Since the passive electrotonic spread of potential along a nerve fibre is an almost instantaneous process, it may be asked why the nerve impulse is not propagated more rapidly than it actually is. In myelinated fibres the explanation is that there is a definite delay of about 0.1 ms at each node (see Fig. 6.4), which represents the time necessary for Na+ ions to move through the membrane at the node in a quantity sufficient to discharge the membrane capacity and build up a reversed potential. Conduction in a non-myelinated fibre is slower than in a myelinated fibre of the same diameter because the membrane capacity per unit length is much greater, and the delay in reversing the potential across it arises everywhere and not just at the nodes. Because the time constant for an alteration of membrane potential depends both on the magnitude of the membrane capacity and on the amount of current that flows into it, conduction velocity is affected by the values of the resistances in the equivalent electrical circuit, and also by the closeness of packing of sodium channels in the membrane, which determines the sodium current density. The effects of changing R and R; can best be seen in isolated axons. Thus Hodgkin (1939) showed that when Ro was increased by raising an axon out of a large volume of sea water into a layer of liquid paraffin, the conduction velocity fell by about 20% in a 30 fxm crab nerve fibre and by 50% in a 500 fxm squid axon; and when the axon was mounted in a moist chamber lying across a series of metal bars which could be connected together by a trough of mercury, the act of short-circuiting the bars increased the velocity by 20%. More recently, del Castillo and Moore (1959) showed that a reduction in R. brought about by inserting a silver wire down the centre of a squid axon could greatly speed up conduction.
One of the reasons why large non-myelinated fibres conduct faster than small ones is the decrease of R with an increase of fibre diameter. Assuming the properties of the membrane to be identical for fibres of all sizes, it can be shown that conduction velocity should be proportional to the square root of diameter. Experimentally this does not always seem to hold good, a possible explanation being that one of the ways in which giant axons are specially adapted for rapid conduction is through an increase in the number of sodium channels in the membrane. Measurements of the binding of labelled TTX have shown that the smallest fibres of all, those in garfish olfactory nerve, have the fewest channels, the site density being 35 fxm-2 as compared with 90 and 100 fxm-2 in lobster leg nerve and rabbit vagus nerve respectively (Ritchie and Rogart, 1977). However, in the squid giant axon there are about 290 TTX binding sites ^m-2 (Keynes and Ritchie, 1984). Since the flow of gating current has the consequence of increasing the effective size of the membrane capacity, there is an optimum sodium channel density above which the conduction velocity would fall off again. Hodgkin (1975) has calculated that the value found in squid is not far from the optimum.
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