Neurons IonicCurrents Records

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Record
  ID Neurons
  ID Methods Electrophysiology
  Current name
  Charge carrier
  Peak conductance
  Peak current
  E rev
  V threshold
  V half activation
  V peak
  Citations
  Reference figures
  Reference text
  Comments
Methods Electrophysiology.ID Ref.
Neurons.ID Ref.
-1725086893 -1725086893 988800474 I(cat) Cations - - - -35 mV - - - Fig. 1B p.2126 - 988800474 -1725086893
-1725086893 -1725086893 988800474 I(NaP) Na+ - 60-3160 pA (median 308 pA) - -60 mV - -25 - -20 mV - Fig. 1-3 pp.2126-2129 Data on time and voltage-dependence of inactivation, responses to conditioning
pulses and pulse-train stimulation. 		988800474 -1725086893
-1041488843 -1041488843 996239748 CaP Ca2+ - - - - - - "The P-current is the dominant high threshold voltage-activated (HVA) current
in cerebellar Purkinje neurones (Llinas, Sugimori, Hillman & Cherksey, 1992).
It is activated over the same range of membrane potentials as the two other
HVA current components and cannot be distinguished by its kinetics, and single
channel recordings have revealed unitary conductance levels in the same range
as for L- and N-channels (Usowicz, Sugimori, Cherksey & Llinas, 1992).
Consequently, evidence for the presence of P-channels has relied on
pharmocological tests."p.197 		- - Blocked specifically by omega-Aga-IVA. Partially supressed by nifedipine.
Constitutes ~30% of HVA. 		996239748 -1041488843
-1041488843 -1041488843 996239748 HVA-Ca Ca2+ - - - - - - "About 11-12% of the HVA current was insensitive to the saturating
concentrations of three organic blocking agents (omega-Aga-IVA, omega-CgTX and
nifedipine). This insensitive component may be due to incomplete inhibition by
one or all of these blocking agents, or it may be due to a separate
unclassified set of calcium channels."p.204 		- p.204 The fourth HVA component was blocked by Cd-ions. 996239748 -1041488843
-1041488843 -1041488843 996239748 L-current Ca2+ - - - - - - "Nevertheless, the results of our experiments in which nifedipine was applied
after the application of both omega-Aga-IVA and omega-CgTX, suggest that about
30% of the HVA current in neocortical neurones are dihydropyridine sensitive
(presumed L-channels)."p.203 		- - Nifedipine is nonspecific blocker of L-channels. 996239748 -1041488843
-1041488843 -1041488843 996239748 N-current Ca2+ - - - - - - "In the present study omega-CgTX blocked about 26% of the HVA current, which is
comparable to the percentages found previously in these cells (20%, Sayer et
al. 1990, 30%, Brown et al. 1993)."p.203 		- p.203 N-current is specifically blocked by omega-CgTX. 996239748 -1041488843
-944650159 -944650159 1004695855 I(Ca) Ca2+ - - - - - - "Plateaus could also be evoked by focal glutamate iontophoresis on basal
dendrites (Oakley et al. 2001). In the present study, the spatial extent of
these plateaus were examined on two cells. Figure 6 shows the results obtained
in one of these cells. Focal glutamate iontophoresis at a site 128 µm from the
soma on a basal dendrite evoked an all-(red trace, bottom)-or-none (gray
trace, bottom) plateau. The corresponding pseudocolor plot (Fog. 6, top) shows
that the plateau was restricted to a small region surrounding the
iontophoretic site (indicated by dashed line in pseudocolor plot). A 50%
contour drawn around the region estimates the proximal extent of the plateau
as 16 µm and the distal extent as 15 µm. In this cell, the spatial extent of
the plateau was no significantly changed when 100 µm AP-5 was added to the
bath and the experiment was repeated (data not shown). In the second cell
tested, iontophoresis at a site 105 µm from the soma evoked a plateau, which
was estimated to extend 20 µm proximally and 10 µm distally."p.510 		Fig. 6 p.510 - 1004695855 -944650159
-866037043 -866037043 999521822 Ca Ca2+ - - - - - - "There were no distinctive features of the Ca2+ currents in the two
nonpyramidal (bipolar) neocortical neurons. Both had high- and low-threshold
components, and the I-V relations had thresholds and maxima within the range
of values for pyramidal neurons.".pp.1599-1600 		- pp.1599-1600 - 999521822 -866037043
-806603121 -806603121 974817158 High-threshold Ca Ca2+ - 264+-116 pA - -45 mV - -20 - -10 mV "These currents were shown to be calcium fluxes by their proportionate
reduction in lowered external calcium (0.1 mM, n=2) and their blockade in 0.4
mM cadmium (n=6). An outward current seen at positive voltage commands was
probably carried by cations passing outward through the calcium channel [8,9]
and was absent when N-methyl-D-glucamine was substituted for Tris in the
electrode solution (n=2)."p.176. 		Fig.1 p.176 - 974817158 -806603121
-806603121 -806603121 974817158 Low-threshold Ca Ca2+ - 75+-32 pA - -65 mV - -30 mV "These currents were shown to be calcium fluxes by their proportionate
reduction in lowered external calcium (0.1 mM, n=2) and their blockade in 0.4
mM cadmium (n=6). An outward current seen at positive voltage commands was
probably carried by cations passing outward through the calcium channel [8,9]
and was absent when N-methyl-D-glucamine was substituted for Tris in the
electrode solution (n=2)."p.176. 		Fig.1 p.176 - 974817158 -806603121
-806603121 -806603121 974903425 High-threshold calcium Ca2+ - - - - - - "Table I lists the responses of currents to application of divalent ions and
organic compounds. The high-threshold currents were more sensitive than the
low-threshold currents to block by Cd2+, while the reverse was true for Ni2+.
Replacement of external Ca2+ by Ba2+ incresed the maximum high-threshold
current and shifted it it approximately 10 mV to the left on the I-V curve.
The low-threshold current was reduced in Ba2+. Nimodipine (Sigma) supressed
both the low-threshold and the high-threshold currents (Fig.2A). Racemic BAY K
8644 (Miles Labs.) had an agonist effect which was most pronounced at command
potentials negative to the maximum of the I-V curve (e.g. Fig. 2B). The
increase at the point of maximum inward current was smaller and more variable
(mean 16%), and the current was reduced at positive potentials. There was no
consistent effect on the low-threshold current. Omega-Conotoxin GVIA
(Peninsula Labs.) reduced the high-threshold current only (Fig. 2C).
Nimodipine and omega-conotoxin attenuated the currents without any voltage
shift in the I-V curves. The effects of all substances were reversed by
washing, except for omega-conotoxin, from which there was only a slight
recovery".pp.176-177. 		Table 1, Fig.2 p.177 No attempt to separate into subcomponents of Ca-conductances. 974903425 -806603121
-806603121 -806603121 974903425 Low-threshold Ca Ca2+ - - - - - - "Table I lists the responses of currents to application of divalent ions and
organic compounds. The high-threshold currents were more sensitive than the
low-threshold currents to block by Cd2+, while the reverse was true for Ni2+.
Replacement of external Ca2+ by Ba2+ incresed the maximum high-threshold
current and shifted it it approximately 10 mV to the left on the I-V curve.
The low-threshold current was reduced in Ba2+. Nimodipine (Sigma) supressed
both the low-threshold and the high-threshold currents (Fig.2A). Racemic BAY K
8644 (Miles Labs.) had an agonist effect which was most pronounced at command
potentials negative to the maximum of the I-V curve (e.g. Fig. 2B). The
increase at the point of maximum inward current was smaller and more variable
(mean 16%), and the current was reduced at positive potentials. There was no
consistent effect on the low-threshold current. Omega-Conotoxin GVIA
(Peninsula Labs.) reduced the high-threshold current only (Fig. 2C).
Nimodipine and omega-conotoxin attenuated the currents without any voltage
shift in the I-V curves. The effects of all substances were reversed by
washing, except for omega-conotoxin, from which there was only a slight
recovery".pp.176-177. 		Table 1, Fig. 2 p.177 Authors claim similarity to T-current (p.177). 974903425 -806603121
-781327707 -781327707 986573713 I(h) Cations - - - - - - "..., whereas in patches from apical dendrites the magnitude of this slow
inward current increased as recordings were made more distally from the soma
(slope of linear regression 9 pA/100 µm; Fig. 1B)." 		Fig.1B. p.3178 - 986573713 -781327707
-625879160 -625879160 1006622979 I(A) K+ - - about -66 mV - - - "Two general classes of outward current were seen in cell-attached patches, as
in nucleated patches. A fast transient current resembled I(A) (Fig. 1A). This
current, when present in a cell-attached patch, was very consistent in all its
properties (below)."p.612

"In some patches, particularly those containing many channels, a mixture of
I(A) and I(K) was seen (Fig. 1D). The same kinetic diversity was also apparent
in outside-out patches (not illustrated)."p.613 		Fig. 1 pp.612-613 - 1006622979 -625879160
-625879160 -625879160 1006622979 I(K) K+ - - -82+-6 mV - - - "Two general classes of outward current were seen in cell-attached patches, as
in nucleated patches. ... A slow transient or plateau current was also
observed, which may correspond to I(K) (Fig. 1B and C). Surprisingly, however,
the I(K)-like current was variable in its inactivation behaviour: in some
cell-attached patches it inactivated like I(K) in nucleated patches (Fig. 1C);
in other patches it did not inactivate at all during a 500 ms test pulse (Fig.
1B). In some patches, particularly those containing many channels, a mixture
of I(A) and I(K) was seen (Fig. 1D). The same kinetic diversity was also
apparent in outside-out patches (not illustrated)."pp.612-613 		Fig. 1 pp.612-613 - 1006622979 -625879160
-381558745 -381558745 986573713 I(h) Cations - - -7.94+-0.77 mV -70.0 mV -92 mV -110 mV - Fig.1 pp.3178-79 Also values on steepness coefficients, activation/deactivation timeconstants 986573713 -381558745
-342234224 -342234224 -1051416814 I(Ca) Ca2+ - - - - - - "To verify directly that increases in dendritic [Ca2+]i result from Ca2+ influx
through voltage-gated Ca2+ channels, iontophoretically evoked changes in
dendritic [Ca2+]i were compared before and after the addition of the Ca2+
channel blocker Cd2+ in three cells. Typical results are shown in Fig. 5. The
iontophoretic current that evoked the plateau and rise of [Ca2+]i shown in
Fig. 5A evoked only a passive membrane potential response and little or no
increase in [Ca2+]i in the presence of 200 µM Cd2+ (Fig. 5B). In this and each
cell tested, a subthreshold iontophoresis also evoked a significant rise of
[Ca2+]i that was also blocked by Cd2+ (data not shown]."pp.509-510 		Fig. 5 pp.509-510 - -1051416814 -342234224
-342234224 -342234224 1004695855 I(Ca) Ca2+ - - - - - - "From the pseudocolor plot, it can be seen that the largest rise in [Ca2+]i
occured at the iontophoretic site (indicated by dashed line on pseudocolor
plot). During the initial Ca2+ and Na+ spikes, [Ca2+]i increased above resting
levels at locations both proximal and distal to the iontophoretic site.
Following these initial spikes, [Ca2+]i decayed to the resting level at these
proximal and distal locations, whereas [Ca2+]i remained above the resting
level near the iontophoresis site for the remainder of the iontophoresis.
After the iontophoresis was terminated, [Ca2+]i decayed to baseline. In this
and all cells examined, an iontophoresis that was subthreshold for either the
plateau or the initial transient Ca2+ spike caused an increase of [Ca2+]i, and
the largest rise in [Ca2+]i ocurred near the iontophoretic site.
In Fig. 2C, the plateau was evoked (red trace at bottom) during a larger [-70
nA) iontophoresis at the same site. As indicated by the pseudocolor plot (Fig.
2C, top), during and immediately after the initial Ca2+ and Na+ spike the
spatial-temporal increase of [Ca2+]i was similar to that of Fig. 2B.
Subsequently, when the plateau was evoked, the increase of [Ca2+]i at the
iontophoretic site was larger than during the subthreshold response of Fig. 2B
or the subthreshold portion of the response that preceeded the plateau in Fig.
2C. In addition, [Ca2+i] rose above its rest value both proximal and distal to
the iontophoretic site following plateau initiation, and this rise persisted
for the duration of the plateau. Thus the plateau was associated with a
[Ca2+]i rise that differed from a subtreshold response in both magnitude and
spatial extent.
Our primary finding is that the rise of [Ca2+]i associated with plateau
generation declined with distance from the iontophoretic spike, both
proximally and distally. This same pattern, highest around the iontophoretic
site and lower at the proximal and distal boundaries of the imaged region, was
evoked during plateau generation in all recorded cells. Assuming for the
moment that the rise of [Ca2+]i is caused entirely by Ca2+ influx through
voltage-gated channels, these results imply that dendritic membrane potential
(i.e., plateau amplitude) also declined with distance. That is, the plateau
propagates decrementally both proximal and distal to its site of initiation.
In contrast, a regenerative response that propagated actively with constant
amplitude, like a Na+ spike propagating down the axon, would be expected to
result in a similar rise of [Ca2+]i along the whole region of active
propagation. The assumptions on which this conclusion is based were tested in
experiments described in the following text."p.507

"Based on the observations and rationale described in the preceeding text, the
proximal and distal extent of the active plateau-generating region was defined
as the most proximal an distal extent of the 50%-of-peak contour line during a
plateau. Using this criterion, the active plateau-generating region was
remarkably small but of similar magnitude among the cells tested. Active
plateau initiation extended 50 µm proximally and 38 µm distally from the
iontophoretic site in the experiment in Fig. 2C. Plateaus were evoked on the
apical dendrite of 12 cells bathed in physiological saline. Data from these 12
plateaus are plotted as squares in Fig. 4. ... In these experiments, the
proximal extent of active initiation ranged from 20 to 113 µm (mean: 63.2 µm),
and the distal extent ranged from 10 to 207 µm (mean: 51.4 µm). The proximal
and distant extents were not significantly different (P = 0.47, paired,
2-tailed, Students t-test).
The plot of Fig. 4 also shows that the plateaus were evoked over the whole
extent of the apical dendrite examined (from 178 to 648 µm from the soma), and
all plateaus were centered spatially on about the iontophoretic site. The
ability to evoke plateaus at sited over this length of the apical dendrite
indicates that Ca2+ channel density is adequate for plateau generation over
(at least) this length of the apical dendrite."p.508

""Since the peak rise of [Ca2+]i always ocurred around the iotophoretic site
at all locations tested (from 178 to 648 µm on the apical dendrite; cf. Fig.
4), it is unlikely that the plateaus were initiated at discrete "hot spots" on
the dendrite. These results strongly suggest that CDRPs can be initiated at
any point on the main apical trunk where the membrane potential reaches
plateau threshold."p.510 		Fig. 2, 3, 4 pp.506-508, 510 No Ca2+ channel "hotspots", - uniform distribution. 1004695855 -342234224
-342234224 -342234224 1023579893 I(Ca) Ca2+ - - - - - - "To confirm that Ca2+ influx through NMDA channels was not a major influence on
the measured rise in [Ca2+]i and to additionally test whether the
voltage-gated Na+ channel activity might influence the initiation site or
spatial extent of the plateau, plateaus were evoked in an additional 10 cells
bathed in 100 µM AP-5 plus 1 µM TTX. Figure 5 illustrates typical results when
both Na+ channels and NMDA receptors were blocked. Plateaus were evoked in
each cell tested under these conditions, and the spatio-temporal pattern of
the rise of [Ca2+]i and the spatial extent of these plateaus were similar to
those obtained in physiological saline. In these experiments, the estimated
proximal extent of the plateaus ranged from 15 to 88 µm (mean: 53.1 µm) and
the distal extent ranged from 22 to 146 µm (mean: 49.5 µm). These values were
not significantly different from those obtained in physiological saline (for
proximal extent P = 0.46; for distal extent P = 0.94; 2-tailed Student's
t-test). As found for physiological saline, the proximal extent of plateaus
evoked in AP-5 plus TTX was not significantly different from teh distal extent
(P = 0.81, 2-tailed Students t-test). Data obtained from plateaus evoked in
AP-5 plus TTX are plotted as triangles in Fig. 4 for comparison with plateaus
evoked in physiological saline."p.509 		Fig. 4, 5 p.509-510 - 1023579893 -342234224
-51689092 -51689092 999521822 CaT Ca2+ - 47+-31 pA - ~ -60 mV - ~ -30 mV "When the depolarizing commands were preceeded by an 800 ms hyperpolarizing
prepulse to -100 mV, there was an additional transient component of inward
current, with a threshold for activation at about -60 mV (low-threshold or
T-type Ca2+ current). The I-V relation for this current (the difference
between the records with and without the prepulse) is plotted as open circles
for the example cell in Fig. 2B. The maximum low-threshold current was evoked
at about -30 mV and was 47+-31 pA (n = 30; excludes 2 cells in which the
current was absent or unmeasurably small, and one in which the leak
subtraction was unsatisfactory)."p.1598

"Steady-state inactivation of the low-threshold Ca2+ current was examined in
four neurons by stepping to a constant test voltage from various prepulse
potentials (each 800 ms duration). Figure 3A shows the inactivation curve
based on data from four cells and example records from one cell. In each
neuron the maximum current was normalized to 1.0 (i.e., inactivation fully
removed), and the data points were then averaged across cells. A Boltzmann
curve was fitted by an algorithm that minimized the sum of squared errors. The
slope factor for the fitted curve was 5.4 mV per e-fold change. The
low-threshold current was almost fully inactivated at -70 mV; inactivation was
half removed at -86 mV and fully removed at about -110 mV."p.1599

"The time course for removal of inactivation of the low-threshold current was
investigated in two neurons. The results from one are shown in Fig. 3B. The
low-threshold current was evoked after hyperpolarizing prepulses of constant
amplitude [to -95 mV in one cell (Fig. 3B) and -110 mV in the other]. In both
cases removal of inactivation occured over hundreds of milliseconds and
appeared almost complete by 800 ms (these cells became progressively leaky
when the durations of hyperpolarizations exceeded 1 s, so longer prepulses
were not examined). These findings indicate that both strong (more negative
than -100 mV) and prolonged (hundreds of ms) hyperpolarization is required for
inactivation of the low-threshold current to be fully removed."p.1599 		Fig. 2, 3 pp.1598-1599 - 999521822 -51689092
-51689092 -51689092 999521822 HVA-Ca Ca2+ - 428+-233 pA >+40 mV ~-45 mV - -10 - -20 mV "From the holding potential of -60 mV, depolarizing current commands evoked a
slowly inactivating inward current, with a threshold at about -45 mV and a
maximum between -10 and -20 mV (high-threshold current; Fig.2, [filled
triangles]). The peak current at the maximum of the I-V was 428+-233 pA for
the pyramidal neurons (n = 33). The currents usually reversed positive to
about +40 mV in the Tris-PO4 internal solution (and at more positive
potentials with the N-methyl-D-glucamine internal solution), probably due to
the outflow of internal cations. The rate of inactivation was variable between
cells, and no attempt was made to quantify it in the experimental situation
with artificial internal Ca2+ buffering."p.1598 		Fig. 2 p.1598 - 999521822 -51689092
-51689092 -51689092 1841045319 CaL Ca2+ - - - - - - "Nifedipine (10 µM) inhibited 48 +-16% of the control amplitude of the
high-threshold current (n = 6; this includes one nonpyramidal neuron in which
the current suppresion was 57%). In three cells tested with 10 µM nimopidine
the Ca2+ current reduction was 43 +- 7.2%. The effects of nifepidine and
nimopidine were reversible."p.1600

"Single-channel studies in other mammalian neurons have attributed ... the
dihydropyridine-sensitive component to L-type channels (Hess 1990), although
concentrations of dihydropyridine Ca2+ antagonists that fully-inhibit L-type
current may weakly suppress other current components as well (Regan et al.
1991)."p.1603 		Fig.4, 5 p.1600, 1603 - 1841045319 -51689092
-51689092 -51689092 1841045319 CaN Ca2+ - - - - - - "In four cells, omega-CgTX (16 µM) reduced the peak Ca2+ current by 21 +- 5.1%
with only slight recovery on washing."p.1600

"Single channel studies in other mammalian neurons have attributed the
omega-CgTX-sensitive component to N-type channels..."p.1603 		Fig. 4 p.1600, 1603 - 1841045319 -51689092
-9806123 -9806123 -232296371 I(Na) Na+ - - - - - - "Fig. 3B, location 1 shows Na+ channel currents (single traces and the ensemble
average) activated by voltage commands in a somatic patch, and Fig. 3B,
location 2 shows comparable recordings from a dendritic patch about 80 µm away
(see locations 1 and 2 in Fig. 3A). Fig. 3B, locations 3 and show recordings
from 2 additional sites [located at the junction of soma and apical dendrite
(location 3 if Fig. 3 A and B) and further distal on the dendrite (location 4
in Fig. 3 A and B)] from the same neuron. Note that although there was Na+
channel activity at each location, the density of channels was not precisely
equivalent at all locations. For example, the dendritic location in Fig. 3A,
location 4 had an unusually high level of Na+ current; this would be
indicative of a " hot spot" (16, 17). All recordings showed transient (about 1
msec) inward openings that were activated in a similar pattern by each voltage
command at a given site (compare sequential sweeps in each vertical column of
Fig.3B)." 		Fig.3 pp.2475-2476 - -232296371 -9806123
-9806123 -9806123 987614460 I(Na) Na+ - - - - - - "The relative density of Na+ currents in proximal (som-basilar dendritic ) and
distal apical dendritic was similar. Regression analysis showed that there was
a significant correlation between area and Na+ current (Fig.2D and Table 1)."

"By using data obtained from differential perfusion experiments, it was also
possible to determine whether there were significant differences between the
properties of Na+ currents on somatic and dendritic membranes....In each case,
no significant differences in theses parameters were found between somatic and
dendritic membranes." 		Fig.2, Table 1. pp.2474-2475 - 987614460 -9806123
5642164 5642164 986573713 I(h) Cations - - - - - - "...Recordings made from axonal and somatic patches revealed little or no slow
inward current..." 		Fig.1B p.3178   986573713 5642164
35614620 35614620 -20718951 I(Na) Na+ 109+-39 pS/µm^2 - - -55 mV -30.6+-2.8 mV - - Table 1-2;Figs. 6-9 - Kinetic parameters fitted; biexponential decay; ratio of slow to fast component
of Na-current = 0.19+-0.030 		-20718951 35614620
35614620 35614620 974208830 I(Na) Na+ - - - - - - "The biexponential nature of Na+ current decay was verified by recording
single-channel Na+ currents from cell-attached patches. Examples of
single-channel currents from a P10 neuron are shown in Fig.10B. Single-step
depolarizations resulted in a barrage of early channel openings, as well as
late individual events with latencies of up to tens of milliseconds.
Occasionally bursts of openings were seen that lasted the duration of of the
depolarization. Ensemble averages of Na+ channel currents demonstrated two
decay components, with similar time constants to those obtained with
whole-cell clamp currents (Fig.10B). No significant differences in the
amplitudes of the early and late single-channel openings could be
detected."pp.790-791. 		Fig.10 pp.790-791 - 974208830 35614620
216257617 216257617 -862865877 I(A) K+ - - - - -31 mV - - Fig.5 pp.55-57 Data from P1 rat. Also data on half-inactivation. -862865877 216257617
216257617 216257617 -862865877 I(K) K+ - - - - - - "...with external and internal solutions (see Table 1) that minimized the
contribution of Ca2+-activated K+-currents, which are not studied here."

"The differences (see legend, Fig. 5A) between the transient and sustained
current are essentially similar to differences reported previously for the A
current and the delayed rectifier, with the A current showing activation and
steady state inactivation at relatively less depolarized potentials and the
delayed K current showing only incomplete inactivation at positive voltages
(Adams et al., 1980; Adams and Galvan, 1984)." 		Fig.4 pp.55-57 Currents in response to voltage steps, normalized current densities (early and
late component) in Fig. 4. 		-862865877 216257617
216257617 216257617 -862865877 I(Kdr) K+ - - - - 10 mV - - Fig. 5 pp.55-57 Data from P1 rat. Also data on half-inactivation. -862865877 216257617
216257617 216257617 -754473072 I(CaL) Ca2+ 40 pS/µm^2 - - - -10 mV - - Fig.6, 7 pp.57-59 Data from P11 rat. Plots of response to voltagesteps, I-V curves, fits. -754473072 216257617
216257617 216257617 -754473072 I(CaT) Ca2+ 20 pS/µm^2 - - - -70 mV - - Fig.6, 7 pp.57-59 Data from P11 rat. Plots of response to voltagesteps, I-V curves, fits. -754473072 216257617
216257617 216257617 1693123346 I(Na) Na+ - - - - - - "However, there is a developmental change in activation in inactivation
kinetics that is evident in both cell types (Huguenard et. Al., 1988). This is
indicated by the residual Na+ current that remains at the end of the 15-ms
current pulse in the P55 neuron but which is absent in the E18 neuron (i.e.
compare current levels at the arrows in Fig. 3A)."

"By contrast, in the mature neuron, complete decay took approximately 10 times
longer and was best fitted with 2 exponentials with fast (3-1 msec) and slow
(30-10 msec) time constants." 		Fig.3 pp.52-55 Responses to voltage steps, normalized conductance densities, steady state
inactivation and peak activation curves and recovery time course plots in
Fig.3. 		1693123346 216257617
406866101 406866101 -1756532732 INa Na+ - - 22.2+-2.7 mV ~ -65 mV -44.8+-1.9 mV - "After papain produced its full effectr, INa became larger at negative
potentials (Figs. 1A, and 2, A and B) and was evoked by depolarizations that
evoked no transient current in control records (starting at about -65 mV for
the cell of Fig. 1A). Papain resulted in a leftward shift of the activation
curve by 7.2 mV in this cell (Fig. 1B). A similar leftward shift (averaging
6.4 mV; see Table 1) was seen in each of the seven cells tested. Peak INa
became 32% larger on average, but there was no significant change in ENa, Gmax
or the slope of the activation curve (see Table 1).
Figure 2, A and B shows how papain modified the time-course of INa during
small and large depolarizations. INa persisted throughout either
depolarization with little decrement from its peak value. During either
depolarization the initial rate of rise of INa was unchanged, but the time to
reach peak current was much greater for the small depolarization (Fig. 2A)
than for the large depolarization (Fig. 2B)."p.2564 		Fig. 2, Table 1 p.2564 Papain removes the inactivation of fast sodium channels. -1756532732 406866101
406866101 406866101 -850117393 INa Na+ - - 25.1+-1.6 mV ~ -55 mV -43.5+-1.1 mV ~ -30 mV "INa was first detected near -55 mV and peaked near -30 mV. ... In five
experiments the activation of INa and INaP were compared in the same cell. In
each cell INaP was first detected at potentials 5-12 mV more negative than for
INa (mean values: -65.2 mV for INaP; -56.6 mV for INa)."p.2564 		Fig. 1, Table 1 pp.2563-2564 I-V relationships and activation curves in Fig. 1. -850117393 406866101
406866101 406866101 1000211302 INaP Na+ - - - ~ -65 mV -50.4+-1.4 mV ~ 40 mV "INaP both activated and peaked at more negative potentials (near -65 and -40
mV, respectively) than INa. In five experiments the activation of INa and INaP
were compared in the same cell. In each cell INaP was first detected at
potentials 5-12 mV more negative than for INa (mean values: -65.2 mV for INaP;
-56.6 mV for INa)."p.2564 		Fig. 1, Table 1 pp.2563-2564 I-V relationships and activation curves in Fig. 1. 1000211302 406866101
481039627 481039627 -1020917390 I(NaP) Na+ - (Fig. 2) - about -60 mV - -40 to - 35 mV "As has also been found for the fast INa during development (Huguenard et al.
1988), the voltage dependence of INaP activation did not change during the
time frame of out study. However, INaP seemed to increase in magnitude during
development (Fig. 1A)."

"As shown in the histogram of Fig. 2A, the strongest increase in INaP
amplitude ocurred between aoung and juvenile rats where the mean peak INaP
amplitude more than doubled, whereas a smaller increase was seen from juvenile
to mature rats."

"Surprisingly, only a rather weak correlation (r=0.61)was found between age
amd maximal current density." 		Fig. 1, 2. pp.291-292 Persistent sodium current was completely blocked by TTX. -1020917390 481039627
987005279 987005279 986573713 I(h) Cations - - - - - - "...Recordings made from axonal and somatic sites revealed little or no slow
inward current..." 		Fig.1B p.3178 - 986573713 987005279
987681444 987681444 987614460 I(Na) Na+ - - - - - - "The relative density of Na+ currents in proximal (som-basilar dendritic ) and
distal apical dendritic was similar. Regression analysis showed that there was
a significant correlation between area and Na+ current (Fig.2D and Table 1)."

"By using data obtained from differential perfusion experiments, it was also
possible to determine whether there were significant differences between the
properties of Na+ currents on somatic and dendritic membranes....In each case,
no significant differences in theses parameters were found between somatic and
dendritic membranes." 		Fig.2, Table 1. pp.2474-2475 - 987614460 987681444
987766595 987766595 -192623055 I(NaP) Na+ - - - - - - "Apparently, the continous Na+ influx associated with INaP was required to
cause a detectable rise of [Na+]i."

"In each neuron tested, INaP-associated reductions of fluorescence in the
apical dendrites were detecable as far as the dye could be visualized
(distance from soma: 50-300 µm, n = 12)." 		Fig.1, 2 p.1190 Amplitude of induced plateau depolarization (PD) during current pulse 54.2+-5.5
mV. 		-192623055 987766595
988292479 988292479 -862865877 I(K) K+ - - - - - - "...with external and internal solutions (see Table 1) that minimized the
contribution of Ca2+-activated K+-currents, which are not studied here."

"In more mature nonpyramidal cells, a transient current did not appear, but
the sustained current became larger."

"The differences (see legend, Fig. 5A) between the transient and sustained
current are essentially similar to differences reported previously for the A
current and the delayed rectifier, with the A current showing activation and
steady state inactivation at relatively less depolarized potentials and the
delayed K current showing only incomplete inactivation at positive voltages
(Adams et al., 1980; Adams and Galvan, 1984)." 		Fig.4 pp.55-57 Currents in response to voltage steps, normalized current densities (early and
late component) in Fig. 4. 		-862865877 988292479
988292479 988292479 -754473072 I(CaL) Ca2+ 60 pS/µm^2 - - - -10 mV - - Fig.6, 7 pp.57-59 Data from P11 rat. Curves of response to voltage-steps, I-V curves, fits. -754473072 988292479
988292479 988292479 -754473072 I(CaT) Ca2+ 5 pS/µm^2 - - - -65 mV - - Fig. 6, 7 pp.57-59 Data from P11 rat. Curves of response to voltage-steps, I-V curves, fits. -754473072 988292479
988292479 988292479 1693123346 I(Na) Na+ - - - - - - "However, there is a developmental change in activation in inactivation
kinetics that is evident in both cell types (Huguenard et. Al., 1988). This is
indicated by the residual Na+ current that remains at the end of the 15-ms
current pulse in the P55 neuron but which is absent in the E18 neuron (i.e.
compare current levels at the arrows in Fig. 3A)."

"By contrast, in the mature neuron, complete decay took approximately 10 times
longer and was best fitted with 2 exponentials with fast (3-1 msec) and slow
(30-10 msec) time constants." 		Fig.3 pp.52-55 Responses to voltage steps, normalized conductance densities, steady state
inactivation and peak activation curves and recovery time course plots in
Fig.3. 		1693123346 988292479
989418859 989418859 -1662948559 I(Na,p) Na+ - - - -60 mV -46.9 mV -30 mV - Fig.1 p.109 Fit to Boltzmann. -1662948559 989418859
989418859 989418859 -1357204228 I(Ca) Ca2+ - - - - - - "The current traces and I-V relationship of the total Ca2+ currents under
control conditions and during ATX II perfusion are shown in Fig.2B, which also
includes a T-type current, as the recording steps were preceded by a 100 ms
hyperpolarizing prepulse at -100 mV." 		Fig.2 pp.109-110 I-V plot. -1357204228 989418859
989418859 989418859 -1322394210 I(Na,f) Na+ - < 1 nA - -60 mV -27.5 mV -15 mV - Fig.1 pp.107-109 Also fit to Boltzmann distribution in fig.1. Inactivation parameters. -1322394210 989418859
989418859 989418859 732686535 I(K) K+ - - - - - - "The current traces traces shown in the figure include Ca2+ -activated K+
currents, as the Ca2+ currents were not blocked but hidden by the outward
current." 		Fig.2 p.109 I-V plot. 732686535 989418859
999088458 999088458 -231029841 CaL Ca2+ - - - - -19+-11/-17+-7 mV - "We operationally defined L-type current as that blocked by a saturating dose
of the DHP antagonist Nif,..."p.1433

"In adult neurons, Nif (5 µM) blocked an average of 32+-15% (n = 40) of the
peak whole cell calcium current (Figs. 4 and 5)."p.1433

"We found that the Nif sensitive current contributed ~30% to the whole cell
calcium current."p.1438 		Fig. 4, 5, 6, 7, 8, 9. Table 1. - Details on activation, deactivation and inactivation in table 1. Ba2+ used as
charge-carrier in experiments. 		-231029841 999088458
999088458 999088458 -231029841 CaN Ca2+ - - - - -17+-8/-16+-7 mV - "We operationally defined...N-type current as that blocked by a saturating dose
of CgTx,..."p.1433

"HVA currents in adult cells were also reduced by CgTx (Fig. 4). CgTx (1 µM)
blocked 33 +- 14% (n = 22) of the whole cell current."p.1434

"In acutely isolated sensorimotor neurons, the CgTx-sensitive current
contributed ~33% to the whole cell calcium current."p.1438 		Fig. 4, 5, 6, 7, 8, 9. Table 1. - Details on activation, deactivation and inactivation in table 1. Ba2+ used as
charge-carrier in experiments. 		-231029841 999088458
999088458 999088458 -231029841 CaP Ca2+ - - - - -20+-7/-15+-7 mV - "We operationally defined... P-type current as that blocked by a saturating
dose of AgTx..."p.1433

"AgTx also reduced the HVA currents (Figs. 4 and 5); 100 nM AgTx blocked 36 +-
16% (n = 18) of the peak current."p.1434

"A third HVA current in rat neocortical neurons was isolated by its
sensitivity to omega-AgTx-IVA (P-type channels). In rat sensorimotor neurons
we found that AgTx blocked 36% of the peak calcium current (see also Brown et
al. 1994; 33% block)."p.1438 		Fig. 4, 5, 6, 7, 8, 9. Table 1. - Details on activation, deactivation and inactivation in table 1. Ba2+ used as
charge-carrier in experiments. 		-231029841 999088458
999088458 999088458 -231029841 HVA-Ca (Nif, CgTx, AgTx res) Ca2+ - - - - -22+-6/-25+-6 mV - "We operationally defined ... resistant current as that current remaining in
the presence of the combination of saturating doses of Nif, CgTx, and
AgTx."p.1433

"An average of 80 +- 11% (n = 9) of the whole cell current was blocked when
Nif, CgTx, and AgTx were applied simultaneously (Fig. 5), with ~20% of the
whole cell current resistant to a combination of these blockers."p.1434

"Our data are consisten with the resistant current being at least partially
due to Q-type current, although the voltage dependency of activation for the
current induced in Xenopus oocytes be injection of the rbA alfa-subunit in the
Sather et al. study (Sather et al. 1993) was shifted to positive voltages
versus that for the L-type current (rbC alfa-subunit)."p.1440 		Fig. 4, 5, 6, 7, 8, 9. Table 1. - Details on activation, deactivation and inactivation in table 1. Ba2+ used as
charge-carrier in experiments. 		-231029841 999088458
999088458 999088458 999005478 HVA-Ca Ca2+ - - - -45 mV -17 +- 1 mV - "Two millimolar Ca2+ is close to the physiological concentration of
extracellular Ca2+. We found that currents obtained with 5 mM Ba2+ exhibited
similar voltage dependence of activation to those obtained with 2 mM Ca2+.
Thus the I-V relationships obtained for 5 mM Ba2+ in this study are likely to
be typical of those for Ca2+ currents under more physiological
conditions."p.1433

"Our principal findings were as follows. 1) Neocortical pyramidal cells
express L-, N-, and P-type calcium channels, as well as a component resistant
to specific blockers of those channels. 2) There were no significant
biophysical differences between physiologically defined L-, N-, and P-type
current components. 3) The resistant current had a shorter time to peak
activation, greater percent inactivation, more rapid inactivation kinetics,
and more negative voltage dependence of activation compared with the other
three types."p.1437

"These results of the present studies are limited to the soma and proximal
dendritic membranes due to the dissociation procedure, and voltage-gated
calcium channels appear to be differentially localized to different parts of
the cell (L-type channesl primarily on soma and proximal dendrites and N- and
P-type channels primarily on distal dendrites) (Ahlijanian et al. 1990;
Westenbroek et al. 1990, 1992, 1993). It is therefore likely that N- and
P-type currents contribute relatively more to the Ca2+ influx of the entire
cell than is suggested by our data."p.1441 		Fig. 1, 2, 3. pp.1432-1433. Ba2+ used in pharmacological experiments with the HVA Ca2+ currents. 999005478 999088458
1000126375 1000126375 -847634651 Ca Ca2+ - - - - - - "Addition of 2-amino-5-phosphonovaleric acid (APV 50-100 µM), an antagonist of
N-methyl-D-aspartate receptors (NMDARs) blocked the initiation of dendritic
action potentials (Fig. 6A and B), and attenuated the peak amplitude of the
associated [Ca2+]i transients (Fig. 6C and D; n=9). Initiation of both Ca2+
action potentials by distal synaptic stimulation and the associated [Ca2+)i
transients were completely blocked by addition of the
alfa-amino-3-hydroxy-5-methyl-4-isoxazolepropionate receptor (AMPAR)
antagonist 6-cyano-7-nitroquinoxaline-2,3-dione (CNQX; 10 µM) to the
extracellular solution (Fig. 6 B and D; n=3). CNQX also reduced the amplitude
of synaptically evoked composite PSPs in dendrites and the soma (not
shown)."p.611

"The dependence of local distal dendritic action potential initiation and the
associated [Ca2+]i transient on activation of NMDA receptors probably resulted
from the relatively slow activation and inactivation kinetics of NMDA
receptors. Thus, it is possible that a train of AMPA-mediated EPSPs could also
evoke Ca2+ actio potentials in distal apical dendrites."p.611 		Fig. 6 p.611 - -847634651 1000126375
1000126375 1000126375 -62810572 Na Na+ - - - - - - "Voltage-dependent Na+ channels contributed also to the initiation of the
dendritic action potentials, as addition of TTX (1 µM) to the bath solution
increased the threshold for action potential initiation by distal current
injection. Dendritic regenerative potentials could still be initiated by
distal synaptic stimulation when voltage-activated Na+ channels were blocked
by dialysis od the neuron with QX-314 (Fig. 5A; 5-10 nM, n=3) or in the
presence of TTX (1 µM) following distal dendritc current injection (Fig. 5B,
n=3)."p.610 		Fig. 5 p.610 - -62810572 1000126375
1000126375 1000126375 999704296 Ca Ca2+ - - - -26.4+-1.9 mV - - "Synaptic stimulation was made via electrodes which had their tips located
either close to the distal branches (layers 1-2) or to the proximal apical
dendritic branches (layers 5-6). Fluoroscence imaging indicated that
stimulation of distal synapses in layers 1-2, which elicited a subtreshold PSP
at the soma, could evoke a large [CA2+]i transient that peaked in the distal
apical branches and gradually decreased in amplitude to undetecable levels
along the main apical trunk (Fig. 2A). The distal dendritic [Ca2+]i transients
(measured at a dendritic region more than 600 µm away from the soma) were
significantly larger than those evoked by either synaptic stimulation of the
proximal apical dendrite (100-300 µm lateral to the somam Fig. 2B and C) or by
action potentials initiated in the axon (by somatic current injection) which
then back-propagate into the distal dendrites (average peak delta(F)/F
amplitude of 16+-15% and average delta(F)/F decay time constant of 338+-54 ms,
n=6). Thus synaptic stimulation which evoked regenerative all-or-none
potentials in the distal dendritic branches, but only subthreshold PSPs at the
soma, elicited a [Ca2+]i transient which remained largely localized to the
distal apical dendrites."p.607

"Simultaneous measurement of dendritic membrane potential (Fig.3C, upper
traces) and dendritic [Ca2+]i transients (Fig.3C, lower traces) evoked by
current injection into distal dendrites via the recording pipette showed that
a transient increase in [Ca2+]i was detectable already at potentials below -30
mV (Fig.3D). Both, the membrane voltage and the [Ca2+]i fluorescence transient
increased abruptly when the stimulus intensity was increased and threshold was
reached (Fig.§C and D). The average threshold potential for the initiation of
all-or-none events was 26.4+-1.9 mV in seven recordings made 700-820 µm for
the soma (Fig. 3C). The largest increase in dendritic [Ca2+]i amplitude
ocurred concomitantly with the initiation of all-or-none regenerative
potential (Fig. 3C and D). The peak of the [Ca2+]i fluorescence transient did
not increase further with increasing stimulus intensity even when a somatic
action potential was initiated by the stimulus, possibly reflecting
significant non-linearity of the fluorescence indicator. Similar imaging
results were obtained in one additional neuron."p.610 		Fig. 2, 3 p.607, p.610 - 999704296 1000126375
1000126375 1000126375 999786975 Ca Ca2+ - - - - - - "Addition of Cd2+ (200 µM) to the bath solution blocked both dendritic
regenerative potentials and dendritic [Ca2+]i transients initiated by distal
dendritic current injection (Fig. 4, n=7). This indicated that these responses
were caused by the activation of voltage-dependent Ca2+ chanels and supports
the view that the dendritic regenerative potentials represent local Ca2+
action potentials."p.610 		Fig. 4 p.610 - 999786975 1000126375
1004375359 1004375359 315966505 I(CaL) Ca2+ - - - - - - "Dihydropyridine antagonists are relatively selective for L channels..."p.1533

"Mean reduction of the HVA current was 31% (range 22-50%, n = 6, P < 0.001)
for 5 µM nifedipine..."p.1534

"Both agents reduced the HVA current uniformly with no shift of the threshold
of maximum current (Fig. 5, B and D). This fact alone suggests that the
voltage dependencies of the residual components do not differ significantly
from the blocked components and was confirmed by comparison of the activation
curves constructed from tail currents (not shown)."p.1534 		Fig. 5, 7 p.1533-1534 - 315966505 1004375359
1004375359 1004375359 315966505 I(CaN) Ca2+ - - - - - - "Whole-cell and single-channel recordings in mammalian neurons have provided
evidence that omega-CgTx blocks N channels specifically (Plummer et al. 1989;
Regan et al. 1991)."p.1533

"Mean reduction of the HVA current was ... 30% (range: 21-43%, n = 5, P <
0.001) for omega-CgTx."

"Both agents reduced the HVA current uniformly with no shift of the threshold
of maximum current (Fig. 5, B and D). This fact alone suggests that the
voltage dependencies of the residual components do not differ significantly
from the blocked components and was confirmed by comparison of the activation
curves constructed from tail currents (not shown)."p.1534 		Fig. 5, 7 p.1533-1534 - 315966505 1004375359
1004375359 1004375359 1003935176 HVA-Ca Ca2+ - 484.9+-42.3 pA - -45 mV - -15 mV "The evoked current was blocked completely and reversibly by 200 µM cadmium
(Fig.2 A) , but a small outward current was revealed at more depolarized
potentials (Fig. 2B). As previously described (Sayer et al. 1990), the HVA
current activated at potentials more positive than -45 mV and peaked near -15
mV. Maximum HVA current was 484.9 +- 42.3 pA, corrensponding to a current
density of 27.7 +- 2.4 µA/cm^2 assuming a uniform distribution of channels on
the membrane."p.1533 		Fig. 2 p.1533 Detailed information on activation/inactivation kinetics and tail-currents. 1003935176 1004375359
1006790213 1006790213 -2086957548 I(K,fast) K+ - - - - - - "This lack of sensitivity of the fast K+ current to TEA allowed us to further
investigate the kinetics of this current. The kinetics were quantified by
fitting the fast K+ current to a Hodgkin-Huxley model. To increase the tail
current amplitude the K+ concentration in the ACSF was increased to 65 mM.
This change in K+ did not change the activation or deactivation kinetics of
the fast K+ current (n = 7, data not shown). A Hodgkin-Huxley model with four
activation gates (Fig. 4B) best desribed the activation and deactivation time
course of the fast K+ current. The time constants, extracted from this
analysis, ranged from 0.31 +- 0.03 ms at +80 mV (n=5) and displayed a
bell-shaped dependence on voltage (Fig. 4C)."pp.625-626

"The inactivation time constant of the fast K+ current was measured by
mono-exponential fits to the decay phase of the current (Fig. 5A). Above -20
mV the inactivation time constant was not dependent on voltage with a mean
value of 8.0 +- 0.3 ms (n=5)."p.626

"The rate of recovery from inactivation ranged from 12.6 +- 1.5 ms (n = 5) at
-110 mV to 64 +- 11 ms (n = 4) at -70 mV."p.626

"4-AP (3 mM) reduced the maximal amplitude of both fast and slow K+ currents
as recorded following a voltage step to +80 mV (Fig. 6A). ... The
concentration of 4-AP yielding half the current observed under control
conditions was 4.2 +- 0.5 mM (Fig. 6B)."p.629 		Fig. 4, 5, 6 pp.624-626 - -2086957548 1006790213
1006790213 1006790213 -2086957548 I(K,slow) K+ - - - - - - "4-AP (10 mM) had no effect on the activation curve of the slow K+ current
(Fig. 7A). ... The activation kinetics of the slow K+ current were quantified
based on a Hodgkin-Huxley kinetic model in the presence of 9 mM 4-AP and 65 mM
K+ in the ACSF. A Hodgkin-Huxley model with two activation gates (Fig. 7B)
best described the time course of activation and deactivation of the slow K+
current. The time constants ranged from 2.4 +- 0.3 ms at +80 mV to 53 +- 4 ms
at -50 mV and were fitted with a single exponential above -50 mV and another
exponential below -50 mV."p.629

"The inactivation time constant of the slow K+ current was measured by fitting
the decay phase of the current to a double exponential function as shown in
Fig. 7A. ... The slow time constant, obtained from the double exponential
curve fit, was slightly voltage sensitive and had a relative contribution of
57 +- 5% to the current (n =5, Fig. 8D) that was independent of voltage. The
faster time constant was more dependent on voltage ranging from 1100 +- 80 ms
(n = 6) at -10 mV to 290 +- 50 ms (n = 4) at +80 mV. ... The time constant of
recovery from inactivation was calculated from mono-exponential fits of the
maximal current amplitude during the second depolarising voltage step. The
rate of recovery from inactivation ranged from 215 +- 12 ms (n = 6) at -110 mV
to 1240 +- 230 ms (n = 4) at -70 mV."pp.629-630

"This double pulse protocol revealed that 10 mM TEA reduced the amplitude of
the slow K+ current without significantly affecting that of the fast K+
current (Fig. 3A, n = 13)."p.624 		Fig. 3 p.624 - -2086957548 1006790213
1006790213 1006790213 -1610535617 I(K,fast) K+ 2.7 +- 0.5 pS/µm^2 - - - -3 +- 1 mV - "Subtraction of the currents obtained by the two voltage protocols revealed a
fast inactivating current (Fig. 1C). This "difference" current decayed with a
time constant of 8.2 +- 0.6 ms (n = 5) at +80 mV to a sustained current (Fig.
1C). ... The difference current (Fig. 1C) will be referred to as the "fast" K+
current ..."p.623 		Fig. 1, 2 p.623 Fit to Boltzmann functions, also for inactivation. -1610535617 1006790213
1006790213 1006790213 -1610535617 I(K,slow) K+ 6.6 +- 0.7 pS/µm^2 - - - -3 +- 1 mV - "This suggested that a 60 ms pre-pulse to -50 mV inactivated, in addition to a
fast inactivating K+ current, a current with slower inactivation kinetics. ...
while the current remaining after the -50 mV pre-pulse (Fig. 1B) will be
reffered to as the "slow" K+ current."p.623 		Fig. 1, 2 p.623 Fit to Boltzmann functions, also for inactivation. -1610535617 1006790213
1927746281 1927746281 1006622979 I(A) K+ - - - - - - "Plots of amplitude of I(A) and I(K) versus distance from the soma showed that
both types of conductance were rather uniformly distributed along the primary
apical dendrite, at least, for distances less than ~400 µm (Fig. 6B; n = 128
patches). The unconstrained fit of a straight line to the data points gave a
slope of 2.3 pA/100 µm for I(A) and -0.4 pA/100 µm for I(K)."p.615 		Fig. 6 p.615 K-channels in apical dendrite were activated by backpropagating action
potentials. 		1006622979 1927746281
1927746281 1927746281 1006622979 I(K) K+ - - - - - - "Plots of amplitude of I(A) and I(K) versus distance from the soma showed that
both types of conductance were rather uniformly distributed along the primary
apical dendrite, at least, for distances less than ~400 µm (Fig. 6B; n = 128
patches). The unconstrained fit of a straight line to the data points gave a
slope of 2.3 pA/100 µm for I(A) and -0.4 pA/100 µm for I(K)."p.615 		Fig. 6 p.615 K-channels in apical dendrite were activated by backpropagating action
potentials. 		1006622979 1927746281
2026686061 2026686061 -20718951 I(Na) Na+ 58.7+-12 pS/µm^2 - - ca. -55 mV -34.1+-1.7 mV - - Table 1-2; Figs. 6-9 - Kinetic parameters fitted; biexponential decay; ratio of slow to fast component
of Na-current = 0.25+-0.051 		-20718951 2026686061