Representative current traces in response to the voltage
protocol (inset). Displayed data in the presence of BTX were recorded
after a 900 pulse train experiment, each lasting 2 s using a frequency of
1 Hz. From a holding potential of )90 mV, a 50 ms pulse was given to
+30 mV (part I) corresponding to the maximum Naþ influx of the
unaffected Nav1.8/b1. Next, a 50 ms pulse to )10 mV (part II) evoked a
transient deactivation response. After 50 ms at +30 mV in the presence
of BTX, the open channel probability is very high caused by the in-
hibition of the inactivation process. As a consequence, the jump to )10
mV causes an initial increase of inward Naþ current due to the in-
creased driving force (this is not instantaneous due to the sluggishness
of TEVC when measuring oocytes). Next, Nav1.8/b1 starts to deacti-
vate at )10 mV which is rather slow and which causes the current
decay over the next 25 ms. The ensuing jump to )120 mV (Part III)
reveals a faster and complete deactivation. In part IV, a pulse is given
to )20 mV in order to reveal a shift in the current–voltage relationship
(I–V curve). In control conditions, Nav1.8/b1 is not yet activated at
)20 mV so there is no current visible. In the presence of BTX, Naþ
ions are passing through even at )20 mV. (B) Corresponding current–
voltage relationship (left panel) before (j) and after addition of 5 lM
(d) and 10 lM (m) BTX. Current traces were evoked using 50 ms step
depolarisations of 10 mV to a voltage range between )70 and 70 mV
from a holding potential of )90 mV. The arrow indicates the shift in
Erev. (C) Superimposed graphics of the corresponding activation and
steady-state inactivation curves. Current traces for the inactivation
protocol were evoked by 50 ms depolarisations from )120 mV to 0 mV
followed by a 50 ms pulse to +30 mV, from a holding potential of )90
mV. As indicated by the arrows, BTX clearly shifts the activation curve
(horizontal arrow) to more negative potentials and inhibits the inac-
tivation process (vertical arrow
Representative current traces in response to the voltageprotocol (inset). Displayed data in the presence of BTX were recordedafter a 900 pulse train experiment, each lasting 2 s using a frequency of1 Hz. From a holding potential of )90 mV, a 50 ms pulse was given to+30 mV (part I) corresponding to the maximum Naþ influx of theunaffected Nav1.8/b1. Next, a 50 ms pulse to )10 mV (part II) evoked atransient deactivation response. After 50 ms at +30 mV in the presenceof BTX, the open channel probability is very high caused by the in-hibition of the inactivation process. As a consequence, the jump to )10mV causes an initial increase of inward Naþ current due to the in-creased driving force (this is not instantaneous due to the sluggishnessof TEVC when measuring oocytes). Next, Nav1.8/b1 starts to deacti-vate at )10 mV which is rather slow and which causes the currentdecay over the next 25 ms. The ensuing jump to )120 mV (Part III)reveals a faster and complete deactivation. In part IV, a pulse is givento )20 mV in order to reveal a shift in the current–voltage relationship(I–V curve). In control conditions, Nav1.8/b1 is not yet activated at)20 mV so there is no current visible. In the presence of BTX, Naþions are passing through even at )20 mV. (B) Corresponding current–voltage relationship (left panel) before (j) and after addition of 5 lM(d) and 10 lM (m) BTX. Current traces were evoked using 50 ms stepdepolarisations of 10 mV to a voltage range between )70 and 70 mVfrom a holding potential of )90 mV. The arrow indicates the shift inErev. (C) Superimposed graphics of the corresponding activation andsteady-state inactivation curves. Current traces for the inactivationprotocol were evoked by 50 ms depolarisations from )120 mV to 0 mVfollowed by a 50 ms pulse to +30 mV, from a holding potential of )90mV. As indicated by the arrows, BTX clearly shifts the activation curve(horizontal arrow) to more negative potentials and inhibits the inac-tivation process (vertical arrow
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