Page 59 - Color_Atlas_of_Physiology_5th_Ed._-_A._Despopoulos_2003
P. 59

Action Potential                resulting in a hyperpolarizing afterpotential
                                                     +
                                                       +
                                       (! A1). Increased Na -K -ATPase pumping
       An action potential is a signal passed on  rates (electrogenic; ! p. 28) can contribute to
       through an axon or along a muscle fiber that  this afterpotential.
       influences other neurons or induces muscle  Very long trains of action potentials can be
       contraction. Excitation of a neuron occurs if the  generated (up to 1000/s in some nerves) since
       membrane potential, E m, on the axon hillock of  the quantity of ions penetrating the mem-
       a motor neuron, for example (! p. 42), or on  brane is very small (only ca. 1/100 000 th the
       the motor end-plate of a muscle fiber changes  number of intracellular ions). Moreover, the
    Nerve and Muscle, Physical Work  rotransmitter-induced opening of postsynap- +  unresponsive to further stimuli; this is called
                                       Na -K -ATPase (! p. 26) ensures the continu-
                                        +
                                          +
       from its resting value (! p. 44) to a less nega-
       tive value (slow depolarization, ! A1). This
                                       ous restoration of original ion concentrations
                                       (! p. 46).
       depolarization may be caused by neu-
                                        During an action potential, the cell remains
       tic cation channels (! p. 50) or by the (elec-
                                       the refractory period. In the absolute refractory
       trotonic) transmission of stimuli from the sur-
                                       period, no other action potential can be trig-
       roundings (! p. 48). If the E m of a stimulated
                                       gered, even by extremely strong stimuli, since
       cell comes close to a critical voltage or thresh-
                                       Na channels in depolarized membranes can-
       old potential (! A1), “rapid” voltage-gated Na
                                        +
       channels are activated (! B4 and B1 ! B2).
                                       not be activated (! B3). This is followed by a
                         +
       This results in increased Na conductance, g Na
                           +
                                       tion potentials of smaller amplitudes and rates
       (! A2). If the threshold potential is not
                                       of rise can be generated, even by strong
    2  (! p. 32), and the entry of Na into the cell  relative refractory period during which only ac-
       reached, this process remains a local (sub-
                                       stimuli. The refractory period ends once the
       threshold) response.            membrane potential returns to its resting
         Once the threshold potential is reached, the  value (! e.g. p. 59 A).
       cell responds with a fast all-or-none depolari-  The extent to which Na channels can be ac-
                                                       +
       zation called an action potential, AP (! A1).  tivated and, thus, the strength of the Na cur-
                                                                +
       The AP follows a pattern typical of the specific  rent, I Na, depends on the pre-excitatory resting
       cell type, irregardless of the magnitude of the  potential, not the duration of depolarization.
                                                      +
       stimulus that generated it. Large numbers of  The activation of the Na channels reaches a
       Na channels are activated, and the influxing  maximum at resting potentials of ca. – 100 mV
         +
       Na accelerates depolarization which, in turn,  and is around 40% lower at – 60 mV. In mam-
         +
                                            +
       increases g Na and so on (positive feedback). As  mals, Na channels can no longer be activated
       a result, the E m rapidly collapses (0.1 ms in  at potentials of –50 mV and less negative
       nerve cells: fast depolarization phase or up-  values (! B3). This is the reason for the abso-
       sweep) and temporarily reaches positive levels  lute and relative refractory periods (see above)
       (overshooting, + 20 to + 30 mV). The g Na drops  and the non-excitability of cells after the ad-
       before overshooting occurs (! A2) because  ministration of continuously depolarizing sub-
       the Na channels are inactivated within 0.1 ms  stances such as suxamethonium (! p. 56). An
           +
       (! B2 ! B3). The potential therefore reverses,  increased extracellular Ca 2+  concentration
       and restoration of the resting potential, the re-  makes it more difficult to stimulate the cell be-
       polarization phase of the action potential,  cause the threshold potential becomes less
       begins. Depolarization increases (relatively  negative. On the other hand, excitability in-
       slowly) the open-probability of voltage-gated  creases (lower threshold) in hypocalcemic
        +
       K channels. This increases the potassium con-  states, as in muscle spasms in tetany
       ductance, g K, thereby accelerating repolariza-  (! p. 290).
       tion.                            The special features of action potentials in
         In many cases, potassium conductance, g K is  cardiac and smooth muscle fibers are de-
       still increased after the original resting poten-  scribed on pages 192, 70 and 59 A.
       tial has been restored (! A2), and E m tem-
   46  porarily approaches E K (! pp. 44 and 32 ff.),
       Despopoulos, Color Atlas of Physiology © 2003 Thieme
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