on to conduct as manyas 1m quite normal action potentials before it gives out. Dr Baker hadsqueezed the life out of the nerve-fibre and turned it into an activeelectrical wire. Cell biology had been reduced to textbook physics.Back to discontinuityDr Hodgkin and Dr Huxley explained the action potential. They did notmanage to show the molecular mechanisms behind it. But those who came laterdid, using similar techniques.In 1976 two German physiologists, Erwin Neher and Bert Sakmann,miniaturised the voltage clamp. Using a pipette with an opening only a fewmillionths of a metre across, the voltage of a minute piece of membrane canbe clamped at any level, and the currents across it measured. The area isso small that current can be seen switching on and off as a single hole inthe membrane opens and closes.These holes--channels--turn out to be either closed or fully open: morelike switches than taps. As the voltage increases, the sodium channelsspend more of their time open. It is the combined effect of billions ofsuch channels that leads to the smooth curves seen by Dr Hodgkin and DrHuxley in a single nerve-fibre. As the channels open, the flow of sodiumboosts the potential even further, opening yet more. Then an automaticshutting-mechanism comes into play. The potassium channels work on similarprinciples, but more slowly; that is why the potassium flow follows thesodium flow.The question remains: how does the nerve membrane suddenly begin to leakions that it barred only a second before? Part of the answer has come fromexperiments using a nerve poison called tetrodotoxin (TTX). It iswell-known in Japan as the ingredient of fugu, the puffer fish, that numbsthe taste buds or, if the chef is careless, kills. TTX blocks sodiumchannels. Caesium blocks the potassium channels. If a nerve is bathed inTTX and caesium, there should be no membrane current at all.At the beginning of the 1970s, two groups of scientists--Clay Armstrong andPancho Bezanilla...
