| First Author | König M | Year | 1996 |
| Journal | Nature | Volume | 383 |
| Issue | 6600 | Pages | 535-8 |
| PubMed ID | 8849726 | Mgi Jnum | J:35826 |
| Mgi Id | MGI:83270 | Doi | 10.1038/383535a0 |
| Citation | Konig M, et al. (1996) Pain responses, anxiety and aggression in mice deficient in pre-proenkephalin. Nature 383(6600):535-8 |
| abstractText | Enkephalins are endogenous opioid peptides that are derived from a pre-proenkephalin precursor protein. They are thought to be vital in regulating many physiological functions, including pain perception and analgesia, responses to stress, aggression and dominance. Here we have used a genetic approach to study the role of the mammalian opioid system. We disrupted the pre-proenkephalin gene using homologous recombination in embryonic stem cells to generate enkephalin-deficient mice. Mutant enk-/- animals are healthy, fertile, and care for their offspring, but display significant behavioural abnormalities. Mice with the enk-/- genotype are more anxious and males display increased offensive aggressiveness. Mutant animals show marked differences from controls in supraspinal, but not in spinal, responses to painful stimuli. Unexpectedly, enk-/- mice exhibit normal stress-induced analgesia. Our results show that enkephalins modulate responses to painful stimuli. Thus, genetic factors may contribute significantly to the experience of pain. |
