Thursday, June 28, 2007

Propagation of a nerve impulse

It is possible to place microelectrodes on the surface
of a myelinated axon at a node of Ranvier and record
spike-like electrical currents that are associated with
changes in potential difference taking place across
the axonal membrane. A nerve impulse is propagated
in the form of an action potential and depends upon
rapid changes in membrane ion permeability. During
the initial phase of the action potential a rapid infl ux
of sodium ions through voltage-gated sodium channels
causes rapid depolarization of the membrane,
i.e. the inside surface of the membrane becomes less
negative relative to the outside of the membrane.
The more a membrane is depolarized, the greater the
number of sodium channels that will be opened. The
entry of Na+ does not continue indefi nitely: it is halted
partly because the membrane potential soon reaches
the sodium ion equilibrium potential, where the net
inward driving force acting on sodium ions becomes
zero, and partly because the rise in sodium permeability
decays inexorably with time from the moment
when it is fi rst triggered. After the peak of the spike
has been reached, therefore, the sodium permeability
is rapidly reduced. At the same time, the opening of
potassium channels and chloride channels allow K+
effux and Cl– infl ux, thereby increasing the degree of
intracellular negativity. This hyperpolarization inhibits
the neuron because the membrane potential is now
further away than ever from the –45 mV threshold for
excitation. The fact that potassium channels are 50
times more numerous than sodium channels (Hille,
1970) ensures that hyperpolarization is rapid. The
membrane then adjusts to its normal resting potential
of –65 mV in readiness for another action potential.
In myelinated fi bres, the sodium channels are concentrated
at the nodes of Ranvier. The function of the
myelin sheath is to restrict the inward and outward
passage of local circuit current to the nodes of Ranvier,
so causing the nerve impulse to be propagated
along myelinated fi bres from node to node in a series
of jumps (saltatory conduction). The generation of an
action potential at each node results in the depolarization
of the next node and subsequently the generation
of an action potential with an internode delay of only
about 20 μs.

No comments: