痛覚、侵害受容

関: nociceptive、pain sensation

WordNet

caused by or in response to pain; "a nociceptive spinal reflex"

Wikipedia preview

出典(authority):フリー百科事典『ウィキペディア（Wikipedia）』「2017/07/04 11:04:13」(JST)

wiki en

Nociception (also nocioception or nociperception, from Latin nocere 'to harm or hurt') is the sensory nervous system's response to certain harmful or potentially harmful stimuli. In nociception, intense chemical (e.g., chili powder in the eyes), mechanical (e.g., cutting, crushing), or thermal (heat and cold) stimulation of sensory nerve cells called nociceptors produces a signal that travels along a chain of nerve fibers via the spinal cord to the brain.^[1] Nociception triggers a variety of physiological and behavioral responses and usually results in a subjective experience of pain in sentient beings.^[2]

Detection of noxious stimuli

Potentially damaging mechanical, thermal, and chemical stimuli are detected by nerve endings called nociceptors, which are found in the skin, on internal surfaces such as the periosteum, joint surfaces, and in some internal organs. The concentration of nociceptors varies throughout the body; they are found in greater numbers in the skin than in deep internal surfaces. Some nociceptors are unspecialized free nerve endings that have their cell bodies outside the spinal column in the dorsal root ganglia.^[3] Nociceptors are categorized according to the axons which travel from the receptors to the spinal cord or brain.

Nociceptors have a certain threshold; that is, they require a minimum intensity of stimulation before they trigger a signal. Once this threshold is reached a signal is passed along the axon of the neuron into the spinal cord.

Nociceptive threshold testing deliberately applies a noxious stimulus to a human or animal subject in order to study pain. In animals, the technique is often used to study the efficacy of analgesic drugs and to establish dosing levels and period of effect. After establishing a baseline, the drug under test is given and the elevation in threshold recorded at specified time points. When the drug wears off, the threshold should return to the baseline (pre-treatment) value.

In some conditions, excitation of pain fibers becomes greater as the pain stimulus continues, leading to a condition called hyperalgesia.

Factors

The gate control theory of pain, proposed by Patrick David Wall and Ronald Melzack, postulates that nociception (pain) is "gated" by non-nociception stimuli such as vibration. Thus, rubbing a bumped knee seems to relieve pain by preventing its transmission to the brain. Pain is also "gated" by signals that descend from the brain to the spinal cord to suppress (and in other cases enhance) incoming nociception (pain) information.^{[citation needed]}

Nociception can also cause generalized autonomic responses before or without reaching consciousness to cause pallor, diaphoresis, tachycardia, hypertension, lightheadedness, nausea and fainting.^[4]

System overview

This diagram linearly (unless otherwise mentioned) tracks the projections of all known structures that allow for pain, proprioception, thermoception, and chemoception to their relevant endpoints in the human brain. Having trouble viewing? Click enlarge.

This overview discusses proprioception, thermoception, chemoception and nociception as they are all integrally connected.

Mechanical

Proprioception is determined by using standard mechanoreceptors (especially ruffini corpuscles (stretch) and transient receptor potential (TRP) channels). Proprioception is completely covered within the somatosensory system as the brain processes them together.

Thermoception refers to stimuli of moderate temperatures (~24-28C), as anything beyond that range is considered pain and moderated by nociceptors. TRP and potassium channels [TRPM (1-8), TRPV (1-6), TRAAK, and TREK] each respond to different temperatures (among other stimuli) which create action potentials in nerves which join the mechano (touch) system in the posterolateral tract. Thermoception, like proprioception, is then covered by the somatosensory system.^[5]^[6]^[7]^[8]^[9]

TRP channels that detect noxious stimuli (mechanical, thermal, and chemical pain) relay that info to nociceptors that generate an action potential. Mechanical TRP channels react to depression of their cells (like touch), thermal TRP change shape in different temperatures, and chemical TRP act like taste buds, signalling if their receptors bond to certain elements/chemicals.

Neural

Ab are the fastest, Aδ fibers are second, and C are slowest at 1/10th (2 m/s:20 m/s) Ao fiber’s speed. A fibers signal initial pain while C fibers signal deep, lasting pain. These fibers synapse on different spinal laminae (1-5).

Laminae 3-5 make up nucleus proprius in spinal grey matter.

Lamina 2 makes up substantia gelatinosa of Rolando, unmyelinated spinal grey matter. Substantia receives input from nucleus proprius and conveys intense, poorly localized pain.

Lamina 1 primarily project to the parabrachial area and periaqueductal grey, which begins the suppression of pain via neural and hormonal inhibition. Lamina 1 receive input from thermoreceptors via the posterolateral tract. Marginal nucleus of the spinal cord are the only unsuppressible pain signals.

The parabrachial area integrates taste and pain info then relays it. Parabrachial checks if the pain is being received in normal temperatures and if the gustatory system is active; if both are so the pain is assumed to be due to poison.

Ao fibers synapse on laminae 1 and 5 while Ab synapses on 1, 3, 5, and C. C fibers exclusively synapse on lamina 2.^[10]^[11]

The amygdala and hippocampus create and encode the memory and emotion due to pain stimuli.

The hypothalamus signals for the release of hormones that make pain suppression more effective, some of these include sex hormones.

Periaqueductal grey (with hypothalamic hormone aid) hormonally signals reticular formation’s raphe nuclei to produce serotonin that inhibits laminae pain nuclei.^[12]

Lateral spinothalamic tract aids in localization of pain.

Spinoreticular and spinotectal tracts are merely relay tracts to the thalamus that aid in the perception of pain and alertness towards it. Fibers cross over (left becomes right) via the spinal anterior white commissure.

Lateral lemniscus is the first point of integration of sound and pain information.^[13]

Inferior colliculus (IC) aids in sound orienting to pain stimuli.^[14]

Superior colliculus receives IC’s input, integrates visual orienting info, and uses the balance topographical map to orient the body to the pain stimuli.^[15]^[16]

Inferior cerebellar peduncle integrates proprioceptive info and outputs to the vestibulocerebellum. The peduncle is not part of the lateral-spinothalamic-tract-pathway; the medulla receives the info and passes it onto the peduncle from elsewhere (see somatosensory system).

The thalamus is where pain is thought to be brought into perception; it also aids in pain suppression and modulation, acting like a bouncer allowing certain intensities through to the cerebrum and rejecting others.^[17]

The somatosensory cortex decodes nociceptor info to determine the exact location of pain and is where proprioception is brought into consciousness; inferior cerebellar peduncle is all unconscious proprioception.

Insula judges the intensity of the pain and provides the ability to imagine pain.^[18]^[19]

Cingulate cortex is presumed to be the memory hub for pain.^[20]

In non-mammalian animals

Nociception has been documented in non-mammalian animals, including fish^[21] and a wide range of invertebrates,^[22] including leeches,^[23] nematode worms,^[24] sea slugs,^[25] and fruit flies.^[26] As in mammals, nociceptive neurons in these species are typically characterized by responding preferentially to high temperature (40° Celsius or more), low pH, capsaicin, and tissue damage.

History of term

The term "nociception" was coined by Charles Scott Sherrington to distinguish the physiological process (nervous activity) from pain (a subjective experience).^[27] It is derived from the Latin verb "nocēre", which means "to harm".

References

^ Portenoy, Russell K.; Brennan, Michael J. (1994). "Chronic Pain Management". In Good, David C.; Couch, James R. Handbook of Neurorehabilitation. Informa Healthcare. ISBN 0-8247-8822-2.
^ "Assessing Pain and Distress: A Veterinary Behaviorist's Perspective by Kathryn Bayne". Definition of Pain and Distress and Reporting Requirements for Laboratory Animals. Proceedings of the Workshop Held June 22, 2000. 2000.
^ Purves, D. (2001). "Nociceptors". In Sunderland, MA. Neuroscience. Sinauer Associates.
^ Feinstein, B.; Langton, J.; Jameson, R.; Schiller, F. (1954). "Experiments on pain referred from deep somatic tissues". J Bone Joint Surg. 36–A (5): 981–97. PMID 13211692. Retrieved 2007-01-06. ^{[permanent dead link]}
^ Tillotson, Joanne. McCann, Stephanie. Kaplan’s Medical Flashcards. Apr. 02. 2013.
^ Albertine, Kurt. Barron’s Anatomy Flash Cards
^ Hofmann, Thomas, and Michael Schaefer. "Subunit Composition of Mammalian Transient Receptor Potential Channels in Living Cells." PNAS. 21 Mar. 2002. Web. 28 Mar. 2016.
^ Noel, Jacques, and Katharina Zimmermann. "The Mechano‐activated K Channels TRAAK and TREK‐1 Control Both Warm and Cold Perception." EMBO Press. 11 Feb. 2009. Web. 28 Mar. 2016.
^ Scholz, Joachim, and Clifford J. Woolf. "Can We Conquer Pain?" Nature Neuroscience. 28 Oct. 2002. Web. 28 Mar. 2016.
^ Braz, Joao M., and Mohammed A. Nassar. "Parallel “Pain” Pathways Arise from Subpopulations of Primary Afferent Nociceptor." Science Direct. 15 Sept. 2005. Web. 28 Mar. 2016.
^ Brown, A. G. "Organization in the Spinal Cord: The Anatomy and Physiology of Identified Neurones." Google Books. Springer, 06 Dec. 2012. Web. 28 Mar. 2016.
^ Van Den Pol, Anthony D. "Hypothalamic Hypocretin (Orexin): Robust Innervation of the Spinal Cord." JNeurosci. 15 Apr. 1999. Web. 28 Mar. 2016.
^ Bajo, Victoria M., and Miguel A. Merchan. "Topographic Organization of the Dorsal Nucleus of the Lateral Lemniscus in the Cat." Wiley Online Library. 10 May 1999. Web. 27 Mar. 2016.
^ Oliver, Douglas M. "Neuronal Organization in the Inferior Colliculus." Springer. 2005. Web. 27 Mar. 2016.
^ Corneil, Brian D., and Etienne Olivier. "Neck Muscle Responses to Stimulation of Monkey Superior Colliculus. I. Topography and Manipulation of Stimulation Parameters." ARTICLES. 01 Oct. 2002. Web. 28 Mar. 2016.
^ May, Paul J. "The Mammalian Superior Colliculus: Laminar Structure and Connections." Science Direct. 2006. Web. 28 Mar. 2016.
^ Benevento, Louis A., and Gregg P. Strandage. "The Organization of Projections of the Retinorecipient and Nonretinorecipient Nuclei of the Pretectal Complex and Layers of the Superior Colliculus to the Lateral Pulvinar and Medial Pulvinar in the Macaque Monkey." Wiley Online Library. 01 Jul. 1983. Web. 27 Mar. 2016.
^ Sawamoto, Nobukatsu, and Manabu Honda. "Expectation of Pain Enhances Responses to Nonpainful Somatosensory Stimulation in the Anterior Cingulate Cortex and Parietal Operculum/Posterior Insula: An Event-Related Functional Magnetic Resonance Imaging Study." JNeurosci. 01 Oct. 2000. Web. 28 Mar. 2016.
^ Menon, Vinod, and Lucina Q. Uddin. "Saliency, Switching, Attention and Control: A Network Model of Insula." Springer. 29 May 2010. Web. 28 Mar. 2016.
^ Shackman, Alexander J., and Tim V. Salomons. "The Integration of Negative Affect, Pain and Cognitive Control in the Cingulate Cortex." Nature.com. Nature Publishing Group, Mar. 2011. Web. 28 Mar. 2016.
^ Sneddon, L. U.; Braithwaite, V. A.; Gentle, M. J. (2003). "Do fishes have nociceptors? Evidence for the evolution of a vertebrate sensory system". Proceedings of the Royal Society B. 270 (1520): 1115–1121. PMC 1691351 . PMID 12816648. doi:10.1098/rspb.2003.2349.
^ Jane A. Smith (1991). "A Question of Pain in Invertebrates". Institute for Laboratory Animals Journal. 33 (1–2).
^ Pastor, J.; Soria, B.; Belmonte, C. (1996). "Properties of the nociceptive neurons of the leech segmental ganglion". Journal of Neurophysiology. 75 (6): 2268–2279. PMID 8793740.
^ Wittenburg, N.; Baumeister, R. (1999). "Thermal avoidance in Caenorhabditis elegans: an approach to the study of nociception". PNAS. 96 (18): 10477–10482. doi:10.1073/pnas.96.18.10477.
^ Illich, P. A.; Walters, E. T. (1997). "Mechanosensory neurons innervating Aplysia siphon encode noxious stimuli and display nociceptive sensitization". Journal of Neuroscience. 17 (1): 459–469. PMID 8987770.
^ Tracey, J.; Daniel, W.; Wilson, R. I.; Laurent, G.; Benzer, S. (2003). "painless, a Drosophila gene essential for nociception". Cell. 113 (2): 261–273. PMID 12705873. doi:10.1016/S0092-8674(03)00272-1.
^ Sherrington, C. (1906). The Integrative Action of the Nervous System. Oxford: Oxford University Press.

UpToDate Contents

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English Journal

Negative cerebral blood volume fMRI response coupled with Ca(2+)-dependent brain activity in a dopaminergic road map of nociception.

Hsu YH1, Chang C1, Chen CC2.Author information 1Institute of Pharmacology, School of Medicine, National Yang-Ming University, Taipei, Taiwan; Institute of Biomedical Sciences, Academic Sinica, Taipei, Taiwan.2Institute of Biomedical Sciences, Academic Sinica, Taipei, Taiwan. Electronic address: ccchentw@ibms.sinica.edu.tw.AbstractDecreased cerebral blood volume/flow (CBV/CBF) contributes to negative blood-oxygen-level-dependent (BOLD) functional MRI (fMRI) signals. But it is still strongly debated whether these negative BOLD or CBV/CBF signals are indicative of decreased or increased neuronal activity. The fidelity of Ca(2+) signals in reflecting neuronal excitation is well documented. However, the roles of Ca(2+) signals and Ca(2+)-dependent activity in negative fMRI signals have never been explored; an understanding of this is essential to unraveling the underlying mechanisms and correctly interpreting the hemodynamic response of interest. The present study utilized a nociception-induced negative CBV fMRI response as a model. Ca(2+) signals were investigated in vivo using Mn(2+)-enhanced MRI (MEMRI), and the downstream Ca(2+)-dependent signaling was investigated using phosphorylated cAMP response-element-binding (pCREB) immunohistology. The results showed that nociceptive stimulation led to (1) striatal CBV decreases, (2) Ca(2+) increases via the nigrostriatal pathway, and (3) substantial expression of pCREB in substantia nigra dopaminergic neurons and striatal neurons. Interestingly, the striatal negative fMRI response was abolished by blocking substantia nigra activity but was not affected by blocking the striatal activity. This suggests the importance of input activity other than output in triggering the negative CBV signals. These findings indicate that the striatal negative CBV fMRI signals are associated with Ca(2+) increases and Ca(2+)-dependent signaling along the nigrostriatal pathway. The obtained data reveal a new brain road map in response to nociceptive stimulation of hemodynamic changes in association with Ca(2+) signals within the dopaminergic system.
NeuroImage.Neuroimage.2014 Apr 15;90:43-51. doi: 10.1016/j.neuroimage.2013.12.028. Epub 2013 Dec 22.
Decreased cerebral blood volume/flow (CBV/CBF) contributes to negative blood-oxygen-level-dependent (BOLD) functional MRI (fMRI) signals. But it is still strongly debated whether these negative BOLD or CBV/CBF signals are indicative of decreased or increased neuronal activity. The fidelity of Ca(2+)
PMID 24369291

The role of kinin receptors in cancer and therapeutic opportunities.

da Costa PL1, Sirois P2, Tannock IF3, Chammas R4.Author information 1Laboratório de Oncologia Experimental, Faculdade de Medicina da Universidade de São Paulo and Instituto do Câncer do Estado de São Paulo, Brazil.2CHUL Research Center, Laval University, Quebec City, Canada.3Princess Margaret Cancer Centre and University of Toronto, Toronto, ON, Canada.4Laboratório de Oncologia Experimental, Faculdade de Medicina da Universidade de São Paulo and Instituto do Câncer do Estado de São Paulo, Brazil. Electronic address: rchammas@lim24.fm.usp.br.AbstractKinins are generated within inflammatory tissue microenvironments, where they exert diverse functions, including cell proliferation, leukocyte activation, cell migration, endothelial cell activation and nociception. These pleiotropic functions depend on signaling through two cross talking receptors, the constitutively expressed kinin receptor 2 (B2R) and the inducible kinin receptor 1 (B1R). We have reviewed evidence, which supports the concept that kinin receptors, especially kinin receptor 1, are promising targets for cancer therapy, since (1) many tumor cells express aberrantly high levels of these receptors; (2) some cancers produce kinins and use them as autocrine factors to stimulate their growth; (3) activation of kinin receptors leads to activation of macrophages, dendritic cells and other cells from the tumor microenvironment; (4) kinins have pro-angiogenic properties; (5) kinin receptors have been implicated in cancer migration, invasion and metastasis; and (6) selective antagonists for either B1R or B2R have shown anti-proliferative, anti-inflammatory, anti-angiogenic and anti-migratory properties. The multiple cross talks between kinin receptors and renin-angiotensin system (RAS) as well as its implications for targeting KKS or RAS for the treatment of malignancies are also discussed. It is expected that B1R antagonists would interfere less with housekeeping functions and therefore would be attractive compounds to treat selected types of cancer. Reliable clinical studies are needed to establish the translatability of these data to human settings and the usefulness of kinin receptor antagonists.
Cancer letters.Cancer Lett.2014 Apr 1;345(1):27-38. doi: 10.1016/j.canlet.2013.12.009. Epub 2013 Dec 11.
Kinins are generated within inflammatory tissue microenvironments, where they exert diverse functions, including cell proliferation, leukocyte activation, cell migration, endothelial cell activation and nociception. These pleiotropic functions depend on signaling through two cross talking receptors,
PMID 24333733

Deletion of GABA-B Receptor in Schwann Cells Regulates Remak Bundles and Small Nociceptive C-fibers.

Faroni A1, Castelnovo LF, Procacci P, Caffino L, Fumagalli F, Melfi S, Gambarotta G, Bettler B, Wrabetz L, Magnaghi V.Author information 1Dipartimento di Scienze Farmacologiche e Biomolecolari, Università degli Studi di Milano, Via Balzaretti 9, 20133, Milan, Italy; Blond McIndoe Laboratories, The University of Manchester, Institute of Inflammation and Repair, M13 9PT, Manchester, United Kingdom.AbstractThe mechanisms regulating the differentiation into non-myelinating Schwann cells is not completely understood. Recent evidence indicates that GABA-B receptors may regulate myelination and nociception in the peripheral nervous system. GABA-B receptor total knock-out mice exhibit morphological and molecular changes in peripheral myelin. The number of small myelinated fibers is higher and associated with altered pain sensitivity. Herein, we analyzed whether these changes may be produced by a specific deletion of GABA-B receptors in Schwann cells. The conditional mice (P0-GABA-B1(fl/fl) ) show a morphological phenotype characterized by a peculiar increase in the number of small unmyelinated fibers and Remak bundles, including nociceptive C-fibers. The P0-GABA-B1(fl/fl) mice are hyperalgesic and allodynic. In these mice, the morphological and behavioral changes are associated with a downregulation of neuregulin 1 expression in nerves. Our findings suggest that the altered pain sensitivity derives from a Schwann cell-specific loss of GABA-B receptor functions, pointing to a role for GABA-B receptors in the regulation of Schwann cell maturation towards the non-myelinating phenotype. GLIA 2014;62:548-565.
Glia.Glia.2014 Apr;62(4):548-65. doi: 10.1002/glia.22625. Epub 2014 Jan 29.
The mechanisms regulating the differentiation into non-myelinating Schwann cells is not completely understood. Recent evidence indicates that GABA-B receptors may regulate myelination and nociception in the peripheral nervous system. GABA-B receptor total knock-out mice exhibit morphological and mol
PMID 24474699

Japanese Journal

Nociceptor-Enriched Genes Required for Normal Thermal Nociception

Cell reports 16(2), 295-303, 2016-07
NAID 120005838217

未然に抗血小板薬の投与を把握することができなかった硬膜外ブロック後の急性硬膜外血腫の1例

日本ペインクリニック学会誌 23(2), 93-96, 2016
NAID 130005160437

The use of autologous neurogenically-induced bone marrow-derived mesenchymal stem cells for the treatment of paraplegic dogs without nociception due to spinal trauma

Journal of Veterinary Medical Science advpub(0), 2016
NAID 130005156401

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★リンクテーブル★

リンク元	「痛覚」「侵害受容」「nociceptive」「pain sensation」「侵害感覚」
拡張検索	「antinociception」

「痛覚」

　　[★]

英: pain sensation, algesthesia, algesia
同: 痛感覚、侵害感覚 nociception
関: 上行性伝導路、痛覚の中枢

2007年度後期生理学授業プリント

痛みの分類

表在痛皮膚の痛み

鋭痛(Aδ線維)
鈍痛(C線維)

深部痛：関節や筋など深部組織の痛み
内臓痛
関連痛
放散痛

内因性発痛物質

ブラディキニン・ヒスタミン・セロトニン・プロスタグランジン・乳酸・K+

痛覚過敏

痛覚の伝導路

「侵害受容」

　　[★]

英: nociception、nociceptive
関: 痛覚、侵害受容性

「nociceptive」

　　[★]

侵害受容性の、侵害受容の

関: nociception

「pain sensation」

　　[★]

痛覚

関: nociception

同: pain sense

同: 痛覚

「侵害感覚」

　　[★]

英: nociception
関: 痛覚

「antinociception」

　　[★]

抗侵害受容、抗侵害

関: antinociceptive

[1] Portenoy, Russell K.; Brennan, Michael J. (1994). "Chronic Pain Management". In Good, David C.; Couch, James R. Handbook of Neurorehabilitation. Informa Healthcare. ISBN 0-8247-8822-2.

[Bayne-2] "Assessing Pain and Distress: A Veterinary Behaviorist's Perspective by Kathryn Bayne". Definition of Pain and Distress and Reporting Requirements for Laboratory Animals. Proceedings of the Workshop Held June 22, 2000. 2000.

[3] Purves, D. (2001). "Nociceptors". In Sunderland, MA. Neuroscience. Sinauer Associates.

[4] Feinstein, B.; Langton, J.; Jameson, R.; Schiller, F. (1954). "Experiments on pain referred from deep somatic tissues". J Bone Joint Surg. 36–A (5): 981–97. PMID 13211692. Retrieved 2007-01-06. ^{[permanent dead link]}

[5] Tillotson, Joanne. McCann, Stephanie. Kaplan’s Medical Flashcards. Apr. 02. 2013.

[6] Albertine, Kurt. Barron’s Anatomy Flash Cards

[7] Hofmann, Thomas, and Michael Schaefer. "Subunit Composition of Mammalian Transient Receptor Potential Channels in Living Cells." PNAS. 21 Mar. 2002. Web. 28 Mar. 2016.

[8] Noel, Jacques, and Katharina Zimmermann. "The Mechano‐activated K Channels TRAAK and TREK‐1 Control Both Warm and Cold Perception." EMBO Press. 11 Feb. 2009. Web. 28 Mar. 2016.

[9] Scholz, Joachim, and Clifford J. Woolf. "Can We Conquer Pain?" Nature Neuroscience. 28 Oct. 2002. Web. 28 Mar. 2016.

[10] Braz, Joao M., and Mohammed A. Nassar. "Parallel “Pain” Pathways Arise from Subpopulations of Primary Afferent Nociceptor." Science Direct. 15 Sept. 2005. Web. 28 Mar. 2016.

[11] Brown, A. G. "Organization in the Spinal Cord: The Anatomy and Physiology of Identified Neurones." Google Books. Springer, 06 Dec. 2012. Web. 28 Mar. 2016.

[12] Van Den Pol, Anthony D. "Hypothalamic Hypocretin (Orexin): Robust Innervation of the Spinal Cord." JNeurosci. 15 Apr. 1999. Web. 28 Mar. 2016.

[13] Bajo, Victoria M., and Miguel A. Merchan. "Topographic Organization of the Dorsal Nucleus of the Lateral Lemniscus in the Cat." Wiley Online Library. 10 May 1999. Web. 27 Mar. 2016.

[14] Oliver, Douglas M. "Neuronal Organization in the Inferior Colliculus." Springer. 2005. Web. 27 Mar. 2016.

[15] Corneil, Brian D., and Etienne Olivier. "Neck Muscle Responses to Stimulation of Monkey Superior Colliculus. I. Topography and Manipulation of Stimulation Parameters." ARTICLES. 01 Oct. 2002. Web. 28 Mar. 2016.

[16] May, Paul J. "The Mammalian Superior Colliculus: Laminar Structure and Connections." Science Direct. 2006. Web. 28 Mar. 2016.

[17] Benevento, Louis A., and Gregg P. Strandage. "The Organization of Projections of the Retinorecipient and Nonretinorecipient Nuclei of the Pretectal Complex and Layers of the Superior Colliculus to the Lateral Pulvinar and Medial Pulvinar in the Macaque Monkey." Wiley Online Library. 01 Jul. 1983. Web. 27 Mar. 2016.

[18] Sawamoto, Nobukatsu, and Manabu Honda. "Expectation of Pain Enhances Responses to Nonpainful Somatosensory Stimulation in the Anterior Cingulate Cortex and Parietal Operculum/Posterior Insula: An Event-Related Functional Magnetic Resonance Imaging Study." JNeurosci. 01 Oct. 2000. Web. 28 Mar. 2016.

[19] Menon, Vinod, and Lucina Q. Uddin. "Saliency, Switching, Attention and Control: A Network Model of Insula." Springer. 29 May 2010. Web. 28 Mar. 2016.

[20] Shackman, Alexander J., and Tim V. Salomons. "The Integration of Negative Affect, Pain and Cognitive Control in the Cingulate Cortex." Nature.com. Nature Publishing Group, Mar. 2011. Web. 28 Mar. 2016.

[21] Sneddon, L. U.; Braithwaite, V. A.; Gentle, M. J. (2003). "Do fishes have nociceptors? Evidence for the evolution of a vertebrate sensory system". Proceedings of the Royal Society B. 270 (1520): 1115–1121. PMC 1691351 . PMID 12816648. doi:10.1098/rspb.2003.2349.

[22] Jane A. Smith (1991). "A Question of Pain in Invertebrates". Institute for Laboratory Animals Journal. 33 (1–2).

[23] Pastor, J.; Soria, B.; Belmonte, C. (1996). "Properties of the nociceptive neurons of the leech segmental ganglion". Journal of Neurophysiology. 75 (6): 2268–2279. PMID 8793740.

[24] Wittenburg, N.; Baumeister, R. (1999). "Thermal avoidance in Caenorhabditis elegans: an approach to the study of nociception". PNAS. 96 (18): 10477–10482. doi:10.1073/pnas.96.18.10477.

[25] Illich, P. A.; Walters, E. T. (1997). "Mechanosensory neurons innervating Aplysia siphon encode noxious stimuli and display nociceptive sensitization". Journal of Neuroscience. 17 (1): 459–469. PMID 8987770.

[26] Tracey, J.; Daniel, W.; Wilson, R. I.; Laurent, G.; Benzer, S. (2003). "painless, a Drosophila gene essential for nociception". Cell. 113 (2): 261–273. PMID 12705873. doi:10.1016/S0092-8674(03)00272-1.

[27] Sherrington, C. (1906). The Integrative Action of the Nervous System. Oxford: Oxford University Press.

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