Serotonin-operated potassium current in CA1 neurons dissociated from rat hippocampus

1993 ◽  
Vol 69 (4) ◽  
pp. 1044-1052 ◽  
Author(s):  
H. Uneyama ◽  
S. Ueno ◽  
N. Akaike
Keyword(s):  
Pyramidal Neurons ◽  
Muscarinic Acetylcholine Receptor ◽  
Outward Current ◽  
Membrane Conductance ◽  
External Solution ◽  
Equilibrium Potential ◽  
Dependent Manner ◽  
Concentration Dependent Manner ◽  
Hippocampal Pyramidal Neurons ◽  
Outward Currents

1. The intracellular mechanisms of serotonin (5-HT) response were investigated in dissociated rat hippocampal pyramidal neurons using the nystatin-perforated patch technique. 2. Under voltage-clamp conditions, 5-HT evoked outward currents (I5-HT) with an increase in membrane conductance at a holding potential of -40 mV. The outward current reversed at the K+ equilibrium potential, which shifted 59.4 mV with a 10-fold change in extracellular K+ concentration. 3. The first application of 5-HT on neurons perfused with Ca(2+)-free external solution induced outward currents of I5-HT but the amplitude was diminished dramatically with successive applications. Pretreatment with the membrane-permeant Ca2+ chelator 1,2-bis-(O-aminophenoxy)ethane-N,N,N',N'-tetraacetic acid, tetraacetoxymethyl ester (BAPTA-AM) also diminished the I5-HT amplitude. 4. Pretreatment with pertussis toxin (PTX) had no effect on I5-HT. 5. The I5-HT was not cross-desensitized with the caffeine-induced outward current but with outward current mediated by the muscarinic acetylcholine receptor. Pretreatment with Li+ significantly enhanced the I5-HT, indicating that I5-HT is involved in the elevation of intracellular free Ca2+ released from inositol triphosphate (IP3)-sensitive Ca2+ store sites but not from the caffeine-sensitive ones. 6. The calmodulin (CaM) antagonists, trifluoperazine and N-(6-aminohexyl)-5-chloro-1-naphthalenesulfonamide (W-7), inhibited I5-HT in a concentration-dependent manner. 7. The Ca2+/CaM-dependent protein kinase II inhibitor 1-[N,O-Bis (5-isoquinolinesulfonyl)-N-methyl-L-tyrosil]-4-phenylpiperazine depressed the I5-HT.(ABSTRACT TRUNCATED AT 250 WORDS)

Muscarinic receptor activation of potassium channels in rat dentate gyrus neurons

1993 ◽  
Vol 70 (4) ◽  
pp. 1544-1552 ◽  
Author(s):  
J. Nabekura ◽  
S. Ebihara ◽  
N. Akaike
Keyword(s):  
Dentate Gyrus ◽  
Reversal Potential ◽  
Outward Current ◽  
External Solution ◽  
Receptor Activation ◽  
Hill Coefficient ◽  
Equilibrium Potential ◽  
Maximal Response ◽  
Dependent Manner ◽  
Concentration Dependent Manner

1. The effects of acetylcholine (ACh) on granule cells freshly dissociated from rat dentate gyrus (DG) were studied using the nystatin perforated patch technique. This method allowed us to study ACh-induced currents (IACh) under voltage clamp without "run-down" of the ACh response. In some experiments, we used the conventional whole-cell method for intracellular application of drugs not permeable to cell membrane. 2. At a holding potential of -40 mV, ACh induced an outward current. The amplitude of IACh increased in a sigmoidal fashion with increasing ACh concentration. The half-maximal response and the Hill coefficient determined from the relation between ACh concentration and response were 4.98 x 10(-7) M and 1.70, respectively. 3. The reversal potential of IACh was close to the K+ equilibrium potential. The IACh was accompanied by an enhancement of the K+ current. 4. Muscarine and McN-A-343 mimicked the ACh response, whereas oxotremorine induced no response. 5. Muscarinic antagonists reversibly suppressed the IACh (10(-5) M) in a concentration-dependent manner, where the values of half-inhibition concentration (IC50) were 1.03 x 10(-6) M for pirenzepine and 2.21 x 10(-5) M for AF-DX-116. 6. Intracellular perfusion with GDP-beta S suppressed the IACh greatly. The IACh persisted in the neurons pretreated with an external solution containing pertussis toxin (IAP) for 18 h. 7. In the neurons perfused with Ca(2+)-free external solution containing 2 mM ethylene glycol-O,O'-bis (beta-aminoethyl ether)-N,N,N',N'-tetraacetic acid and 10 mM Mg2+, the first application of ACh induced the IACh with an amplitude similar to that in the standard solution.(ABSTRACT TRUNCATED AT 250 WORDS)

Metabotropic glutamate receptor agonist-induced hyperpolarizations in rat basolateral amygdala neurons: receptor characterization and ion channels

1996 ◽  
Vol 76 (5) ◽  
pp. 3059-3069 ◽  
Author(s):  
K. H. Holmes ◽  
N. B. Keele ◽  
V. L. Arvanov ◽  
P. Shinnick-Gallagher
Keyword(s):  
Dicarboxylic Acid ◽  
Glutamate Receptor ◽  
Basolateral Amygdala ◽  
Metabotropic Glutamate Receptor ◽  
Outward Current ◽  
Channel Blockers ◽  
Dependent Manner ◽  
Concentration Dependent Manner ◽  
Metabotropic Glutamate ◽  
Outward Currents

1. Metabotropic glutamate receptor (mGluR)-agonist-induced hyperpolarizations and corresponding outward currents were analyzed in basolateral amygdala (BLA) neurons in rat brain slice preparations with current-clamp and single-electrode voltage-clamp recording to characterize the mGluR subtype(s) and the ion channel(s) mediating this response. 2. The mGluR agonist (1S,3R)-1-amino-cyclopentane-1,3-dicarboxylic acid (1S,3R-ACPD) induced a membrane hyperpolarization or outward current in BLA neurons in a concentration-dependent manner (median effective concentration = 34 microM; range = 10-200 microM); the 1S,3R-ACPD hyperpolarizations are recorded in 89% of neurons that accommodate or cease firing in response to a 400-ms depolarizing current injection (0.5 nA). 3. mGluR agonists elicited hyperpolarizations or outward currents in a concentration-dependent manner in the following rank order of potency: (2S,3S,4S)-alpha-(carboxycyclopropyl)glycine (L-CCG-I) > 1S,3R-ACPD > (s)-4-carboxyphenylglycine = (RS)-4-carboxy-3-hydroxyphenylglycine (4C3HPG) > L-aminophosphonobutyric acid > (1S,3S)-1-amino-cyclopentane-1,3-dicarboxylic acid. In contrast, the mGluR agonists quisqualate and ibotenate induced only depolarizations in the presence of D-2-amino-5-phosphonovalerate and 6-cyano-7-nitroquinoxaline-2,3-dione in BLA neurons. 4. The 1S,3R-ACPD-induced outward current is mediated through a large-conductance calcium-dependent potassium (BK) conductance. The BK channel blockers iberiotoxin and charybdotoxin blocked the response, as did the potassium channel blockers tetraethylammonium and 4-aminopyridine; the small-conductance calcium-activated potassium channel blocker apamin did not affect the response. 5. The mGluR-agonist-induced hyperpolarization is blocked in amygdala slices from animals pretreated with pertussis toxin (PTX). 1S,3R-ACPD hyperpolarizations were recorded in neurons contralateral but not ipsilateral to the site of PTX injection. 6. The antagonist (+/-)-alpha-methyl-4-carboxyphenylglycine (MCPG, 500 microM) reduced significantly the 1S,3R-ACPD-induced hyperpolarization. 7. In conclusion, the relative potency of L-CCG-I and 4C3HPG in evoking only hyperpolarizations (outward currents) in accommodating neurons, and the observation that MCPG (500 microM) reduces the hyperpolarization, suggest that a group-II-like mGluR underlies the hyperpolarizing response. The mGluR-induced response is sensitive to iberiotoxin and to pretreatment with PTX, suggesting activation of BK channels through a group II mGluR linked to a PTX-sensitive G protein in BLA neurons.

Glycine-gated chloride current in acutely isolated rat hypothalamic neurons

1989 ◽  
Vol 62 (6) ◽  
pp. 1400-1409 ◽  
Author(s):  
N. Akaike ◽  
M. Kaneda
Keyword(s):  
Reversal Potential ◽  
External Solution ◽  
Hill Coefficient ◽  
Equilibrium Potential ◽  
Dependent Manner ◽  
Hypothalamic Neurons ◽  
Adult Rats ◽  
Concentration Dependent Manner ◽  
Current Decay ◽  
Continuous Application

1. Electrical and pharmacologic properties of glycine-induced currents were investigated in single hypothalamic neurons acutely isolated from young and adult rats by the use of a "concentration-clamp" technique, which allows both internal perfusion and rapid application of an external solution under single-electrode voltage-clamp. 2. The glycine-induced current reversed at the Cl- equilibrium potential (ECl), and a 10-fold decrease of extracellular Cl- with a large impermeable anion resulted in a 53 mV shift of the glycine reversal potential (EGly). 3. Glycine-induced Cl- currents (ICl) increased sigmoidally in a concentration-dependent manner with a Kd of 9 X 10(-5) M at a Hill coefficient of 1.8. Current inactivation occurred completely at all concentrations within 10 s. EGly remained unchanged during continuous application of glycine, suggesting that the inactivation process is because of desensitization. 4. The glycine-induced conductance exhibited a striking voltage dependency at membrane potentials more negative than -50 mV and reached a steady state value when hyperpolarized beyond -110 mV. 5. Both the activation and inactivation phases of glycine-induced ICl are described by double exponential (fast and slow components) functions with the concentrations used. All four time constants decreased with increasing glycine concentration. 6. The slow time constant of the current decay induced by glycine increased with depolarization and decreased with hyperpolarization, indicating that the rate of desensitization is considerably voltage dependent. The fast decay showed little voltage dependency. 7. Recovery of the glycine response after complete desensitization consisted of two components. 8. The blockade of the glycine response by strychnine and picrotoxin was noncompetitive.

ATP-induced rise in apamin-sensitive Ca(2+)-dependent K+ conductance in adult rat hepatocytes

1996 ◽  
Vol 270 (2) ◽  
pp. G307-G313 ◽  
Author(s):  
Y. Yamashita ◽  
H. Ogawa ◽  
N. Akaike
Keyword(s):  
Rat Hepatocytes ◽  
Female Rats ◽  
Equilibrium Potential ◽  
Dependent Manner ◽  
Calmodulin Antagonists ◽  
Intracellular Perfusion ◽  
Concentration Dependent Manner ◽  
Adult Rat ◽  
Outward Currents ◽  
Adult Rat Hepatocytes

Exogenous ATP-induced transient outward currents (IATP) were investigated in isolated adult rat hepatocytes using conventional whole cell patch and nystatin perforated patch recording modes. The IATP increased in a sigmoidal fashion with an increase in ATP concentration, where the half-maximal concentration was 1.4 microM. The order of current potency was 2-methylthio-ATP > or = UTP = ATP > > alpha, beta-methylene-ATP. IATP was depressed in a concentration-dependent manner by suramin and apamin. IATP reversed its direction at the K+ equilibrium potential. IATP occurred easily in hepatocytes obtained from female rats weighing > 250 g. Removal of extracellular Ca2+ had no effect on the peak amplitude of IATP, but thapsigargin abolished it. Intracellular perfusion with 1,2-bis(2-aminophenoxy)ethane-N,N,N',N'-tetraacetic acid, heparin, guanosine 5'-O-(3-thiotriphosphate), or neomycin also abolished IATP. Pretreatment with pertussis toxin or calmodulin antagonists had no effect on IATP. It was concluded that ATP binding to both P2Y and P2U purinoceptors coupled to G protein may raise apaminsensitive Ca(2+)-dependent K+ conductance via a phospholipase C-inositol trisphosphate-Ca2+ signaling pathway.

K+ Currents Generated by NMDA Receptor Activation in Rat Hippocampal Pyramidal Neurons

2002 ◽  
Vol 87 (6) ◽  
pp. 2983-2989 ◽  
Author(s):  
Mala M. Shah ◽  
Dennis G. Haylett
Keyword(s):  
Nmda Receptor ◽  
Time Course ◽  
Pyramidal Neurons ◽  
Outward Current ◽  
Receptor Activation ◽  
Bk Channel ◽  
Hippocampal Pyramidal Neurons ◽  
Sk Channel ◽  
Outward Currents ◽  
Nmda Receptor Activation

Long lasting outward currents mediated by Ca2+-activated K+ channels can be induced by Ca2+ influx through N-methyl-d-aspartate (NMDA)-receptor channels in voltage-clamped hippocampal pyramidal neurons. Using specific inhibitors, we have attempted to identify the channels that underlie these outward currents. At a holding potential of −50 mV, applications of 1 mM NMDA to the soma of cultured hippocampal pyramidal neurons induced the expected inward currents. In 44% of cells tested, these were followed by outward currents (average amplitude 60 ± 7 pA) that peaked 2.5 s after the initiation of the inward NMDA currents and decayed with a time constant of 1.4 s. In 43% of those cells exhibiting an outward current, SK channel inhibitors, UCL 1848 (100 nM) and apamin (100 nM) abolished the outward current. In the remainder of the cells, the outward currents were either insensitive or only partly inhibited (44 ± 4%) by 100 nM UCL 1848. In these cells, the outward currents were reduced by the slow afterhyperpolarization (sAHP) inhibitors, muscarine (3 μM; 43 ± 9%), UCL 1880 (3 μM; 34 ± 10%), and UCL 2027 (3 μM; 57 ± 6%). Neither the BK channel inhibitor, charybdotoxin (100 nM), nor the Na+/K+ ATPase inhibitor, ouabain (100 μM), reduced these outward currents. Irrespective of the pharmacology, the time course of the outward current did not differ. Interestingly, no correlation was observed between the presence of a slow apamin-insensitive afterhyperpolarization and an outward current insensitive to SK channel blockers following NMDA-receptor activation. It is concluded that an NMDA-mediated rise in [Ca2+]i can result in the activation of apamin-sensitive SK channels and of the channels that underlie the sAHP. The activation of these channels may, however, depend on their location relative to NMDA receptors as well as on the spatial Ca2+ buffering within individual neurons.

Quinolones and fenbufen interact with GABAA receptor in dissociated hippocampal cells of rat

1991 ◽  
Vol 66 (2) ◽  
pp. 497-504 ◽  
Author(s):  
N. Akaike ◽  
T. Shirasaki ◽  
T. Yakushiji
Keyword(s):  
Gabaa Receptor ◽  
Pyramidal Neurons ◽  
Equilibrium Potential ◽  
Dependent Manner ◽  
Gamma Aminobutyric Acid ◽  
Patch Clamp Technique ◽  
Concentration Dependent Manner ◽  
Inflammatory Agent ◽  
Quinolone Antibiotics ◽  
Anti Inflammatory

1. Interaction of quinolone antibiotics and the anti-inflammatory agent fenbufen with the gamma-aminobutyric acid-A (GABAA) receptor-chloride channel complex in pyramidal neurons freshly dissociated from the hippocampal CA1 region of the rats was investigated in whole-cell mode, using the patch-clamp technique under voltage-clamp conditions. 2. Quinolones in clinical doses had no effects on the GABA-gated Cl- current (ICl) but slightly suppressed the response at concentrations greater than 10(-5) M. A metabolite of fenbufen, 4-biphenylacetic acid (BPA), also had little effect on the GABA response at therapeutic concentrations. 3. Coadministration of one of quinolones and BPA suppressed the GABA-gated ICl with increase in each of them in a concentration-dependent manner, and there was a parallel shift of the concentration-response curve for GABA to the right but with no effect on the maximum response, thereby indicating a competitive antagonism. The inhibitory potency of antibiotics in combination with BPA was in the order of norfloxacin much greater than enoxacin greater than cyprofloxacin greater than pipemidic acid much greater than ofloxacin greater than cinoxacin = piromidic acid = nalidixic acid = 0. 4. Norfloxacin and BPA, administered simultaneously, also strongly suppressed pentobarbital sodium (PB)-gated ICl, but they did not act on benzodiazepine (BZP) receptors. 5. Both GABA- and PB-induced ICls reversed at the Cl- equilibrium potential (ECl). In the presence of BPA, the quinolone-induced inhibition of GABA-gated ICls showed no voltage dependence. 6. It was concluded that, in the presence of an anti-inflammatory agent, the quinolone antibiotics decrease the affinity of GABAA receptors, the result being induction of epileptogenic neurotoxicities.

Effects of glucose deprivation on NMDA-induced current and intracellular Ca2+ in rat substantia nigra neurons

1996 ◽  
Vol 75 (2) ◽  
pp. 740-749 ◽  
Author(s):  
Y. Nakashima ◽  
H. Ishibashi ◽  
N. Harata ◽  
N. Akaike
Keyword(s):  
Substantia Nigra ◽  
Outward Current ◽  
Glucose Deprivation ◽  
Equilibrium Potential ◽  
Dependent Manner ◽  
Induced Current ◽  
Patch Clamp Technique ◽  
Concentration Dependent Manner ◽  
Inward Current ◽  
Rat Substantia Nigra

1. The effects of glucose deprivation on N-methyl-D-asparate (NMDA)-induced current (INMDA) and the intracellular free Ca2+ concentration ([Ca2+]i) in the acutely dissociated rat substantia nigra neurons were investigated using the nystatin-perforated patch-clamp technique under voltage clamp and the microfluometry with a fluorescent probe, Indo-1. 2. Application of NMDA induced a peak and a successive steady-state inward current, and an outward current immediately after washout at a holding potential of -40 mV. The amplitudes of the three current components of INMDA were increased by increasing the concentrations of NMDA with half-maximum concentrations (EC50s) of 1.1 x 10(-4) M, 1.2 x 10(-4) M, and 1.6 x 10(-4) M, respectively. 3. The reversal potentials of the peak inward and outward currents were -4 +/- 3 (SE) mV and -76 +/- 2 mV, respectively. The latter was close to the theoretical K+ equilibrium potential (-82 mV). 4. The outward current was potentiated by increase in extracellular Ca2+ concentration and was blocked by Cs+ internal solution and suppressed by 5 x 10(-3) M tetraethylammonium chloride and 10(-7) M charybdotoxin, indicating that it was Ca(2+)-activated K+ current. 5. Application of NMDA increased [Ca2+]i in a concentration-dependent manner with an EC50 of 3.9 x 10(-5) M. 6. Depriving the external solution of glucose induced a slowly developing outward current and increased the basal level of [Ca2+]i. It also prolonged the NMDA-induced outward current without affecting the peak inward current, and prolonged the NMDA-induced increase in [Ca2+]i without changing the peak [Ca2+]i. 7. These findings suggest that the deprivation of glucose did not affect the NMDA-induced influx of Ca2+ into the cells, but it inhibited Ca2+ clearance by affecting the efflux of Ca2+ to the extracellular space, reuptake into the intracellular Ca2+ stores, and/or active extrusion from intracellular stores.

Nociceptin Augments K+ Currents in Hippocampal CA1 Neurons by Both ORL-1 and Opiate Receptor Mechanisms

1999 ◽  
Vol 82 (4) ◽  
pp. 1776-1785 ◽  
Author(s):  
Samuel G. Madamba ◽  
Paul Schweitzer ◽  
George Robert Siggins
Keyword(s):  
Receptor Antagonist ◽  
Pyramidal Neurons ◽  
Partial Agonist ◽  
Opiate Receptors ◽  
Outward Current ◽  
Opiate Receptor ◽  
Equilibrium Potential ◽  
Orphanin Fq ◽  
Hippocampal Pyramidal Neurons ◽  
M Current

We previously reported (see also the accompanying paper) that dynorphin A significantly enhanced the voltage-dependent K+ M-current ( I M) in CA3 and CA1 hippocampal pyramidal neurons (HPNs). Because the opioid-receptor-like-1 (ORL-1) receptor shares a high sequence homology with opioid receptors and is expressed in rat hippocampus, we examined the effects of orphanin FQ or nociceptin, the endogenous ligand for the ORL-1 receptor, using the rat hippocampal slice preparation and intracellular voltage-clamp recording. Current-voltage ( I-V) relationships from CA1 HPNs revealed that nociceptin superfusion induced an outward current reversing near the equilibrium potential for K+ ions. Ba2+ (2 mM) blocked this effect. The nociceptin-induced current was largest at depolarized membrane potentials, where I M is largely activated. Nociceptin concentrations of 0.5–1 μM (but not 0.1 μM) significantly increased I M relaxation amplitudes with recovery on washout. Interestingly, both the general opiate antagonist naloxone and the κ receptor antagonist nor-binaltorphimine (nBNI) inhibited the nociceptin-induced I Mincreases and outward currents in the depolarized range but not the inward current induced at hyperpolarized potentials. The putative ORL-1 receptor antagonist, [Phe1Ψ(CH2-NH)Gly2]NC(1–13)NH2(hereafter ORLAn), blocked most of the nociceptin current near rest but not the I M increase. However, ORLAn alone had direct effects similar to those of nociceptin, indicating that ORLAn might be a partial agonist. Our results suggest that nociceptin postsynaptically modulates the excitability of HPNs through ORL-1 and κ-like opiate receptors linked to different K+channels.

Heterogeneous Actions of Serotonin on Interneurons in Rat Visual Cortex

2003 ◽  
Vol 89 (3) ◽  
pp. 1278-1287 ◽  
Author(s):  
Zixiu Xiang ◽  
David A. Prince
Keyword(s):  
Receptor Antagonist ◽  
Receptor Agonist ◽  
Reversal Potential ◽  
Outward Current ◽  
Membrane Conductance ◽  
Pyramidal Cells ◽  
Equilibrium Potential ◽  
Inward Current ◽  
Outward Currents ◽  
Layer V

The effects of serotonin (5-HT) on excitability of two cortical interneuronal subtypes, fast-spiking (FS) and low threshold spike (LTS) cells, and on spontaneous inhibitory postsynaptic currents (sIPSCs) in layer V pyramidal cells were studied in rat visual cortical slices using whole-cell recording techniques. Twenty-two of 28 FS and 26 of 35 LTS interneurons responded to local application of 5-HT. In the group of responsive neurons, 5-HT elicited an inward current in 50% of FS cells and 15% of LTS cells, an outward current was evoked in 41% of FS cells and 81% of LTS cells, and an inward current followed by an outward current in 9% of FS cells and 4% LTS cells. The inward and outward currents were blocked by a 5-HT3 receptor antagonist, tropisetron, and a 5-HT1A receptor antagonist, NAN-190, respectively. The 5-HT–induced inward and outward currents were both associated with an increase in membrane conductance. The estimated reversal potential was more positive than −40 mV for the inward current and close to the calculated K+equilibrium potential for the outward current. The 5-HT application caused an increase, a decrease, or an increase followed by a decrease in the frequency of sIPSCs in pyramidal cells. The 5-HT3 receptor agonist 1-( m-chlorophenyl) biguanide increased the frequency of larger and fast-rising sIPSCs, whereas the 5-HT1Areceptor agonist (±)8-hydroxydipropylaminotetralin hydrobromide elicited opposite effects and decreased the frequency of large events. These data indicate that serotonergic activation imposes complex actions on cortical inhibitory networks, which may lead to changes in cortical information processing.

Nitric oxide mediates outward potassium currents in opossum esophageal circular smooth muscle

1996 ◽  
Vol 270 (6) ◽  
pp. G932-G938 ◽  
Author(s):  
J. Jury ◽  
K. R. Boev ◽  
E. E. Daniel
Keyword(s):  
Nitric Oxide ◽  
Smooth Muscle ◽  
Circular Muscle ◽  
Outward Current ◽  
Equilibrium Potential ◽  
Patch Clamp Technique ◽  
Pipette Solution ◽  
Whole Cell ◽  
Circular Smooth Muscle ◽  
Outward Currents

Single smooth muscle cells from the opossum body circular muscle were isolated and whole cell currents were characterized by the whole cell patch-clamp technique. When the cells were held at -50 mV and depolarized to 70 mV in 20-mV increments, initial small inactivating inward currents were evoked (-30 to 30 mV) followed by larger sustained outward currents. Depolarization from a holding potential of -90 mV evoked an initial fast inactivating outward current sensitive to 4-aminopyridine but not to high levels of ethylene glycol-bis(beta-aminoethyl ether)-N,N,N',N'-tetraacetic acid (EGTA). The outward currents reversed near K+ equilibrium potential and were abolished when KCl was replaced by CsCl in the pipette solution. The sustained outward current was inhibited by quinine and cesium. High EGTA in the pipette solution reduced but did not abolish the sustained outward currents, suggesting that both Ca(2+)-dependent and -independent currents were evoked. The nitric oxide (NO)-releasing agents Sin-1 and sodium nitroprusside increased outward K+ currents. High levels of EGTA in the pipette solution abolished the increase in outward current induced by Sin-1. The presence of cyclopiazonic acid, an inhibitor of the sarcoplasmic reticulum (SR) Ca2+ pump, blocked the effects of NO-releasing agents. We conclude that NO release activates K+ outward currents in opossum esophagus circular muscle, which may depend on Ca2+ release from the SR stores.

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