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The Journal of Neuroscience, 1999, 19:RC33:1-5
RAPID COMMUNICATION
Activity-Dependent Regulation of Potassium Currents in an
Identified Neuron of the Stomatogastric Ganglion of the Crab
Cancer borealis
Jorge
Golowasch,
L. F.
Abbott, and
Eve
Marder
Volen Center and Department of Biology, Brandeis University,
Waltham, Massachusetts 02454
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ABSTRACT |
Identified neurons of the stomatogastric ganglion of the crab
Cancer borealis were voltage-clamped, and the current
densities of three K+ currents were measured. The
current densities of each of the three K+ currents
varied twofold to fivefold in inferior cardiac (IC) neurons from
different animals. Conventionally, this degree of variability has been
attributed to experimental artifacts. Instead, we suggest that it
reflects a natural variability that may be related to an underlying
process of plasticity. First, we found that there is no fixed ratio
among the three K+ currents. Second, we found that
several hours of stimulation with depolarizing current pulses (0.5 sec
duration at 1 Hz) altered the current density of the
Ca2+-dependent outward current,
IK(Ca), and the transient outward current, IA. This stimulation paradigm
mimics the normal pattern of activity for these neurons. The effect of
stimulation on the IA current density was
eliminated when Ca2+ influx was blocked by
extracellular Cd2+. In contrast, the
K+ current densities of the lateral pyloric (LP)
neuron were unaffected by the same pattern of stimulation, and the
currents expressed by both the IC and the LP neurons were insensitive
to hyperpolarizing pulses at the same frequency. We conclude that the
conductance densities expressed by neurons may vary continually
depending on the recent history of electrical activity in the
preparation, and that intracellular Ca2+ may play a
role in the processes by which activity influences the regulation of
current densities in neurons.
Key words:
potassium currents; transient outward current; delayed
rectifier; Ca2+-dependent K+ current; calcium signaling; crustacean; voltage clamp
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INTRODUCTION |
The
intrinsic electrical properties of neurons depend on the ionic currents
they express. Measurements of the densities of ionic currents
frequently exhibit high levels of variability from cell to cell (Liu et
al., 1998 ). This variability has traditionally been attributed to
recording artifacts. However, studies of multiconductance-based model
neurons show that very similar intrinsic patterns of activity can be
produced by neurons with different conductance densities (Liu et al.,
1998; M. S. Goldman, J. Golowasch, E. Marder, and L. F. Abbott, unpublished observations). Moreover, recent experimental and
theoretical work argues that neuronal electrical activity can regulate
and modify ionic conductances (Franklin et al., 1992; Abbott and
LeMasson, 1993; LeMasson et al., 1993; Siegel et al., 1994; Turrigiano
et al., 1994, 1995; Hong and Lnenicka, 1995, 1997; Liu et al., 1998;
Desai et al., 1999; Golowasch et al., 1999; Stemmler and Koch, 1999).
These results suggest that cells do not maintain fixed conductance
densities, but rather regulate their conductances to maintain a
characteristic pattern of activity, and that they do so in an
activity-dependent manner.
The regulation of ionic currents by electrical activity has been most
extensively studied in development or in cell culture (Turrigiano et
al., 1994, 1995; Desai et al., 1999). In this paper, we study different
identified neurons from the crustacean stomatogastric ganglion (STG) to
ask whether altered patterns of activity can produce significant
changes in conductance densities in adult neurons over relatively short
time periods.
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MATERIALS AND METHODS |
STGs of adult Cancer borealis were dissected, pinned
on a Sylgard-lined Petri dish, and superfused with normal saline (in mM: 440 NaCl, 11 KCl, 26 MgCl2, 13 CaCl2, 12 Trizma
base, and 5 maleic acid, pH 7.4-7.5). The STG was desheathed, and
cells were identified (Hooper et al., 1986). Neurons were impaled with two microelectrodes filled with 0.6 M
K2SO4 plus 20 mM KCl (15-25 M resistance) or with 3 M KCl (10-15 M resistance). Results for the
two electrode filling electrolytes showed no difference and have thus
been combined. Ionic currents were measured in two-electrode voltage
clamp (TEVC) using an Axoclamp 2A amplifier, Digidata 1200A interface,
and the pClamp software (Axon Instruments, Foster City, CA) in either
normal saline plus 10 µM picrotoxin (PTX; Sigma, St. Louis, MO) to block glutamatergic synapses or in PTX plus
0.1 µM tetrodotoxin (TTX; Sigma) to
additionally block action potential generation. The presence of PTX
and/or TTX in the bath made no difference to the ionic current
measurements (data not shown). In the absence of TTX, only some extra
current noise from poorly clamped action potentials riding on top of
the outward currents is observed. Current-clamp experiments were
performed with two electrodes (2ECC) in normal saline plus PTX
throughout. Action potential conduction along the input stomatogastric
nerve was blocked by placing a vaseline well filled with
isotonic sucrose (750 mM sucrose plus 1 µM TTX) around it.
We chose to study the three K+ outward
currents in STG neurons. They are easily measured, adequately clamped
with somatic electrodes, and relatively easy to separate by
manipulations of the membrane potential and pharmacological agents. All
three K+ currents activate at membrane
potentials more depolarized than  40 mV. The delayed rectifier current
(IKd) was measured in TEVC from a
holding potential Vh = 40 mV in the
presence of 500 µM Cd2+. The
Ca2+-activated
K+ current
(IK(Ca)) was measured as the current
difference between the current measured in normal saline and the
current remaining in the presence of 500 µM
Cd2+ from
Vh = 40 mV. Finally,
IA was measured either in normal
saline or in the presence of 500 µM
Cd2+ as the difference in currents evoked
from Vh = 80 mV minus
Vh = 40 mV. The peak currents were
measured at +20 mV, and chord conductances were calculated from the
equation g = I/(Vm EREV) with an estimated
EREV value of 80 mV for all three
outward K+ currents, and where
Vm is the membrane potential during a
voltage-clamp pulse. The leak current was measured from fits with a
linear equation, Ileak = gleak · (Vm EREV), and
Vm = 40, 50, 60, and 70 mV. The membrane capacitance (Cm) was
measured by integrating the current over time for short voltage steps
to membrane potentials where no active currents are elicited (80 to
40 mV). All currents are expressed as current densities normalized to
the measured cell capacitance. The stimulation protocol in 2ECC
consisted of 500 msec depolarizing or hyperpolarizing current pulses at
1 Hz. The current injection level was adjusted to depolarize the cells to a baseline Vm ~ 25 mV or to
hyperpolarize them to Vm ~ 90 mV, respectively.
| |
RESULTS |
All STG neurons studied express three outward
K+ currents, a delayed rectifier current
(IKd), a
Ca2+-activated current
(IK(Ca)), and a transient A-type
current (IA) (Graubard and Hartline,
1991; Golowasch and Marder, 1992; Tierney and Harris-Warrick, 1992;
Harris-Warrick et al., 1995; Kloppenburg et al., 1999). We measured the
conductance densities of these three outward
K+ currents in the inferior cardiac (IC)
neuron of 18 preparations (Fig. 1).
Figure 1A shows current traces from two different
neurons, shown in black and gray, respectively. The amplitude of
IK(Ca) was larger in the neuron shown
in gray, but the amplitudes of IA and
IKd were larger in the neuron shown in
black. This suggests that different neurons do not maintain a fixed
ratio of these three K+ currents, but that
they can vary in amplitude independently.
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Figure 1.
Variability of the outward K+
currents in the IC neuron. A, Example of the three
K+ currents in two different IC neurons
(gray and black traces,
respectively). All three currents show large variations between the two
cells. B, Three-dimensional plot showing the mutual
relationship between the conductances of the outward currents (same
data as in C). C, Histograms showing the
variability of the conductance densities of
gKd,
gK(Ca),
gA, and
gleak for identified IC neurons. Each point
corresponds to a different preparation. The peak current was measured
at Vm = +20 mV, and the conductance was
calculated with an estimated EREV value of
80 mV. The ratios between maximum and minimum values for each
conductance are shown above each data set. Notice that the ratios are
between 2.1 and 4.4, except for
gleak, which shows a much higher
variability. The total conductance density,
gtotal, is the sum of the conductance
densities of all three K+ currents. Mean values (± SD) are: membrane capacitance, 0.48 ± 0.09 nF; resting potential,
50.2 ± 6.7 mV; gKd = 0.35 ± 0.13 µS/nF; gK(Ca) = 2.68 ± 0.68 µS/nF; gA = 0.74 ± 0.18 µS/nF; gleak = 0.40 ± 0.24 µS/nF; and gtotal = 3.76 ± 0.76 µS/nF. D, Coefficients of variation (SD/mean) of each
of the data sets shown in C.
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Figure 1B is a three-dimensional plot in which the
conductance densities of the three currents in all 18 IC neurons are
displayed. If the three currents were proportionally scaled, the points
would line up along a straight line going from the lower right front to
the upper left back corner of the graph. Although the points show a
tendency to fall in a plane parallel to such a line, the values show a
great degree of dispersion, showing that proportional scaling is not
occurring. Instead, the broad distribution observed indicates a lack of
correlation between the conductance densities of these three currents
(three-dimensional regression analyses with a plane: r = 0.406; p = 0.26; with a hyperbola: r = 0.527; p = 0.34).
Figure 1C shows the peak conductance densities for each of
the three K+ currents, for the sum of the
K+ currents
(gtotal), and the conductance
density for the leak current. The ratios between the maximum and the
minimum measured conductance densities for each ionic current are shown
above each set of data. The conductance densities of the
K+ currents range between 2.1 and 4.4 over
the 18 neurons studied, and the leak conductances vary even more.
Interestingly, the sum of the three K+
currents varies less than either those of the delayed rectifier and
Ca2+-activated
K+ currents (Fig. 1C). Figure
1D shows the coefficient of variation (SD/mean) for the three voltage-dependent and the leak currents. By this measure, the total of the K+
conductance densities is marginally less variable than any of the
individual currents.
To test whether patterned activity imposed experimentally could alter
the conductance density of one or more of the
K+ currents, we stimulated the IC neuron
rhythmically (1 Hz, 50% duty cycle) for several hours under current
clamp. Every 60 min, the recording configuration was switched to
voltage clamp, and the ionic currents were measured. Figure
2A illustrates the
effects of this stimulation. The dark traces correspond to the current elicited before stimulation and the lighter traces to those elicited after 240 min of patterned depolarizing current injection. The top
traces correspond to the sum of IKd
and IK(Ca), and the bottom traces
correspond to IA. In these
experiments, IKd and
IK(Ca) cannot effectively be separated
because separating these currents involves applying, and then washing
Cd2+ (see Materials and Methods) during
every ionic current measurement (e.g., every 60 min). Therefore, the
sum of these two currents is reported throughout the remainder of this
paper. Notice that IKd plus
IK(Ca) decreased, and
IA markedly increased in amplitude as
a consequence of the stimulation, whereas
Itotal decreases because of the
decrease of the dominant IKd plus
IK(Ca).
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Figure 2.
Effect of patterned stimulation of the IC
neuron. The peak current measured at +20 mV every 60 min was normalized
to the peak current level at time 0, i.e., immediately before the
beginning of stimulation (downward arrow).
Negative time indicates time before stimulation begins.
Dashed lines indicate control values (i.e., 100%).
Numbers of measurements are indicated in
parentheses under the time axes below the time label;
the variability in these numbers is caused by the fact that different
preparations survived different amounts of time and that in some cases
stimulation was begun immediately after impalement. Values in
B-D are mean ± SEM. A, Ionic
current raw traces before (black traces) and after 4 hr
of stimulation (gray traces).
IKd and IK(Ca)
are measured together from a Vh = 40
mV, and IA is measured separately from a
Vh = 80 mV. B, The
neurons were stimulated for as long as they survived. Before
stimulation begins, current amplitudes are not statistically
significantly different from control. Black bars
correspond to IK(Ca) + IKd, hatched bars to
IA, and gray bars to
Ileak. Statistical significance of the
changes is shown above the bars for the other currents:
NS, not statistically significant;
*p < 0.05; **p < 0.01;
***p < 0.001; ANOVA. C, Three
neurons were stimulated for 3 hr (between arrows) and
finally held for 3 hr without stimulation to observe the recovery of
the maximum current amplitudes. Ileak is
omitted for clarity because no statistically significant changes were
observed. D, Same protocol as in B but in
the presence of 200 µM Cd2+ to block
Ca2+ entry to the cells via Ca2+
channels (Golowasch and Marder, 1992).
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Figure 2B summarizes the effect of patterned
depolarizing stimulation on 14 IC neurons. Before the beginning of
stimulation (time, 120-0 min) the measured current densities were
stable. Within the first hour of stimulation (which begins at the
arrow), however, IKd plus
IK(Ca) began to decrease until it
reached a minimum value of ~70% of control after ~2 hr, whereas
IA increased its amplitude with a
similar time course to reach a maximum value ~250% of control. These
trends are statistically significant for IKd plus
IK(Ca) and
IA. In contrast, the leak current
showed no statistically significant variation in amplitude during the
same period of time. The change in IKd
plus IK(Ca) is likely to be mainly a
result of IK(Ca), because the largest
IKd measured in an IC neuron is of
lower amplitude than the activity-induced current change.
Figure 2C shows a similar result for three IC neurons that
were recorded long enough to demonstrate that this effect fully reverses over time after the stimulation was terminated. Notice that
the phenomenon reverses with approximately the same time course as the
onset of the current changes during stimulation. Figure
2D shows the effect of stimulating six IC neurons in
the presence of Cd2+ to block the
Ca2+ current expressed by these cells
(Golowasch and Marder, 1992). Here we observe that the effect on
IA is completely abolished. The effect
on IK(Ca) is occluded by the fact that
IK(Ca) activation depends on
Ca2+ entering the cell through
Ca2+ channels, but no effect on
IKd (the current remaining in the presence of Cd2+) can be observed under
these conditions. These results indicate that the conductance density
changes observed in response to the imposed activity pattern in IC
depend on Ca2+ influx into the cell.
Figure 3A shows that the same
stimulus paradigm that alters the conductance densities measured in the
IC neuron failed to elicit equivalent changes in another cell type in
the STG, the lateral pyloric (LP) neuron. Figure 3, B and
C, shows that neither the IC nor the LP neuron are affected
by hyperpolarizing current stimulation. Taken together, this indicates
that identified neurons in the STG respond differentially to specific
patterns of activity and the polarity of the stimulus.
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Figure 3.
Effect of other stimulation paradigms and cell
types. The temporal aspect of the stimulation protocol was identical to
that used in Figure 2, but the polarity of the injected current was
varied. Peak currents normalized to the peak current level at time 0, immediately before the beginning of stimulation. Dashed
lines indicate control values (100%). Numbers
of measurements are indicated in parentheses under the
time axes below the time label. Values are mean ± SEM.
A, Stimulation of the LP neuron with depolarizing
current. No effect of stimulation is observed. B, Effect
of hyperpolarizing stimulation of the IC neuron, and of the LP neuron
(C). No effect was observed with hyperpolarizing current
in either B or C.
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DISCUSSION |
Ion channel proteins turn over rapidly relative to the lifetime of
neurons, so ion channels must continually be replaced. Control of this
process requires that the number, open conductance, and distribution of
ion channels be regulated by feedback mechanisms related to the firing
properties of the neuron (LeMasson et al., 1993; Liu et al., 1998;
Stemmler and Koch, 1999). One of the salient observations of this paper
and our previous work (Liu et al., 1998) is that there is considerable
variation in conductance densities for different currents when
individual neurons of the same class are compared (Fig. 1). Modeling
work indicates that such a high degree of variability is consistent
with a relatively constant pattern of activity (Liu et al., 1998; M.S.
Goldman, J. Golowasch, E. Marder, and L.F. Abbott, unpublished data).
The type of neuronal plasticity we report in this paper may act as a
driving force for this variability by linking the conductances of a
neuron to its recent history of activity.
Under physiological conditions, neurons of the STG are rhythmically
active. The pattern of activity is influenced by sensory and modulatory
inputs that can alter the ongoing motor pattern for either short or
long periods of time. The activity-dependent changes in conductances
reported here suggest that the conductance densities expressed by each
neuron will depend on its history, with an "integration time
constant" of several hours. Variability in measured conductances may
thus reflect the variability in the activity of the STG before the
recording. Interestingly, the changes produced, in the experiments
reported here, by "natural" imposed patterns of depolarization fall
within the range of variability observed among different preparations
(Fig. 1).
Our data demonstrate that even 2 or 3 hr of stimulation can
significantly alter the currents that are measured in single IC neurons
(Fig. 2). It is interesting that another neuronal type, the LP neuron,
did not respond to the same pattern of depolarization. Each cell type
may have a different sensitivity to activity so that stimulation with
different frequencies or durations, or for much longer time periods
(Desai et al., 1999), may be needed to elicit measurable changes in
conductances in some neurons. This is consistent with a growing body of
literature that argues that a variety of cellular processes may be
sensitive to different temporal patterns of activity (Fields et al.,
1990; Turrigiano et al., 1994; Itoh et al., 1995, 1997; Stevens et al.,
1998). In our experiments, blocking the influx of
Ca2+ into the cells abolished the effects
of stimulation (Fig. 2C). Further support for the plasticity
of conductances in the STG is provided by recent experiments that show
that removal of modulatory inputs is first followed by loss of
rhythmicity in the STG motor circuits followed by resumption of
activity one to several days later (Thoby-Brisson and Simmers, 1998;
Golowasch et al., 1999), presumably as the neurons that make up these
circuits respond to changes in their activity levels and loss of
modulatory inputs.
Because the intrinsic properties of neurons depend on the number and
type of all of their ionic currents, the variability and fluctuations
reported here have several important consequences. One possibility is
that changes in current densities alter the firing properties of
neurons to compensate for other changes (Desai et al., 1999).
Alternatively, it is possible that neurons with many different current
types maintain relatively constant intrinsic electrical properties,
although each current density can individually be quite variable (Liu
et al., 1998; M. S. Goldman, J. Golowasch, E. Marder, and L.F. Abbott,
unpublished data).
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FOOTNOTES |
Received June 4, 1999; revised July 21, 1999; accepted July 27, 1999.
This work was supported by National Institutes of Mental Health Grant
MH 46742 and the W. M. Keck Foundation.
Correspondence should be addressed to Dr. Jorge Golowasch, Volen Center
Mail Stop 013, Brandeis University, 415 South Street, Waltham, MA 02454.
This article is published in
The Journal of Neuroscience, Rapid Communications Section,
which publishes brief, peer-reviewed papers online, not in print. Rapid
Communications are posted online approximately one month earlier than
they would appear if printed. They are listed in the Table of Contents
of the next open issue of JNeurosci. Cite this article as:
JNeurosci, 1999, 19:RC33 (1-5). The
publication date is the date of posting online at
www.jneurosci.org.
| |
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Copyright © 0000 Society for Neuroscience 0270-6474/0/$05.00/0
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R. H. Cudmore and G. G. Turrigiano
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J. C. Choi, D. Park, and L. C. Griffith
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E. S. Piedras-Renteria, J. L. Pyle, M. Diehn, L. L. Glickfeld, N. C. Harata, Y. Cao, E. T. Kavalali, P. O. Brown, and R. W. Tsien
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A. A. Prinz, C. P. Billimoria, and E. Marder
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J. A. Luther, A. A. Robie, J. Yarotsky, C. Reina, E. Marder, and J. Golowasch
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Y. Zhang, J. N. MacLean, W. F. An, C. C. Lanning, and R. M. Harris-Warrick
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TOP
ABSTRACT
INTRODUCTION
Compound via MeSH
