Pain and the genome

  • M. E. Ferrero
  • A. Fulgenzi
  • M. Tiengo
Part of the Topics in Anaesthesia and Critical Care book series (TIACC)


There is increasing evidence that genotype affects pain sensitivity and pain modulation. As an example in humans, 10% of a Caucasian population studied only poorly metabolized the liver isozyme P450IID6 (required for the O-demethylation of the widely used opiate drug codeine to morphine) [1]. So, for such people codeine is an inefficient analgesic. The enzymatic defect is related to a mutation in the CYP2D6 gene [2]. As an experimental example, a recent study in rats demonstrated that a form of stress-induced analgesia was naloxone-insensitive, but attenuated by dizocilpine in male C57BL/6J mice. The same type of analgesia in male DBA/2J mice was significantly attenuated by naloxone but was insensitive to dizocilpine antagonism, indicating the role exerted by the different rat strain (i.e., genetic factors) in determining the selective recruitment of alternative central mechanisms of pain inhibition [3].


Nerve Growth Factor Carpal Tunnel Syndrome CYP2D6 Gene Nerve Growth Factor Expression Hereditary Sensory Neuropathy 
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© Springer Verlag Italia, Milano 1999

Authors and Affiliations

  • M. E. Ferrero
  • A. Fulgenzi
  • M. Tiengo

There are no affiliations available

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