Disuse supersensitivity, also pharmacological disuse supersensitivity or pharmacological denervation supersensitivity, is the increased sensitivity by a postsynaptic cell because of decreased input by incoming axons, e.g., due to the exposure to an antagonist drug.[1][2]
Jaffe and Sharpless pointed out that withdrawal syndrome after the cessation of a chronically used drug often shows an exaggerated response which is normally suppressed by the drug which produced a dependence. They suggested the model according to which a drug has both excitatory and depressive effects. Depressive effects generate hypersensitivity, but at the same time they mask it. When drug usage stops, hypersensitivity becomes unmasked.[3]
See also
editReferences
edit- ^ Yarbrough GG, Phillis JW., "Supersensitivity of central neurons--a brief review of an emerging concept", Can J Neurol Sci. 1975 Aug;2(3):147–52. PMID 169978
- ^ Jaffe JH, Sharpless SK., "Pharmacological denervation supersensitivity in the central nervous system: a theory of physical dependence.", Res Publ Assoc Res Nerv Ment Dis. 1968;46:226–46. PMID 5749386
- ^ Drug Addiction I: Morphine, Sedative/Hypnotic and Alcohol Dependence, Springer Science & Business Media, 2013, ISBN 3642666124, p. 636
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