Decreased nociceptive sensitization in mice lacking the fragile X mental retardation protein: role of mGluR1/5 and mTOR.

Fragile X mental retardation is caused by silencing of the gene (FMR1) that encodes the RNA-binding protein (FMRP) that influences translation in neurons. A prominent feature of the human disorder is self-injurious behavior, suggesting an abnormality in pain processing. Moreover, FMRP regulates group I metabotropic glutamate receptor (mGluR1/5)-dependent plasticity, which is known to contribute to nociceptive sensitization.

Estrogen modulation of ovariectomy-induced hyperalgesia in adult mice.

Some chronic pain conditions are more prevalent in women. However, the evidence from both human and animal studies as to whether estrogen is pro- or anti-nociceptive is inconsistent. We have used a model of functional abdominal pain in mice to examine the role of estrogen in the modulation of a hyperalgesic state induced by ovariectomy.

Spinal NKCC1 blockade inhibits TRPV1-dependent referred allodynia.

Background: The Na+, K+, 2Cl- type I cotransporter (NKCC1) and TRPV1 receptors, at the level of the dorsal horn, have been implicated in mediating allodynia in response to an inflammatory insult. The NKCC1 cotransporter regulates intracellular [Cl-] and thus the magnitude and polarity of GABAA receptor responses in neurons. TRPV1 receptors transduce diverse chemical and natural stimuli in nociceptors and are critical for inflammatory hyperalgesia.