The key words for me were "central sensitization". You can also look up "wind up". Amitriptylene could be reducing it by blocking sodium channels.Here's a paper on amitriptyline's anti-pain mechanism.
So they are basically concluding that it reduces pain because it reduces pain. What am I missing?
Arch Pharm Res. 2008 Feb;31(2):178-82.
Effects of carbamazepine and amitriptyline on tetrodotoxinresistant Na+ channels in immature rat trigeminal ganglion neurons.
Hur YK, Choi IS, Cho JH, Park EJ, Choi JK, Choi BJ, Jang IS.
Department of Oral Medicine, School of Dentistry, Kyungpook National University, Daegu 700-412, Korea.
Although anticonvulsant drugs that block voltage-dependent Na+ channels have been widely used for neuropathic pain, including peripheral nerve injury-induced pain, much less is known about the actions of these drugs on immature trigeminal ganglion (TG) neurons. Here we report the effects of carbamazepine (CBZ) and amitriptyline (ATL) on tetrodotoxin-resistant (TTX-R) Na' channels expressed on immature rat TG neurons. TTX-R Na+ currents (I(Na)) were recorded in the presence of 300 nM TTX by use of a conventional whole-cell patch clamp method. Both CBZ and ATL inhibited TTX-R I(Na) in a concentration-dependent manner, but ATL was more potent. While CBZ and ATL did not affect the overall voltage-activation relationship of TTX-R Na+ channels, both drugs shifted the voltage-activation relationship to the left, indicating that they inhibited TTX-R Na+ channels more efficiently at depolarized membrane potentials. ATL showed a profound use-dependent blockade of TTX-R I(Na), but CBZ had little effect. The present results suggest that both CBZ and ATL, common drugs used for treating neuropathic pain, efficiently inhibit TTX-R Na+ channels expressed on immature TG neurons, and that these drugs might be useful for the treatment of trigeminal nerve injury-induced neuropathic pain, as well as the inhibition of ongoing central sensitization, even during immature periods.
PMID: 18365687