For as long as I have been in pain research (and long before I ever even thought about pain research) the topic of mechanically-gated ion channels has been a huge deal. The reasons are simple:
1) We obtain information about our environment through touch (among other things) but in certain conditions touch can become painful. We call this allodynia. The problem is we don’t know how this happens (but we have some good ideas — more on this later) and, ostensibly, identifying ion channels involved in mechanosensation would go a long way toward helping us understand this.
2) Certain types of mechanical inputs are painful (e.g. pinch or pin-prick) and these types of input become even more painful after injury. We call this hyperalgesia and, again, we have some good ideas of the processes that underlie this hyperalgesia but, ultimately, without knowledge of the initial transducer of mechanical inputs, it is hard to understand this fully.
3) Time for the most obvious reason, we just flat out don’t know how we feel mechanical stimulation. There are hundreds (or thousands, depending how you think about it) of papers out there on this but, to date, no one has clearly identified a mechanically-gated channel expressed by vertebrate sensory neurons.
Until now. There were all types of rumors flying around about this at IASP. This is not unusual, however, as I have heard similar rumors at SfN and IASP meetings in the past. On Sept 2, a paper was published in Science from the Patapoutian lab at Scripps, La Jolla, that may open the flood gates in terms of describing how mechanical stimulation is transduced into signals that can be transmitted to the CNS.
How’d they do it? Continue reading