PubMed Health⌕ Search

Biomedical subjects

S Y Chiu

Publications and source records attributed to S Y Chiu.

At least 37 records · Page 2Linked to original sources
PubMed1994

Axons regulate the expression of Shaker-like potassium channel genes in Schwann cells in peripheral nerve.

We examined potassium channel gene expression of two members of the Shaker subfamily, MK1 and MK2, in sciatic nerves from rats and mice. In Northern blot analysis, MK1 and MK2 probes detected single transcripts of approximately 8 kb and approximately 9.5 kb, respectively, in sciatic nerve and brain from both species. Polymerase chain reaction amplification of a cDNA library of cultured rat Schwann cells using MK1- and MK2- specific primers produced DNA fragments that were highly homologous to MK1 and MK2. To determine whether these channel genes were axonally regulated, we performed Northern blot analysis of developing, permanently transected, and crushed rat sciatic nerves. The mRNA levels for both MK1 and MK2 increased from P1 to P15 and then declined modestly. Permanent nerve transection in adult animals resulted in a dramatic and permanent reduction in the mRNA levels for both MK1 and MK2, whereas normal levels of MK1 and MK2 were restored when regeneration was allowed to occur following crush injury. In all cases, MK1 and MK2 mRNA levels paralleled that of the myelin gene P0. Elevating the cAMP in cultured Schwann cells by forskolin, which mimics axonal contact but not myelination, did not induce detectable levels of MK1 and MK2 mRNA by Northern blot analysis. Further, the level of MK1 mRNA in the vagus nerve, which contains relatively fewer myelinating Schwann cells and relatively more non-myelinating Schwann cells than the sciatic nerve, is reduced relative to the sciatic nerve. In conclusion, we have identified two Shaker-like potassium channel genes in sciatic nerves whose expressions are regulated by axons. We suggest that MK1 and MK2 mRNA are expressed in high levels only in myelinating Schwann cells and that these Shaker-like potassium channel genes have specialized roles in these cells.

Animals↗
PubMed1994

Transcription factor expression is induced by axonal stimulation and glutamate in the glia of the developing optic nerve.

Recent experiments have demonstrated that stimulation of the developing optic nerve affects several glial cell characteristics, such as ionic fluxes and cell proliferation. This investigation asked if transcription factor expression may be another stimulation-dependent process in the glia of the developing optic nerve. In unstimulated optic nerves, an antibody to c-fos-related antigens demonstrated positive cell body staining at postnatal days (P) 2, 7, 14, and 60. This nuclear staining was most prominent at early postnatal ages, although young adult (P60) optic nerves showed occasional positive cells. To demonstrate the inducibility of transcription factor antigens, optic nerves from P7 animals received intermittent 15-20 Hz electrical stimulation for 5-15 min. Two hours after this stimulation, an increased number of immunoreactive cells for c-fos-related antigens, c-jun, and NGFI-A was demonstrated. Additionally, optic nerves were exposed for 5-30 min to a solution of 300 microM glutamate, latter maintained in a glutamate-free solution for 2 h, and then quickly frozen. Glutamate-treated nerves showed an increased expression of c-fos-related antigens compared to control nerves. No c-fos increase was seen in the absence of calcium. Expression of c-fos or NGFI-A occurred in cells that were S-100 positive, and most likely represented type 1 astrocytes. These studies indicate that developing (P7) optic nerves show a baseline expression of c-fos-related antigens, c-jun and NGFI-A. Stimulation through electrical nerve stimulation or glutamate results in an increased expression of these transcription factors.

Action Potentials↗
PubMed1993

Differential expression of sodium channels in acutely isolated myelinating and non-myelinating Schwann cells of rabbits.

1. Single channel recordings were made of voltage-sensitive sodium channels in outside-out patches excised from the cell body region of Schwann cells. The cells were freshly isolated from sciatic nerves of 10-week-old rabbits and both myelinating and non-myelinating Schwann cells were visually identified for recordings. 2. Sodium channel activities were observed in approximately 75% of patches (n = 41) obtained from cell bodies of non-myelinating Schwann cells. In contrast, sodium channels were not observed in patches (n = 78) obtained from cell bodies of myelinating Schwann cells. 3. Transection of the sciatic nerves and allowing Wallerian degeneration to occur for 5-11 days in vivo prior to recording resulted in the appearance of sodium channel activities in approximately 30% of the patches (n = 33) obtained from the cell body of the myelinating cells. 4. It is interesting that although immunocytochemical and saxitoxin binding experiments indicate the clear presence of sodium channels in the plasmalemma of myelinating Schwann cells (both at the cell body and at the paranodal region), the present study suggests that these channels are absent from the soma region of normal myelinating Schwann cells.

Animals↗
PubMed1993

Mitogenic factors regulate ion channels in Schwann cells cultured from newborn rat sciatic nerve.

1. Patch clamp studies were carried out in Schwann cells cultured from newborn rat sciatic nerve to determine the effects of mitogens on voltage-gated currents without the confounding influences of axonal contact and myelin present in vivo. The relevance of the various Schwann cell currents to proliferation was assessed using assays of [3H]thymidine incorporation. 2. Treatment of cultured Schwann cells with known mitogens, namely axon fragments (AF), myelin fragments (MF), or glial growth factor in combination with forskolin (GGF+F), increased the magnitudes of delayed rectifying potassium (K+) and sodium (Na+) currents. 3. In both control and mitogen-treated cells, the magnitude of net outward current paralleled clearly the magnitude of the cells' proliferative response. 4. The K+ channel-blocking quaternary ammonium ions, tetrabutylammonium (TBuA), tetrapentylammonium (TPeA) and tetrahexylammonium (THeA), but not the Na+ channel blocker tetrodotoxin (TTX), reduced proliferation in a dose-dependent fashion offering further evidence for a role for K+ channels in Schwann cell proliferation. 5. Voltage-gated chloride (Cl-) currents were observed in both control and mitogen-treated cells. Addition of the Cl- channel blockers, 4-acetamido-4'-isocyanatostilbene-2,2'-disulphonate (SITS) or 4,4'-diisothiocyanatostilbene-2,2'-disulphonate (DIDS), to the culture media enhanced proliferation. 6. The possible intermediary role of the Schwann cell resting potential was explored in ion substitution experiments by increasing the K+ concentration of the media and by adding ouabain. Both manipulations inhibited Schwann cell mitosis. 7. Comparison of the expression of functional ion channels in vitro with that previously described for Schwann cells in vivo suggests a difference in the Schwann cell response to the membrane fragment mitogens and their intact counterparts in regard to the regulation of ion channels. MF up-regulates the number of functional channels, whereas the elaboration of myelin (or a factor related to its presence) in vivo appears to down-regulate channel expression, at the cell soma of myelinating Schwann cells. In addition, axonal contact may be required for normal expression of functional inwardly rectifying K+ channels.

Animals↗
PubMed1993

Calcium signaling of glial cells along mammalian axons.

Glial [Ca2+]i signaling was examined in a mammalian white matter lacking neuronal cell bodies and synapses. Rat optic nerves (postnatal days 2 and 7) were stained with calcium indicator dyes and confocal images of [Ca2+bdi were recorded at approximately 25 degrees C or approximately 37 degrees C. Glial cell bodies showed spiking or sustained [Ca2+], response to bath-applied glutamate (50-500 microM). The metabotropic glutamate agonist trans-ACPD elicited transient, sometimes spiking, [Ca2+], responses, whereas ionotropic agonists kainate and AMPA elicited a 6,7-dinitroquinoxaline-2,3-dione-sensitive, mostly sustained [Ca2+]i response. Transient and spiking glial [Ca2+]i responses also were elicited by adenosine and ATP (0.1-100 microM). Repetitive nerve stimulation (10-20 Hz) elicited [Ca2+bdi spiking in 15-25% of glial cells in postnatal day 7 nerves, with spiking typically occurring 15-60 sec after onset of nerve stimulation. At 37 degrees C, the frequency of glial [Ca2+]i spikes increased from approximately 0.06 Hz to approximately 0.11 Hz when axonal stimulation was increased from 10 to 20 Hz. This activity-dependent glial spiking was inhibited by TTX, could not be mimicked by increasing the bath K+ by 20 mM, and occurred when nerves were stimulated in the absence of bath calcium. Activity-dependent and glutamate-induced glial spiking could be mimicked by altering ionic gradients known to favor release of glutamate via glutamate transporters, including elevation of intracellular Na+ by veratridine concurrent with external K+ elevation. We suggest that glial [Ca2+]i spiking observed during electrical activity resulted from activation of glial receptors (e.g., metabotropic glutamate receptor, adenosine receptor) by substances (e.g., glutamate, adenosine) released from the optic nerve in a nonvesicular fashion, possibly through a reversal of sodium-coupled transporters when Na+ and K+ gradients are altered by prolonged nerve activity.

Action Potentials↗
PubMed1993

Expression of glutamate receptor genes in white matter: developing and adult rat optic nerve.

We have identified the glutamate receptor genes expressed by developing and adult rat optic nerve. Results from PCR suggested that of the ionotropic glutamate receptor (GluR) gene family, only GluR1 and GluR3 subunits are expressed by optic nerve. However, Northern blot analysis demonstrated that only the GluR1 subtype is expressed at appreciable levels. In situ hybridization histochemistry of GluR1 was performed and a diffuse pattern of expression was observed in both postnatal day 15 and adult optic nerve. Restriction mapping of the GluR1 PCR product indicated the expression of the flip alternative splice version in optic nerve. The detected GluR1 message was not due to axons because no loss of expression was observed after the degeneration of axons. PCR analysis also revealed the presence of a metabotropic glutamate receptor in optic nerve.

Aging↗
PubMed1991

Functions and distribution of voltage-gated sodium and potassium channels in mammalian Schwann cells.

Recent patch-clamp studies on freshly isolated mammalian Schwann cells suggest that voltage-gated sodium and potassium channels, first demonstrated in cells under culture conditions, are present in vivo. The expression of these channels, at least at the cell body region, appears to be dependent on the myelinogenic and proliferative states of the Schwann cell. Specifically, myelin elaboration is accompanied by a down regulation of functional potassium channel density at the cell body. One possibility to account for this is a progressive regionalization of ion channels on a Schwann cell during myelin formation. In adult myelinating Schwann cells, voltage-gated potassium channels appear to be localized at the paranodal region. Theoretical calculations have been made of activity-dependent potassium accumulations in various compartments of a mature myelinated nerve fibre; the largest potassium accumulation occurs not at the nodal gap but rather at the adjacent 2-4 microns length of periaxonal space at the paranodal junction. Schwann cell potassium channels at the paranode may contribute to ionic regulation during nerve activities.

Animals↗
PubMed1991

Differential intracellular calcium responses to glutamate in type 1 and type 2 cultured brain astrocytes.

Fluorescence image analysis using the calcium indicator fluo-3 was used to examine changes in [Ca2+]i induced by glutamate in mixed glia populations cultured from neonatal rat brains. [Ca2+]i responses were correlated with glia type by performing immunohistochemistry using markers specific for type 1 and type 2 astrocytes on the same cells used in the imaging experiments. Glutamate (30-500 microM) induced two markedly different [Ca2+]i responses in the two astrocyte types: the response in type 1 astrocytes consisted of an initial fast transient followed by varying degrees of oscillations, whereas the predominant response in type 2 astrocytes was a slow rise in [Ca2+]i to a more or less sustained and nonoscillatory level. In some type 2 astrocytes, an initial spikelike transient similar to that in type 1 astrocytes was observed; the overall size of the spike, however, was smaller than in type 1 astrocytes. Two agonists for the ionotropic glutamate receptor, alpha-amino-3-hydroxy-5-methylisoxazole-4-propionate (AMPA) and kainate, elicited a 6-cyano-7-dinitroquinoxaline-2,3-dione (CNQX)-sensitive, external Ca(2+)-dependent, sustained [Ca2+]i rise in type 2 but not type 1 astrocytes. The initial spike in type 2 astrocytes was less dependent on external Ca2+ and not blocked by CNQX. [Na+]i as measured by the Na(+)-fluorescence dye SBFI, was elevated by kainate in both astrocyte types, though the increase was larger in type 2 astrocytes. This increase was reduced by CNQX, suggesting this [Ca2+]i increase was mediated, at least in part, by ionotropic glutamate receptors. The results are discussed in terms of the relative distribution of two classes of glutamate receptors on these two astrocyte types: one, the ionotropic class, is linked directly to an ion channel, and the other, the metabotropic class, induces internal mobilization of Ca2+ via inositol phospholipid hydrolysis.

6-Cyano-7-nitroquinoxaline-2,3-dione↗
PubMed1990

Ion channels in axon and Schwann cell membranes at paranodes of mammalian myelinated fibers studied with patch clamp.

While recent studies have established the presence of voltage-gated ion channels on Schwann cells in culture and on freshly isolated fibers from mature mammals, an important issue not yet explored is whether Schwann cell channels are regionally specialized. In the nodal region, the intimate association between the Schwann cell and its axon suggests that this is a likely site for functional specialization. Here, we examine whether there is a localized expression of channels in the Schwann cell paranodal regions, in a manner similar to that already shown for the nodal axon. Cell-attached and outside-out patch-clamp recordings were made from paranodal regions of rat myelinated sciatic nerve fibers where the myelin on both sides of the node was retracted by enzymatic treatment. Even though no myelin was visible on the surface of the retracted paranode, significant portions of this surface were found to stain positively with a marker (anti-galactocerebroside) for Schwann cell membranes, suggesting that part of the axon still was covered by glial membranes. Using Lucifer yellow in the recording pipettes, we observed that the dye diffused into either axons or Schwann cells when the membrane under the tip was ruptured. Using this as a criterion to identify membranes obtained from retracted paranodes, we found delayed and inwardly rectifying potassium channels on both axon- and Schwann-derived patches. However, sodium channels were detected only in axon patches. This is the first report that voltage-gated glial channels are present in immediate vicinity to axons of the PNS. This finding, coupled with earlier reports that functional channels are absent in soma of mature myelinating Schwann cells, suggests that ion channels in these cells are regionally specialized for functional interaction with axons.

Animals↗
PubMed1990

Fluorescence measurement of changes in intracellular calcium induced by excitatory amino acids in cultured cortical astrocytes.

Population response of [Ca2+]i in cultured cortical astrocytes to excitatory amino acids was measured at room temperature using the calcium-sensitive dye fura-2. Quisqualic acid (QA), glutamate (Glu), and kainic acid (KA) caused a peak increase in [Ca2+]i in the order QA greater than Glu greater than KA. No response to N-methyl-D-aspartic acid (NMDA) was observed whether or not Mg2+ was present externally. Both QA and Glu (100 microM) frequently elicited a decaying oscillatory [Ca2+]i response during sustained agonist application; the period of oscillations initially was 23.5 sec and increased as the response was damped. Comparatively, the [Ca2+]i response to KA was nonoscillatory. Both responses to Glu and KA were reduced slightly by antagonist gamma-D-glutamylaminomethyl-sulfonic acid (1 mM), but virtually were abolished by kynurenic acid (3 mM). Replacement of external Na+ by choline had no significant effect on the Glu response. Removal of external Ca2+ reduced the peak response to QA, Glu, and KA to 40, 34, and 18%, respectively; and markedly reduced the degree of QA- and Glu-induced [Ca2+]i oscillations. Pretreatment with phorbol esters, a potent activator of protein kinase C, blocked the [Ca2+]i response to Glu but not KA. It is concluded that cortical astrocytes express Glu receptors of the non-NMDA type in culture and that receptor activation leads to Ca2+ influx and release of internal Ca2+. Mobilization of Ca2+ apparently occurs via the known Glu-mediated hydrolysis of inositol lipids, which may come under negative-feed-back control by protein kinase C activation. Oscillatory [Ca2+]i signaling offers the possibility of a dynamic population response in an electrically coupled glial network.

Amino Acids↗
PubMed1990

Potassium channel regulation in Schwann cells during early developmental myelinogenesis.

The presence of neuronal-like, voltage-gated ion channels on glia has raised questions concerning their physiological roles. Insights into glial channel function can be gained by examining regulation of channel expression during axoglial interactions. We examine the regulation of Schwann cell potassium channels in developing sciatic nerves of newborn rats when myelin is first laid down. During the initial postnatal week, cell-attached patch-clamp recordings at soma of Schwann cells with visible myelin revealed an inward rectifying potassium channel (KIR), to date described only in CNS glia but not Schwann cells, as well as an outward potassium channel (KO). Around the resting potential, the KO channel is virtually closed, while the KIR channel appears maximally open. Compared with the KO channel, the KIR channel is blocked by low concentrations of Cs+ and exhibits higher sensitivity to 4-aminopyridine (4AP). Further, the KIR channel appears similar to other mammalian inward rectifiers and rectification depends, in part, on cytoplasmic Mg2+. Channel regulation bears an interesting relation to early myelination: as the average number of myelin lamellae increases from 6 to 21 from day 2 to day 8, currents decrease by 80-90%. The reduction in KO current also parallels the known decrease in proliferation of Schwann cells as they are being committed to myelination, supporting the recently proposed notion of a functional link between potassium channels and proliferation. The KIR channels, by virtue of being open at the resting potential, may play a role in buffering activity-dependent K+ accumulation during early myelin formation. The subsequent reduction in somal channel density may parallel a diminished need for K+ buffering as electrogenesis is restricted to nodal regions.

Animals↗
PubMed1989

The role of potassium channels in Schwann cell proliferation in Wallerian degeneration of explant rabbit sciatic nerves.

1. Patch clamp studies of whole-cell ionic currents and biochemical studies of proliferation were carried out on Schwann cells of myelinated axons in explant segments of sciatic nerves of adult rabbit maintained in culture for 0-10 days. 2. Schwann cell proliferation, as assayed by [3H]thymidine incorporation and by electron microscopic autoradiography, showed an increase following nerve explant. Proliferation proceeded in parallel with a gradual hyperpolarization of the resting potential and an increase in K+ currents in Schwann cells of myelinated axons. 3. The relation between K+ channels and proliferation was studied by incubating explant nerves in the presence of various K+ channel blockers. Quinine, TEA and 4-aminopyridine (4-AP), which blocked K+ currents in Schwann cells, were found also to block Schwann cell proliferation in a dose-dependent fashion and over similar concentrations. Electron microscopy showed that TEA did not retard myelin and axonal break-down which is thought to be the source of mitogens for Schwann cell proliferation. 4. The relation between resting potential and proliferation was studied by incubating explant nerves in depolarizing culture media. Depolarizing monovalent cations (K+ and Rb+) led to a marked inhibition of Schwann cell proliferation. However, Cs+ and NH4+, which did not depolarize Schwann cells in patch clamp studies, also inhibited proliferation. Gramicidin and veratridine also inhibited proliferation. 5. The results suggest that the expression of K+ channels is functionally important for Schwann cell proliferation in Wallerian degeneration. A possible link between K+ channel and proliferation might be via a hyperpolarization of the resting membrane potential which occurs when Schwann cells proliferate.

4-Aminopyridine↗
PubMed1988

Changes in excitable membrane properties in Schwann cells of adult rabbit sciatic nerves following nerve transection.

1. Whole-cell patch clamp studies were carried out on Schwann cells associated with myelinated and non-myelinated axons in the distal nerve stump of transected adult rabbit sciatic nerves which had undergone in vivo degeneration for 0-13 days. 2. Voltage-gated sodium current of Schwann cells associated with non-myelinated axons decreased in amplitude following nerve transection; the peak current density decreased to about 51% by day 3, and to 27% by day 6. The number of non-myelinated axons, determined from cross-sectional electron microscopy of the whole nerve bundle, also exhibited a similar decline to 48% (day 3) and 17% (day 6) of the control values. 3. In contrast, both voltage-gated sodium and potassium currents of Schwann cells associated with myelinated axons showed an increase following nerve transection. These two currents, normally not detectable in these Schwann cells, first appeared at around day 4 after nerve transection and increased progressively with time thereafter as Wallerian degeneration persisted. 4. The whole-cell membrane capacity of Schwann cells also exhibited different pattern of changes, depending on whether the cell normally lacked or produced myelin. In the former, the cell capacity remained relatively constant following nerve transection. In the latter, the whole cell capacity was reduced to 11% of control values by day 13. This capacity decline is consistent with the observed detachment of myelin membranes from these latter Schwann cells. 5. There was an apparent inverse relation between the whole-cell capacity and the density of sodium and potassium currents in Schwann cells undergoing progressive myelin loss. It is suggested that the appearance of sodium and potassium currents in these cells might be related to myelin degeneration. 6. A hypothesis is proposed that the expression of excitable ion channels (sodium and potassium) on a Schwann cell is under opposing regulation by degenerating myelin and by axons. Axonal degeneration leads to a decline of Schwann cell sodium currents. Myelin degeneration, in contrast, leads to an increase of both Schwann cell sodium and potassium currents. 7. The above hypothesis that axons normally exert a positive trophic influence on Schwann cells to express sodium channels is discussed in relation to a recent speculation of a Schwann-to-axon transfer of excitable ion channels.

Action Potentials↗
PubMed1987

Optical recording of action potential propagation in demyelinated frog nerve.

Conduction in focally demyelinated frog nerves has been measured optically using potential-sensitive dyes. Absorption changes were recorded with an array of photodiodes positioned in the image plane of a microscope. Both the amplitude and conduction velocity of the optical signals decreased in the demyelinated region. Conduction was improved after exposure to the potassium channel blocking agent 4-aminopyridine.

Action Potentials↗
PubMed1987

Sodium currents in axon-associated Schwann cells from adult rabbits.

1. Patch-clamp and electron-microscopic studies were carried out on individual axon-Schwann-cell complexes 2-6 h after they were isolated from the sciatic nerves of rabbits 5, 10 and 20 weeks old. 2. Under Hoffman modulation contrast optics Schwann cells associated with both myelinated and non-myelinated axons could be seen. Frequently, fine cable-like structures about 1 micron in diameter, which are presumably axons, could be seen in isolation from a Schwann cell. 3. Cross-sectional electron-microscopic studies directly demonstrated the presence of axons engulfed by Schwann cells. For Schwann cells associated with non-myelinated axons, multiple fine axons (approximately 1 micron) could be seen enclosed by one or few turns of spiralling tongues of Schwann cells. Schwann cells associated with a single large myelinated axon showed characteristic compact myelin wrappings. No membrane fusion between Schwann cells and the axons could be detected. 4. Giga-seals could readily be formed when a patch pipette was pressed against the body region of a Schwann cell associated with either non-myelinated or myelinated axons. In contrast, giga-seals were only infrequently obtained on fine cable-like structures (1 micron) visually identified to be separated from the Schwann cell body. 5. Whole-cell recordings made from the body region of a Schwann cell revealed a TTX-sensitive fast inward current. Intriguingly, the expression of this current appeared to be dependent on the type of associated axon; this current was detectable in virtually all recordings made at the body region of Schwann cells associated with small non-myelinated axons, but not from those associated with large myelinated axons. 6. The inward current was like a neuronal sodium current; it had voltage-gated kinetics similar to the Hodgkin-Huxley sodium current, and exhibited a reversal potential close to the expected Nernstian potential for sodium ions. 7. From the observed size of the whole-cell membrane capacity and the electron-microscopic observations that the surface area of the Schwann cell at the body region was much larger than that of a 1 micron non-myelinated axon, it was argued that the whole-cell recordings were from Schwann cells rather than from single axons. Furthermore, the peak sodium current density was similar to that of Schwann cells cultured from new-born rabbits in which axons were presumed to be absent. 8. The results suggested that Schwann cells normally associated with non-myelinated axons in the rabbit sciatic nerves maintain an active synthesis of neuronal-like sodium channels throughout normal development.

4-Aminopyridine↗
PubMed1987

Sodium and potassium currents in acutely demyelinated internodes of rabbit sciatic nerves.

1. Voltage-clamp experiments were performed on single internodes isolated from rabbit sciatic nerve fibres acutely demyelinated with the detergent lysolecithin or a synthetic analogue, lysophosphatidyl choline palmitoyl. 2. The extent of demyelination was monitored by a gradual increase in the internodal leak conductance and capacitance. Voltage- and time-dependent inward and outward currents, absent during the early phase (30-40 min) of detergent treatment, appeared during the final phase (40-60 min) of treatment. 3. The internodal ionic currents elicited by depolarizations consisted of three components pharmacologically identified as (a) a transient sodium current which was inhibited by tetrodotoxin, (b) a delayed rectifying potassium current which was inhibited by internal caesium and (c) a time-dependent current that was abolished by replacement of external chloride with ascorbate. 4. The current-voltage relations and h infinity curves for the internodal sodium current were similar in shapes to those of the nodal sodium current. 5. The amplitudes of the three internodal currents increased with the increase in the measured internodal capacity during the final phase of demyelination. 6. At high degrees of demyelination a peak sodium current of about 90 nA could be observed in an internodal segment of 100 micron length. 7. Interestingly, the membrane capacity measured at the time of such a large sodium current was about 10 times larger than could be accounted for by the axonal membrane in the recording pool alone. A suggestion is made that this represents lysolecithin-induced membrane fusion between the Schwann cell and the internodal axon.

Action Potentials↗
PubMed1986

Ion channels in rabbit cultured fibroblasts.

Large outward currents are recorded with the whole-cell patch-clamp technique on depolarization of rabbit cultured fibroblasts. Our findings suggest that these outward currents consist of two voltage-dependent components, one of which also depends on cytoplasmic calcium concentration. Total replacement of external Cl- by the large anion ascorbate does not affect the amplitude of the currents, indicating that both components must be carried by K+. Consistent with these findings with whole-cell currents, in single channel recordings from fibroblasts we found that most patches contain high-conductance potassium-selective channels whose activation depends on both membrane potential and the calcium concentration at the cytoplasmic surface of the membrane. In a smaller number of patches, a second population of high-conductance calcium-independent potassium channels is observed having different voltage-dependence. The calcium- and voltage-dependence suggest that these two channels correspond with the two components of outward current seen in the whole-cell recordings. The single channel conductance of both channels in symmetrical KCl (150 mM) is 260-270 pS. Both channels are highly selective for K+ over both Na+ and Cl-. The conductance of the channels when outward current is carried by Rb+ is considerably smaller than when it is carried by K+. Some evidence is adduced to support the hypothesis that these potassium channel populations may be involved in the control of cell proliferation.

4-Aminopyridine↗