Sensitization

For other uses, see Sensitization (disambiguation).

Sensitization is a non-associative learning process in which repeated administrations of a stimulus results in the progressive amplification of a response.[1] Sensitization often is characterized by an enhancement of response to a whole class of stimuli in addition to the one that is repeated. For example, repetition of a painful stimulus may make one more responsive to a loud noise.

History

Eric Kandel was one of the first to study the neural basis of sensitization, conducting experiments in the 1960s and 1970s on the gill withdrawal reflex of the seaslug Aplysia. Kandel and his colleagues first habituated the reflex, weakening the response by repeatedly touching the animal's siphon. They then paired noxious electrical stimulus to the tail with a touch to the siphon, causing the gill withdrawal response to reappear. After this sensitization, a light touch to the siphon alone produced a strong gill withdrawal response, and this sensitization effect lasted for several days. (After Squire and Kandel, 1999[2]). In 2000, Eric Kandel was awarded the Nobel Prize in Physiology or Medicine for his research in neuronal learning processes.

Neural substrates of sensitization

Addiction and dependence glossary[3][4][5]
addiction – a state characterized by compulsive engagement in rewarding stimuli despite adverse consequences
addictive behavior – a behavior that is both rewarding and reinforcing
addictive drug – a drug that is both rewarding and reinforcing
dependence – an adaptive state associated with a withdrawal syndrome upon cessation of repeated exposure to a stimulus (e.g., drug intake)
drug sensitization or reverse tolerance – the escalating effect of a drug resulting from repeated administration at a given dose
drug withdrawal – symptoms that occur upon cessation of repeated drug use
physical dependence – dependence that involves persistent physical–somatic withdrawal symptoms (e.g., fatigue and delirium tremens)
psychological dependence – dependence that involves emotional–motivational withdrawal symptoms (e.g., dysphoria and anhedonia)
reinforcing stimuli – stimuli that increase the probability of repeating behaviors paired with them
rewarding stimuli – stimuli that the brain interprets as intrinsically positive or as something to be approached
sensitization – an amplified response to a stimulus resulting from repeated exposure to it
tolerance – the diminishing effect of a drug resulting from repeated administration at a given dose

The neural basis of behavioral sensitization is often not known, but it typically seems to result from a cellular receptor becoming more likely to respond to a stimulus. Several examples of neural sensitization include:

Cross-sensitization

Cross-sensitization is a phenomenon in which sensitization to a stimulus is generalized to a related stimulus, resulting in the amplification of a particular response to both the original stimulus and the related stimulus. For example, cross-sensitization to the neural and behavioral effects of addictive drugs are well characterized, such as sensitization to the locomotor response of a stimulant resulting in cross-sensitization to the motor-activating effects of other stimulants. Similarly, reward sensitization to a particular addictive drug often results in reward cross-sensitization, which entails sensitization to the rewarding property of other addictive drugs in the same drug class or even certain natural rewards.

As a causal factor in pathology

Sensitization has been implied as a causal or maintaining mechanism in a wide range of apparently unrelated pathologies including addiction, allergies, asthma, and some medically unexplained syndromes such as fibromyalgia and multiple chemical sensitivity. Sensitization may also contribute to psychological disorders such as post-traumatic stress disorder, panic anxiety and mood disorders.[17][18][19]

See also

References

  1. Shettleworth, S. J. (2010). Cognition, Evolution and Behavior (2nd ed.). New York: Oxford.
  2. Squire LR, Kandel ER (1999). Memory: From Mind to Molecules. New York: Scientific American Library; New York: W.H. Freeman. ISBN 0-7167-6037-1.
  3. Nestler EJ (December 2013). "Cellular basis of memory for addiction". Dialogues Clin. Neurosci. 15 (4): 431–443. PMC 3898681. PMID 24459410.
  4. Malenka RC,Nestler EJ, Hyman SE (2009). "Chapter 15: Reinforcement and Addictive Disorders". In Sydor A, Brown RY. Molecular Neuropharmacology: A Foundation for Clinical Neuroscience (2nd ed.). New York: McGraw-Hill Medical. pp. 364–375. ISBN 9780071481274.
  5. "Glossary of Terms". Mount Sinai School of Medicine. Department of Neuroscience. Retrieved 9 February 2015.
  6. Collingridge GL, Isaac JT, Wang YT (2004). "Receptor trafficking and synaptic plasticity". Nat Rev Neurosci 5(12): 952–962, PMID 15550950, doi:10.1038/nrn1556.
  7. Morimoto K, Fahnestock M, Racine RJ (2004). "Kindling and status epilepticus models of epilepsy: Rewiring the brain". Prog Neurobiol 73(1): 1–60, PMID 15193778, doi:10.1016/j.pneurobio.2004.03.009.
  8. Teicher MH, Glod CA, Surrey J, Swett C, Jr (1993). "Early childhood abuse and limbic system ratings in adult psychiatric outpatients". J Neuropsychiatry Clin Neurosci 5(3): 301–306, PMID 8369640.
  9. Ji RR, Kohno T, Moore KA, Woolf CJ (2003). "Central sensitization and LTP: Do pain and memory share similar mechanisms?". Trends Neurosci 26(12): 696–705, PMID 14624855.
  10. Gudin J. (2004). Medscape Neurobiology: Expanding Our Understanding of Central Sensitization. Medscape: Medscape Education.
  11. Robinson TE, Berridge KC (1993). "The neural basis of drug craving: An incentive-sensitization theory of addiction". Brain Res Brain Res Rev 18(3): 247–291, PMID 8401595.
  12. Janeway, Charles; Paul Travers, Mark Walport, and Mark Shlomchik (2001). Immunobiology; Fifth Edition. New York and London: Garland Science. pp. e–book. ISBN 978-0-8153-4101-7.
  13. Janeway C, Travers P, Walport M, Shlomchik M, eds. (2001). Immunobiology 5: The Immune System in Health and Disease. New York: Garland Pub., ISBN 0-8153-3642-X
  14. 1 2 Croner S (1992). "Prediction and detection of allergy development: influence of genetic and environmental factors". J. Pediatr. 121 (5 Pt 2): S58–63. doi:10.1016/S0022-3476(05)81408-8. PMID 1447635.
  15. De Swert LF (1999). "Risk factors for allergy". Eur. J. Pediatr. 158 (2): 89–94. doi:10.1007/s004310051024. PMID 10048601.
  16. Barnes KC, Grant AV, Hansel NN, Gao P, Dunston GM (2007). "African Americans with asthma: genetic insights". Proc Am Thorac Soc 4 (1): 58–68. doi:10.1513/pats.200607-146JG. PMC 2647616. PMID 17202293. Archived from the original on 2010-11-16.
  17. Rosen JB, Schulkin J (1998). "From normal fear to pathological anxiety". Psychol Rev 105(2): 325–350, doi:10.1037/0033-295X.105.2.325 PMID 9577241.
  18. Antelman SM (1988). "Time-dependent sensitization as the cornerstone for a new approach to pharmacotherapy: drugs as foreign/stressful stimuli". Drug Development Research 14: 1–30.
  19. Post RM (1992). "Transduction of psychosocial stress into the neurobiology of recurrent affective disorder". Am J Psychiatry 149(8): 999–1010, PMID 1353322.
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