, which in turn effects how much dopamine comes in contact with dopamine receptors in the CTZ. Other antiemetic medications work similarly by lowering a different substance in the brain that is known to interact with chemoreceptors in the CTZ that cause emesis. Some examples of antiemetic medications include Dolasetron, Aprepitant, Cyclizine, and Hyoscine.

Antiemetic drugs coupled with pain relieving medications

Oftentimes, doctors will "pre-treat" patients who he/she believes might exhibit emetic responses due to drugs they prescribe them. Usually pain relieving drugs such as opioids are co-prescribed with anti-emetic drugs to stop the emetic response due to the pain reliever before it can even mediate its effects on the CTZ. This way, the patient does not have to worry about the doctors prescription to treat their pain causing them to be in severe discomfort via vomiting.

Chemotherapy

Chemotherapy is a big cause of emesis, and often can cause severe and frequent emetic responses. This is because chemotherapy agents circulating in the blood activate the CTZ in such a way as to cause emesis.^[13] Patients receiving chemotherapy are often prescribed antiemetic medications.

References

^ editors, Ansgar M. Brambrink, Jeffrey R. Kirsch, (2012). Essentials of neurosurgical anesthesia & critical care : strategies for prevention, early detection, and successful management of perioperative complications (2012 ed.). New York: Springer. p. 716. ISBN 0387095616. Retrieved 16 August 2014.
^ ^a ^b Pierre, S.; Whelan, R. (11 August 2012). "Nausea and vomiting after surgery". Continuing Education in Anaesthesia, Critical Care & Pain 13 (1): 28–32. doi:10.1093/bjaceaccp/mks046.
^ ^a ^b ^c Miller AD, Leslie RA. The area postrema and vomiting. Frontiers in Neuroendocrinology. 1994 Dec;15(4):301-20. PMID 7895890
^ Roth, G. and Dicke, U. (2005). Evolution of the brain and intelligence. Trends in Cognitive Sciences. 9(5): 250-257.
^ ^a ^b ^c Hori,N. et al. (2000). Brainstem slice studies of receptor activation in the mouse area postrema. Society for Neuroscience Abstracts. 26(1-2) Abstract No.-716.13.
^ ^a ^b ^c ^d ^e ^f ^g ^h Porreca, F., & Ossipov, M. H. (2009). Nausea and Vomiting Side Effects with Opioid Analgesics during Treatment of Chronic Pain: Mechanisms, Implications, and Management Options. Pain Medicine, 10(4), 654-662. doi: 10.1111/j.1526-4637.2009.00583.x
^ ^a ^b Hornby, P. J. (2001). Central Neurocircuitry Associated With Emesis. American Journal of Medicine. 111(8a), 106S-112S.
^ ^a ^b Bhargava, K.P. (1968). Role Of Chemoreceptor Trigger Zone In Histamine-induced Emesis. British Journal of Pharmacology. 34(3): 508-&
^ ^a ^b ^c ^d ^e Mori, F. et al. (2010). The human area postrema and other nuclei related to the emetic reflex express cAMP phosphodiesterases 4B and 4D. Journal of Chemical Neuroanatomy. 40(1): 36-42.
^ ^a ^b ^c Shinpo, K. et al. (2012). The role of area postrema neurons expressing H-channels in the induction mechanism of nausea and vomiting. Physiology and Behavior. 107(1): 98-103
^ Encarnacion, H. J. et al. (2009). Vomiting. Compendium-Continuing Education for Veterinarians. 31(3): 122-+.
^ ^a ^b ^c Mortazavi, M. M. (2010). Chronic emesis due to compression of the area postrema by the posterior inferior cerebellar artery resolution following microvascular decompression. Journal of Neurosurgery-Pediatrics. 6(6): 583-585
^ Edwards, C.M. (1988). Chemotherapy induced emesis -mechanisms and treatment: a review. Journal of the Royal Society of Medicine. 81(11): 658-662.

UpToDate Contents

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1. 悪心および嘔吐を伴う成人に対するアプローチ approach to the adult with nausea and vomiting
2. 化学療法誘発性悪心および嘔吐の病態生理および予測 pathophysiology and prediction of chemotherapy induced nausea and vomiting
3. オピオイド系薬剤を用いた癌疼痛のマネージメント：副作用の予防およびマネージメント cancer pain management with opioids prevention and management of side effects
4. 緩和ケア：人生最後の数時間 palliative care the last hours and days of life
5. 悪性腫瘍関連胃不全麻痺：病態生理およびマネージメント malignancy associated gastroparesis pathophysiology and management

English Journal

Lessons learned from hospice care.

Martin CM.Author information Greensboro, North Carolina.AbstractPharmaceutical care of the hospice patient offers unique challenges in the management of pain and other symptoms. Lessons learned in providing hospice care can be used in the care of nonterminal patients as well to optimize patient-specific care, regardless of care setting or life expectancy.
The Consultant pharmacist : the journal of the American Society of Consultant Pharmacists.Consult Pharm.2013 Oct;28(10):605-12. doi: 10.4140/TCP.n.2013.605.
Pharmaceutical care of the hospice patient offers unique challenges in the management of pain and other symptoms. Lessons learned in providing hospice care can be used in the care of nonterminal patients as well to optimize patient-specific care, regardless of care setting or life expectancy.
PMID 24129218

Cyclic vomiting associated with excessive dopamine in Riley-day syndrome.

Norcliffe-Kaufmann LJ, Axelrod FB, Kaufmann H.Author information Department of Physiology and Neuroscience, New York University School of Medicine, New York, NY, USA. Horacio.Kaufmann@nyumc.orgAbstractGOALS: To analyze the neurochemical profile during the recurrent attacks of nausea and vomiting in patients with Riley-day syndrome.
Journal of clinical gastroenterology.J Clin Gastroenterol.2013 Feb;47(2):136-8. doi: 10.1097/MCG.0b013e3182582cbf.
GOALS: To analyze the neurochemical profile during the recurrent attacks of nausea and vomiting in patients with Riley-day syndrome.BACKGROUND: One of the most disabling features of patients with Riley-day syndrome are recurrent attacks of severe nausea/retching/vomiting accompanied by hypertension,
PMID 22739220

Long-term use of intrathecal droperidol as an excellent antiemetic in nonmalignant pain--a retrospective study.

Ahmad-Sabry MH, Shareghi G.Author information Alexandria Faculty of Medicine, Alexandria University, Alexandria, Egypt. Mohammad_hazem@yahoo.comAbstractOver the past five years our pain practice encountered eight patients (5 female, 3 male) with chronic non-malignant pain syndromes, in whom any meaningful pain reduction via opioid analgesics (either by oral or systemic and/or intraspinal route) had resulted in profound nausea and/or vomiting despite generous use of available and/or affordable anti-emetics. After obtaining proper consents, small, incremental doses of intrathecal droperidol were added to these patients having implanted intrathecal narcotic drug delivery system. Significant reduction of nausea and vomiting without any side effects from droperidol was obtained while adequate pain reduction is achieved.
Middle East journal of anesthesiology.Middle East J Anesthesiol.2012 Oct;21(6):857-62.
Over the past five years our pain practice encountered eight patients (5 female, 3 male) with chronic non-malignant pain syndromes, in whom any meaningful pain reduction via opioid analgesics (either by oral or systemic and/or intraspinal route) had resulted in profound nausea and/or vomiting despit
PMID 23634568

Japanese Journal

悪心,嘔吐 (特集研修・当直医必携シリーズ(3)消化器救急) -- (症状からみた消化器救急診療)

前田彰,坂本照夫
救急医学 32(5), 528-530, 2008-05
NAID 40016050721

光刺激による摂食行動の制御に関するラット最後野構成細胞の形態学的研究

玉田善堂,諏訪文彦,竹村明道,安田久理人
歯科医学 67(3_4), 279-284, 2004-12-25
… )の相互関係について明らかにすることが,本研究の目的である.嘔吐は生体防御反応として,摂食行動の一部と考えられていることから,嘔吐と摂食行動の研究に着手した.嘔吐誘発のchemoreceptor trigger zoneは延髄の最後野およびその近傍の領域であると考えられている.最後野は,神経細胞,アストロサイトおよび有窓性内皮の洞様毛細血管の要素から構成されていることが明らかにされ …
NAID 110001724745

Related Pictures

★リンクテーブル★

リンク元	「嘔吐」「化学受容器引金帯」「CTZ」「化学受容器誘発帯」
関連記事	「zone」「trigger」

「嘔吐」

　　[★]

英: vomiting, emesis
ラ: vomitus
関: 悪心、嘔気 nausea、悪心・嘔吐 nausea and vomiting

概念

胃の内容物をはき出す現象。
胃または腸内容が食道を経て口腔より吐出される現象。

嘔吐中枢

延髄網様体中の迷走神経背側核付近
第4脳室底の化学受容体誘発帯 chemoreceptor trigger zone CTZ

嘔吐中枢の近傍に存在するもの

呼吸中枢、血管運動中枢、消化管運動中枢、唾液分泌中枢、前庭神経核

随伴症状

発汗、唾液分泌、顔面蒼白、脈拍微弱、徐脈、頻脈、血圧の動揺、めまいなど

生理的変化：バソプレシン分泌刺激

症状の出現形式と原因の所在

突然の嘔吐：中枢性
消化器症状を伴う：末梢性

噴水状、噴射状嘔吐

projectile vomiting is where stomach contents 'shoot out' (like a fountain) to a distance sometimes many feet away.

乳児の肥厚性幽門狭窄症や水頭症・中枢神経系の異常
幼児期以降、脳腫瘍などによる頭蓋内圧亢進

嘔吐に関わる経路

IMD.351

1. 嘔吐中枢(延髄網様体背側神経背側核近傍)への直接刺激(脳圧亢進、循環障害)
2. 化学受容体誘発帯(CTZ; 第四脳室底)への刺激(代謝異常や中毒による化学物質の作用)　→　1.
3. 大脳皮質(中枢神経など高位中枢)からの入力　→　1.
4. 求心性迷走神経や交感神経を介する入力　→　1.

原因

中枢性刺激	化学受容器引金帯刺激	薬物	アポモルヒネ、モルヒネ、ジギタリス、抗菌薬、抗癌薬、降圧薬、アミノフイリン、コルヒチン、アルコール
		毒物	重金属、ガス
		放射線	各種癌治療後
		感染症	細菌毒素
		内分泌疾患	肝性脳症、糖尿病性ケトアシドーシス/高血糖高浸透圧症候群、尿毒症、妊娠悪阻、妊娠高血圧症候群
		代謝疾患	甲状腺クリーゼ、副腎不全、Addison病
	直接刺激	脳圧亢進	頭部外傷、脳腫瘍、脳出血、くも膜下出血、髄膜炎、脳への放射線療法後
		脳循環障害	ショック、低酸素脳症、脳梗塞、片頭痛、脳炎、髄膜炎
		上位中枢刺激	神経性食思不振症、不快感、てんかん、ヒステリー、抑うつ状態、うつ病、過度の嫌悪感、不快感、拘禁反応による恐怖、ストレス、視覚・嗅覚・味覚的刺激
末梢性刺激	消化管疾患	舌咽頭疾患	アデノイド、咽頭炎
		食道疾患	胃食道逆流症、食道裂孔ヘルニア、食道癌
		胃腸疾患	急性胃炎、急性胃十二指腸粘膜病変、急性腸炎、急性虫垂炎、消化性潰瘍、食中毒、消化管腫瘍、寄生虫、食中毒、Mallory-Weiss症候群
		消化管通過障害	腸閉塞、胃幽門部狭窄、輸入脚症候群
		腹膜疾患	腹膜炎
		胆膵疾患	急性胆嚢炎、急性胆管炎、急性膵炎、膵癌、胆管癌
		肝疾患	急性肝炎
	循環器疾患		うっ血性心不全、狭心症、急性心筋梗塞
	泌尿器科疾患		尿路結石、腎結石、急性腎炎、腎盂腎炎、腎不全
	耳鼻咽喉科疾患		中耳炎、Meniere病、乗り物酔い
	眼科疾患		緑内障
	呼吸器科疾患		肺結核、胸膜炎、肺癌、咳嗽発作
	婦人科疾患		子宮付属器炎、月経前症候群、更年期障害
	脊髄疾患		脊髄癆、多発性硬化症
	膠原病		結節性多発動脈炎、強皮症、側頭動脈炎

小児科で遭遇する嘔吐の原因

	新生児	乳児	幼児～学童
消化器疾患以外で見・落とさないよう注意する疾患	敗血症・髄膜炎・水頭症・脳奇形・尿路感染症	髄膜炎・脳炎・脳症・虐待児・尿路感染症・呼吸器感染症・心疾患・薬物中毒・誤嚥	脳炎・脳症・脳腫瘍・肺炎・中耳炎・頭部外傷・薬物中毒・心筋炎・不整脈
よくある消化器疾患	溢乳・空気嚥下・哺乳過誤・初期嘔吐・胃食道逆流現象・胃腸軸捻転・腸管感染症・壊死性腸炎	食事過誤・空気嚥下・便秘・腸管感染症・幽門狭窄症・腸重積症・胃食道逆流現象・胃長軸捻転・食事アレルギー	腸管感染症・急性虫垂炎・肝・腹部外傷・肝炎・胆嚢炎・膵炎・腹部外傷・食事アレルギー・好酸球性胃腸症
主な代謝性疾患	先天性副腎過形成・ガラク卜ース血症	先天性副腎過形成・Reye症候群	アセトン血性嘔吐症・ケトン性低血糖症・糖尿病性ケトアシドーシス・Reye症候群
その他			起立性調節障害・神経性食思不振症
外科的疾患	食道閉鎖・狭窄症・胃軸捻転・十二指腸閉鎖・狭窄症・腸回転異常・捻転・小腸閉鎖症・Hirschsprung病・胎便性イレウス・稀に腸重積・肥厚性幽門狭窄・特発性腸管偽性閉鎖症	肥厚性幽門狭窄症・腸重積・腸回転異常・捻転・Hirschsprung病・虫垂炎	虫垂炎・腸重積・腸回転異常・捻転・上腸間膜動脈症候群・腫瘍・嚢胞

「化学受容器引金帯」

　　[★]

英: chemoreceptor trigger zone, CTZ
関: 嘔吐、嘔吐中枢、催吐薬、鎮吐薬

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化学受容器引き金帯 : 約 11,900 件
化学受容器引金帯 : 約 11,100 件
化学受容器誘発帯 : 1 件
化学受容器引き金領域 : 0 件
化学受容器引金領域 : 2 件
化学受容器誘発領域 : 0 件
化学受容体引き金帯 : 約 11,900 件
化学受容体引金帯 : 約 42 件
化学受容体誘発帯 : 約 21 件
化学受容体引き金領域 : 
化学受容体引金領域 : 2 件
化学受容体誘発領域 : 2 件

化学受容器引き金帯 CTZ : 91 件
化学受容器引金帯 CTZ : 99 件
化学受容器誘発帯 CTZ : 1 件
化学受容器引き金領域 CTZ : 0 件
化学受容器引金領域 CTZ : 2 件
化学受容器誘発領域 CTZ : 0 件
化学受容体引き金帯 CTZ : 28 件
化学受容体引金帯 CTZ : 41 件
化学受容体誘発帯 CTZ : 約 15 件
化学受容体引き金領域 CTZ : 
化学受容体引金領域 CTZ : 2 件
化学受容体誘発領域 CTZ : 1 件