358
M. V. L. BENNETT
where different and more less-specific ions can enter or leave the cell.
These sites are intermixed in varying degrees and proportions to account
for the different kinds of membrane activity. The membrane separating
the sites has a bimolecular lipid core that presumably is of very high
resistance and inactive in ion movement. Most of the membrane capacity
can be assigned to this part of the surface. For most cells the specific
capacitance is about 1 pF/ cm2 while membrane resistance-reflecting
the number and nature of sites for ionic movement-can vary over a
range of six or seven orders of magnitude. This concept of localized
sites of ion movement has received strong support from recent experiments using artificial bimolecular lipid membranes. These membranes
are similar to ordinary membranes in dimensions and capacitance but
have an extraordinarily high resistivity. A number of compounds lower
the resistance into the physiological range by providing sites for movement of ions or by acting as carrier molecules (e.g., Cass et d., 1970).
In impulse responses of electrocytes there appear to be three types of
sites that change their properties as a function of membrane potential.
When the membrane is moderately depolarized, the conductance at
sodium sites increases (sodium activation) allowing influx of sodium and
further depolarization. This process is responsible for the active rising
phase of the spike. If depolarization is maintained, the sodium conductance decreases again (sodium inactivation) and this change is a
factor in return of the membrane potential to its resting level. At the
resting potential the inactivated sodium sites gradually recover their
ability to increase in conductance when the membrane is depolarized.
(Any remaining activated sites rapidly return to their low, resting conductance at the resting potential and can be rapidly activated again
without further delay.) One kind of potassium site in electrocytes increases in conductance when the membrane is depolarized (potassium
activation or delayed rectification), but the change is delayed compared
to sodium activation. The increased potassium conductance tends to
restore the cell to the resting potential where the conductance gradually
returns to normal. If the membrane is kept depolarized, the increase in
potassium conductance can also reverse (potassium inactivation), a
process which is generally much slower than either the reversal at the
resting potential or sodium inactivation. So far these changes are like
those of ordinary nerve (Hodgkin, 1964; Hille, 1970). Another kind of
potassium site decreases in conductance when an outward current is
passed through it. This change is very rapid in onset and reverses very
rapidly when the outward current is reduced. It resembles and probably
has the same mechanism as anomalous or outward rectification in muscle
M. V. L. BENNETT
where different and more less-specific ions can enter or leave the cell.
These sites are intermixed in varying degrees and proportions to account
for the different kinds of membrane activity. The membrane separating
the sites has a bimolecular lipid core that presumably is of very high
resistance and inactive in ion movement. Most of the membrane capacity
can be assigned to this part of the surface. For most cells the specific
capacitance is about 1 pF/ cm2 while membrane resistance-reflecting
the number and nature of sites for ionic movement-can vary over a
range of six or seven orders of magnitude. This concept of localized
sites of ion movement has received strong support from recent experiments using artificial bimolecular lipid membranes. These membranes
are similar to ordinary membranes in dimensions and capacitance but
have an extraordinarily high resistivity. A number of compounds lower
the resistance into the physiological range by providing sites for movement of ions or by acting as carrier molecules (e.g., Cass et d., 1970).
In impulse responses of electrocytes there appear to be three types of
sites that change their properties as a function of membrane potential.
When the membrane is moderately depolarized, the conductance at
sodium sites increases (sodium activation) allowing influx of sodium and
further depolarization. This process is responsible for the active rising
phase of the spike. If depolarization is maintained, the sodium conductance decreases again (sodium inactivation) and this change is a
factor in return of the membrane potential to its resting level. At the
resting potential the inactivated sodium sites gradually recover their
ability to increase in conductance when the membrane is depolarized.
(Any remaining activated sites rapidly return to their low, resting conductance at the resting potential and can be rapidly activated again
without further delay.) One kind of potassium site in electrocytes increases in conductance when the membrane is depolarized (potassium
activation or delayed rectification), but the change is delayed compared
to sodium activation. The increased potassium conductance tends to
restore the cell to the resting potential where the conductance gradually
returns to normal. If the membrane is kept depolarized, the increase in
potassium conductance can also reverse (potassium inactivation), a
process which is generally much slower than either the reversal at the
resting potential or sodium inactivation. So far these changes are like
those of ordinary nerve (Hodgkin, 1964; Hille, 1970). Another kind of
potassium site decreases in conductance when an outward current is
passed through it. This change is very rapid in onset and reverses very
rapidly when the outward current is reduced. It resembles and probably
has the same mechanism as anomalous or outward rectification in muscle