共查询到20条相似文献,搜索用时 15 毫秒
1.
2.
Selective Dephosphorylation of the Subunits of Skeletal Muscle Calcium Channels by Purified Phosphoprotein Phosphatases 总被引:2,自引:0,他引:2
Abstract: Multiple sites on the α1 and β subunits of purified skeletal muscle calcium channels are phosphorylated by cyclic AMP-dependent protein kinase, resulting in three different tryptic phosphopeptides derived from each subunit. Phosphoprotein phosphatases dephosphorylated these sites selectively. Phosphoprotein phosphatase 1 (PP1) and phosphoprotein phosphatase 2A (PP2A) dephosphorylated both α1 and β subunits at similar rates, whereas calcineurin dephosphorylated β subunits preferentially. PP1 dephosphorylated phosphopeptides 1 and 2 of the α1 subunit more rapidly than phosphopeptide 3. In contrast, PP2A dephosphorylated phosphopeptide 3 of the α1 subunit preferentially. All three phosphoprotein phosphatases preferentially dephosphorylated phosphopeptide 1 of the β subunit and dephosphorylated phosphopeptides 2 and 3 more slowly. Mn2+ increased the rate and extent of dephosphorylation of all sites by calcineurin so that >80% dephosphorylation of both α1 and β sub-units was obtained. The results demonstrate selective dephosphorylation of different phosphorylation sites on the α1 and β subunits of skeletal muscle calcium channels by the three principal serine/threonine phosphoprotein phosphatases. 相似文献
3.
The role of glycosylation on voltage-dependent channel gating for the cloned human cardiac sodium channel (hH1a) and the
adult rat skeletal muscle isoform (μl) was investigated in HEK293 cells transiently transfected with either hH1a or μl cDNA.
The contribution of sugar residues to channel gating was examined in transfected cells pretreated with various glycosidase
and enzyme inhibitors to deglycosylate channel proteins. Pretreating transfected cells with enzyme inhibitors castanospermine
and swainsonine, or exo-glycosidase neuroaminidase caused 7 to 9 mV depolarizing shifts of V
1/2 for steady-state activation of hH1a, while deglycosylation with corresponding drugs elicited about the same amount of depolarizing
shifts (8 to 9 mV) of V
1/2 for steady-state activation of μl. Elevated concentrations of extracellular Mg2+ significantly masked the castanospermine-elicited depolarizing shifts of V
1/2 for steady-state activation in both transfected hH1a and μl. For steady-state activation, deglycosylation induced depolarizing
shifts of V
1/2 for hH1a (10.6 to 12 mV), but hyperpolarizing shifts for μl (3.6 to 4.4 mV). Pretreatment with neuraminidase had no significant
effects on single-channel conductance, the mean open time, and the open probability. These data suggest that glycosylation
differentially regulates Na channel function in heart and skeletal muscle myocytes.
Received: 8 April 1999/Revised: 18 June 1999 相似文献
4.
Roura-Ferrer M Solé L Martínez-Mármol R Villalonga N Felipe A 《Biochemical and biophysical research communications》2008,369(4):1094-1097
Voltage-dependent K+ channels (Kv) are involved in myocyte proliferation and differentiation by triggering changes in membrane potential and regulating cell volume. Since Kv7 channels may participate in these events, the purpose of this study was to investigate whether skeletal muscle Kv7.1 and Kv7.5 were involved during proliferation and myogenesis. Here we report that, while myotube formation did not regulate Kv7 channels, Kv7.5 was up-regulated during cell cycle progression. Although, Kv7.1 mRNA also increased during the G1-phase, pharmacological evidence mainly involves Kv7.5 in myoblast growth. Our results indicate that the cell cycle-dependent expression of Kv7.5 is involved in skeletal muscle cell proliferation. 相似文献
5.
J.I. Kourie 《The Journal of membrane biology》1999,167(1):73-83
The understanding of the role of cytoplasmic pH in modulating sarcoplasmic reticulum (SR) ion channels involved in Ca2+ regulation is important for the understanding of the function of normal and adversely affected muscles. The dependency of
the SR small chloride (SCl) channel from rabbit skeletal muscle on cytoplasmic pH (pH
cis
) and luminal pH (pH
trans
) was investigated using the lipid bilayer-vesicle fusion technique. Low pH
cis
6.75–4.28 modifies the operational mode of this multiconductance channel (conductance levels between 5 and 75 pS). At pH
cis
7.26–7.37 the channel mode is dominated by the conductance and kinetics of the main conductance state (65–75 pS) whereas
at low pH
cis
6.75–4.28 the channel mode is dominated by the conductance and kinetics of subconductance states (5–40 pS). Similarly, low
pH
trans
4.07, but not pH
trans
6.28, modified the activity of SCl channels. The effects of low pH
cis
are pronounced at 10−3 and 10−4
m [Ca2+]
cis
but are not apparent at 10−5
m [Ca2+]
cis
, where the subconductances of the channel are already prominent. Low pH
cis
-induced mode shift in the SCl channel activity is due to modification of the channel proteins that cause the uncoupling of
the subconductance states. The results in this study suggest that low pH
cis
can modify the functional properties of the skeletal SR ion channels and hence contribute, at least partly, to the malfunction
in the contraction-relaxation mechanism in skeletal muscle under low cytoplasmic pH levels.
Received: 20 May 1998/Revised: 24 September 1998 相似文献
6.
R. Barrett-Jolley A. Comtois N.W. Davies P.R. Stanfield N.B. Standen 《The Journal of membrane biology》1996,152(2):111-116
We investigated the action of adenosine and GTP on KATP channels, using inside-out patch clamp recordings from dissociated single fibers of rat flexor digitorum brevis (FDB) skeletal
muscle. In excised patches, KATP channels could be activated by a combination of an extracellular adenosine agonist and intracellular Mg2+-ATP and GTP or GTP-γ-S. The activation required hydrolyzable ATP and could be partially reversed with Mg2+, suggesting that it may involve a G-protein dependent phosphorylation of KATP channels. We found that KATP channels of the rat FDB could not be activated by Mg2+-ATP alone or by Mg2+-ATP in the presence of extracellular adenosine. Patches whose channel activity had been `rundown' by Ca2+ could not be recovered by adenosine, GTP or Mg2+-ATP. KATP channels activated by adenosine receptor agonists had a similar ATP sensitivity to those under control conditions; but adenosine
appears to be able to switch these KATP channels from an inactive to an active mode.
Received: 29 December 1995/Revised: 22 March 1996 相似文献
7.
8.
MicroRNAs Involved in Skeletal Muscle Differentiation 总被引:1,自引:0,他引:1
MicroRNAs (miRNAs) negatively regulate gene expression by promoting degradation of target mRNAs or inhibiting their translation. Previous studies have expanded our understanding that miRNAs play an important role in myogenesis and have a big impact on muscle mass, muscle fiber type and muscle-related diseases. The muscle-specific miRNAs, miR-206, miR-1 and miR-133, are among the most studied and best characterized miRNAs in skeletal muscle differentiation. They have a profound influence on multiple muscle differ-entiation processes, such as alternative splicing, DNA synthesis, and cell apoptosis. Many non-muscle-specific miRNAs are also required for the differentiation of muscle through interaction with myogenic factors. Studying the regulatory mechanisms of these miRNAs in muscle differentiation will extend our knowledge of miRNAs in muscle biology and will improve our understanding of the myogenesis regulation. 相似文献
9.
Role of Voltage-gated Potassium Channels in Cancer 总被引:3,自引:0,他引:3
Pardo LA Contreras-Jurado C Zientkowska M Alves F Stühmer W 《The Journal of membrane biology》2005,205(3):115-124
Ion channels are being associated with a growing number of diseases including cancer. This overview summarizes data on voltage-gated
potassium channels (VGKCs) that exhibit oncogenic properties: ether-à-go-go type 1 (Eag1). Normally, Eag1 is expressed almost
exclusively in tissue of neural origin, but its ectopic expression leads to uncontrolled proliferation, while inhibition of
Eag1 expression produces a concomitant reduction in proliferation. Specific monoclonal antibodies against Eag1 recognize an
epitope in over 80% of human tumors of diverse origins, endowing it with diagnostic and therapeutic potential. Eag1 also possesses
unique electrophysiological properties that simplify its identification. This is particularly important, as specific blockers
of Eag1 currents are not available. Molecular imaging of Eag1 in live tumor models has been accomplished with dye-tagged antibodies
using 3-D imaging techniques in the near-infrared spectral range.
Abbreviations: EAG: Ether-à-go-go, VGKCs: voltage-gated potassium channels 相似文献
10.
J.I. Kourie 《The Journal of membrane biology》1998,164(1):47-58
The lipid bilayer technique was used to examine the effects of the ATP-sensitive K+ channel inhibitor (glibenclamide) and openers (diazoxide, minoxidil and cromakalim) and Cl− channel activators (GABA and diazepam) on two types of chloride channels in the sarcoplasmic reticulum (SR) from rabbit skeletal
muscle. Neither diazepam at 100 μm nor GABA at 150 μm had any significant effect on the conductance and kinetics of the 75 pS small chloride (SCl) channel.
Unlike the 150 pS channel, the SCl channel is sensitive to cytoplasmic glibenclamide with K
i
∼ 30 μm. Glibenclamide induced reversible decline in the values of current (maximal current amplitude, I
max and average mean current, I′) and kinetic parameters (frequency of opening F
o
, probability of the channel being open P
o
and mean open time, T
o
, of the SCl channel. Glibenclamide increased mean closed time, T
c
, and was a more potent blocker from the cytoplasmic side (cis) than from the luminal side (trans) of the channel.
Diazoxide increased I′, P
o
, and T
o
in the absence of ATP and Mg2+ but it had no effect on I
max and also failed to activate or remove the glibenclamide- and ATP-induced inhibition of the SCl channel. Minoxidil induced
a transient increase in I′ followed by an inhibition of I
max, whereas cromakalim reduced P
o
and I′ by increasing channel transitions to the closed state and reducing T
o
without affecting I
max. The presence of diazoxide, minoxidil or cromakalim on the cytoplasmic side of the channel did not prevent [ATP]
cis
or [glibenclamide]
cis
from blocking the channel.
The data suggest that the action(s) of these drugs are not due to their effects on the phosphorylation of the channel protein.
The glibenclamide- and cromakalim-induced effects on the SCl channel are mediated via a ``flicker' type block mechanism.
Modulation of the SCl channel by [diazoxide]
cis
and [glibenclamide]
cis
highlights the therapeutic potential of these drugs in regulating the Ca2+-counter current through this channel.
Received: 2 September 1997/Revised: 20 March 1998 相似文献
11.
Effects of Cannabinoids on Caffeine Contractures in Slow and Fast Skeletal Muscle Fibers of the Frog
Miguel Huerta Mónica Ortiz-Mesina Xóchitl Trujillo Enrique Sánchez-Pastor Clemente Vásquez Elena Castro Raymundo Velasco Rocío Montoya-Pérez Carlos Onetti 《The Journal of membrane biology》2009,229(2):91-99
The effect of cannabinoids on caffeine contractures was investigated in slow and fast skeletal muscle fibers using isometric
tension recording. In slow muscle fibers, WIN 55,212-2 (10 and 5 μM) caused a decrease in tension. These doses reduced maximum
tension to 67.43 ± 8.07% (P = 0.02, n = 5) and 79.4 ± 14.11% (P = 0.007, n = 5) compared to control, respectively. Tension-time integral was reduced to 58.37 ± 7.17% and 75.10 ± 3.60% (P = 0.002, n = 5), respectively. Using the CB1 cannabinoid receptor agonist ACPA (1 μM) reduced the maximum tension of caffeine contractures by 68.70 ± 11.63% (P = 0.01, n = 5); tension-time integral was reduced by 66.82 ± 6.89% (P = 0.02, n = 5) compared to controls. When the CB1 receptor antagonist AM281 was coapplied with ACPA, it reversed the effect of ACPA on caffeine-evoked tension. In slow and
fast muscle fibers incubated with the pertussis toxin, ACPA had no effect on tension evoked by caffeine. In fast muscle fibers,
ACPA (1 μM) also decreased tension; the maximum tension was reduced by 56.48 ± 3.4% (P = 0.001, n = 4), and tension-time integral was reduced by 57.81 ± 2.6% (P = 0.006, n = 4). This ACPA effect was not statistically significant with respect to the reduction in tension in slow muscle fibers.
Moreover, we detected the presence of mRNA for the cannabinoid CB1 receptor on fast and slow skeletal muscle fibers, which was significantly higher in fast compared to slow muscle fiber expression.
In conclusion, our results suggest that in the slow and fast muscle fibers of the frog cannabinoids diminish caffeine-evoked
tension through a receptor-mediated mechanism. 相似文献
12.
Dissociated single fibers from the mouse flexor digitorum brevis (FDB) muscle were used in patch clamp experiments to investigate the mechanisms of activation and inactivation of KATP in mammalian skeletal muscle. Spontaneous rundown of channel activity, in many excised patches, occurred gradually over a period of 10–20 min. Application of 1.0 mm free-Ca2+ to the cytoplasmic side of the patch caused irreversible inactivation of KATP within 15 sec. Ca2+-induced rundown was not prevented by the presence of 1.0 m okadaic acid or 2.0 mg ml– of an inhibitor of calcium-activated neutral proteases, a result consistent with the conclusion that phosphatases or calcium-activated neutral proteases were not involved in the rundown process. Application of 1.0 mm Mg.ATP to Ca2+inactivated KATP caused inhibition of residual activity but little or no reactivation of the channels upon washout of ATP, even in the presence of the catalytic subunit of cyclic AMP-dependent protein kinase (10 U ml–1). Mg.ATP also failed to reactivate KATP, even after only partial spontaneous rundown, despite the presence of channels that could be activated by the potassium channel opener BRL 38227. Nucleotide diphosphates (500 m; CDP, UDP, GDP and IDP) caused immediate and reversible opening of Ca2+-inactivated KATP. Reactivation of KATP by ADP (100 m) increased further upon removal of the nucleotide. In contrast to KATP from cardiac and pancreatic cells, there was no evidence for phosphorylation of KATP from the surface sarcolemma of dissociated single fibers from mouse skeletal muscle. The small degree of activation occasionally observed following application of 10 m or 1.0 mm Mg.ATP could have been due to the generation of ADP from ATP hydrolysis and not through phosphorylation. Data are consistent with the suggestion that Ca2+ inactivation of KATP involves a gating mechanism that can be reopened by nucleotide diphosphates.M.H. is supported by the Medical Research Council. 相似文献
13.
García MC Farías JM Escamilla J Sánchez-Armass S Sánchez JA 《The Journal of membrane biology》1999,168(2):141-148
The effects of a long-term blockade of L-type Ca2+ channels on membrane currents and on the number of dihydropyridine binding sites were investigated in skeletal muscle fibers.
Ca2+ currents (I
Ca) and intramembrane charge movement were monitored using a voltage-clamp technique. The peak amplitude of I
Ca increased by more than 40% in fibers that were previously incubated for 24 hr in solutions containing the organic Ca2+ channel blocker nifedipine or in Ca2+-free conditions. A similar incubation period with Cd2+, an inorganic blocker, produced a moderate increase of 20% in peak I
Ca. The maximum mobilized charge (Q
max) increased by 50% in fibers preincubated in Ca2+-free solutions or in the presence of Cd2+.
Microsomal preparations from frog skeletal muscle were isolated by differential centrifugation. Preincubation with Cd2+ prior to the isolation of the microsomal fraction doubled the number of 3H-PN200-110 binding sites and produced a similar increase in the values of the dissociation constant. The increase in the
number of binding sites is consistent with the increase in the peak amplitude of I
Ca as well as with the increase in Q
max.
Received: 31 August 1998/Revised: 7 December 1998 相似文献
14.
The superficial (tonic) abdominal flexor muscles of Atya lanipes do not generate Ca2+ action potentials when depolarized and have no detectable inward Ca2+ current. These fibers, however, are strictly dependent on Ca2+ influx for contraction, suggesting that they depend on Ca2+-induced Ca2+ release for contractile activation. The nature of the communication between Ca2+ channels in the sarcolemmal/tubular membrane and Ca2+ release channels in the sarcoplasmic reticulum in this crustacean muscle was investigated. The effects of dihydropyridines
on tension generation and the passive electrical response were examined in current-clamped fibers: Bay K 8644 enhanced tension
about 100% but did not alter the passive electrical response; nifedipine inhibited tension by about 70%. Sr2+ and Ba2+ action potentials could be elicited in Ca2+-free solutions. The spikes generated by these divalent cations were abolished by nifedipine. As the Sr2+ or Ba2+ concentrations were increased, the amplitudes of the action potentials and their maximum rate of rise, V
max
, increased and tended towards saturation. Three-microelectrode voltage-clamp experiments showed that even at high (138 mm) extracellular Ca2+ concentration the channels were silent, i.e., no inward Ca2+ current was detected. In Ca2+-free solutions, inward currents carried by 138 mm Sr2+ or Ba2+ were observed. The currents activated at voltages above −40 mV and peaked at about 0 mV. This voltage-activation profile
and the sensitivity of the channels to dihydropyridines indicate that they resemble L-type Ca2+ channels. Peak inward current density values were low, ca.−33 μA/cm2 for Sr2+ and −14 μA/cm2 for Ba2+, suggesting that Ca2+ channels are present at a very low density. It is concluded that Ca2+-induced Ca2+ release in this crustacean muscle operates with an unusually high gain: Ca2+ influx through the silent Ca2+ channels is too low to generate a macroscopic inward current, but increases sufficiently the local concentration of Ca2+ in the immediate vicinity of the sarcoplasmic reticulum Ca2+ release channels to trigger the highly amplified release of Ca2+ required for tension generation.
Received: 5 April 1999/Revised: 15 September 1999 相似文献
15.
本文对玉米花粉肌动蛋白和兔骨骼肌肌动蛋白进行了比较研究。玉米花粉肌动蛋白与兔骨骼肌肌动蛋白具有相同的分子量(42KD)。玉米花粉肌动蛋白可与兔抗鸡胃肌动蛋白抗血清产生免疫沉淀反应。玉米花粉肌动蛋白与兔骨骼肌肌动蛋白的氨基酸组成以及胰蛋白酶水解所得到的肽谱都相似。它们的羧基未端氨基酸顺序完全一致,其顺序都是Lys.Cys.Phe(COOH)。它们的圆二色谱基本相同,由圆二色谱计算得到的二级结构数据也相近。以上的结果表明了玉米花粉肌动蛋白与兔骨骼肌肌动蛋白的相似性。 相似文献
16.
Properties of Shaker-type Potassium Channels in Higher Plants 总被引:2,自引:0,他引:2
Potassium (K+), the most abundant cation in biological organisms, plays a crucial role in the survival and development of plant cells,
modulation of basic mechanisms such as enzyme activity, electrical membrane potentials, plant turgor and cellular homeostasis.
Due to the absence of a Na+/K+ exchanger, which widely exists in animal cells, K+ channels and some type of K+ transporters function as K+ uptake systems in plants. Plant voltage-dependent K+ channels, which display striking topological and functional similarities with the voltage-dependent six-transmembrane segment
animal Shaker-type K+ channels, have been found to play an important role in the plasma membrane of a variety of tissues and organs in higher plants.
Outward-rectifying, inward-rectifying and weakly-rectifying K+ channels have been identified and play a crucial role in K+ homeostasis in plant cells. To adapt to the environmental conditions, plants must take advantage of the large variety of
Shaker-type K+ channels naturally present in the plant kingdom. This review summarizes the extensive data on the structure, function, membrane
topogenesis, heteromerization, expression, localization, physiological roles and modulation of Shaker-type K+ channels from various plant species. The accumulated results also help in understanding the similarities and differences
in the properties of Shaker-type K+ channels in plants in comparison to those of Shaker channels in animals and bacteria. 相似文献
17.
Christoph Fahlke Christine Dürr Alfred L. George Jr. 《The Journal of general physiology》1997,110(5):551-564
Voltage-gated Cl− channels belonging to the ClC family exhibit unique properties of ion permeation and gating. We functionally probed the conduction pathway of a recombinant human skeletal muscle Cl− channel (hClC-1) expressed both in Xenopus oocytes and in a mammalian cell line by investigating block by extracellular or intracellular I− and related anions. Extracellular and intracellular I− exert blocking actions on hClC-1 currents that are both concentration and voltage dependent. Similar actions were observed for a variety of other halide (Br−) and polyatomic (SCN−, NO3
−, CH3SO3
−) anions. In addition, I− block is accompanied by gating alterations that differ depending on which side of the membrane the blocker is applied. External I− causes a shift in the voltage-dependent probability that channels exist in three definable kinetic states (fast deactivating, slow deactivating, nondeactivating), while internal I− slows deactivation. These different effects on gating properties can be used to distinguish two functional ion binding sites within the hClC-1 pore. We determined K
D values for I− block in three distinct kinetic states and found that binding of I− to hClC-1 is modulated by the gating state of the channel. Furthermore, estimates of electrical distance for I− binding suggest that conformational changes affecting the two ion binding sites occur during gating transitions. These results have implications for understanding mechanisms of ion selectivity in hClC-1, and for defining the intimate relationship between gating and permeation in ClC channels. 相似文献
18.
Role of Potassium Channels in Amyloid-Induced Cell Death 总被引:20,自引:1,他引:19
Luis V. Colom Maria E. Diaz David R. Beers Alan Neely Wen-jie Xie Stanley H. Appel 《Journal of neurochemistry》1998,70(5):1925-1934
Abstract: Basal forebrain cholinergic neurons are severely depleted early in Alzheimer's disease and appear particularly susceptible to amyloid β-peptide (Aβ) toxicity in vivo. To model this effect in vitro, a cholinergic septal cell line (SN56) was exposed to Aβ. SN56 cells exhibited a tetraethylammonium (TEA)-sensitive outward K+ current with delayed rectifier characteristics. Increases of 64% (±19; p < 0.02) and 44% (±12; p < 0.02) in K+ current density were noted 6–12 and 12–18 h following the addition of Aβ to SN56 cell cultures, respectively. Morphological observation and staining for cell viability showed that 25 ± 4 and 39 ± 4% of SN56 cells were dead after 48- and 96-h exposures to Aβ, respectively. Perfusion of SN56 cells with 10–20 mM TEA blocked 71 ± 6 to 92 ± 2% of the outward currents, widened action potentials, elevated [Ca2+]i, and inhibited 89 ± 14 and 68 ± 14% of the Aβ toxicity. High [K+]o, which depolarizes cell membranes and increases [Ca2+]i, also protected SN56 cells from Aβ toxicity. This effect appeared specific since glucose deprivation of SN56 cells did not alter K+ current density and TEA did not protect these cells from hypoglycemic cell death. Furthermore, Aβ was toxic to a dopaminergic cell line (MES23.5) that expressed a K+ current with delayed rectifier characteristics; K+ current density was not altered by Aβ and MES23.5 cells were not protected by TEA from Aβ toxicity. In contrast, a noncholinergic septal cell line (SN48) that shows minimal outward K+ currents was resistant to the toxicity of Aβ. These data suggest that a K+ channel with delayed rectifier characteristics may play an important role in Aβ-mediated toxicity for septal cholinergic cells. 相似文献
19.
钾离子通道为组织细胞内分布最广、种类最多的离子通道,在细胞增殖、分化及肿瘤细胞的侵袭转移中起着关键作用。神经胶质瘤是颅内最多发的恶性肿瘤,目前其主要治疗方式为手术加术后放化疗,术后五年生存率较低,寻找其相关发病机制及化疗靶点具有重要意义。目前已有多项研究表明,多种钾离子通道在胶质瘤中呈特异性高表达,且与胶质瘤的增殖、分化有密切关系,一些钾离子通道可作为胶质瘤的诊断和预防因子,有望成为未来胶质瘤化疗的新靶点,研究钾离子通道与神经胶质瘤的关系对胶质瘤的诊断、预防和治疗有重要意义。本文主要对近年来钾离子通道与神经胶质瘤关系研究的新进展进行综述。 相似文献
20.
1. Glucose is one of the most important substrates for generating metabolic energy required for the maintenance of cellular functions. Glucose-mediated changes in neuronal firing pattern have been observed in the central nervous system of mammals. K+ channels directly regulated by intracellular ATP have been postulated as a linkage between cellular energetic metabolism and excitability; the functional roles ascribed to these channels include glucose-sensing to regulate energy homeostasis and neuroprotection under energy depletion conditions. The hippocampus is highly sensitive to metabolic insults and is the brain region most sensitive to ischemic damage. Because the identity of metabolically regulated potassium channels present in hippocampal neurons is obscure, we decided to study the biophysical properties of glucose-sensitive potassium channels in hippocampal neurons.2. The dependence of membrane potential and the sensitivity of potassium channels to glucose and ATP in rat hippocampal neurons were studied in cell-attached and excised inside-out membrane patches.3. We found that under hypoglycemic conditions, at least three types of potassium channels were activated; their unitary conductance values were 37, 147, and 241 pS in symmetrical K+, and they were sensitive to ATP. For K+ channels with unitary conductance of 37 and 241, when the membrane potential was depolarized the longer closed time constant diminished and this produced an increase in the open-state probability; nevertheless, the 147-pS channels were not voltage-dependent.4. We propose that neuronal glucose-sensitive K+ channels in rat hippocampus include subtypes of ATP-sensitive channels with a potential role in neuroprotection during short-term or prolonged metabolic stress. 相似文献