Apamin: A highly neurotoxic polypeptide from the venom of the honey bee (Apis mellifera). It consists of 18 amino acids with two disulfide bridges and causes hyperexcitability resulting in convulsions and respiratory paralysis.Bee Venoms: Venoms obtained from Apis mellifera (honey bee) and related species. They contain various enzymes, polypeptide toxins, and other substances, some of which are allergenic or immunogenic or both. These venoms were formerly used in rheumatism to stimulate the pituitary-adrenal system.Charybdotoxin: A 37-amino acid residue peptide isolated from the scorpion Leiurus quinquestriatus hebraeus. It is a neurotoxin that inhibits calcium activated potassium channels.Small-Conductance Calcium-Activated Potassium Channels: A major class of calcium-activated potassium channels that are found primarily in excitable CELLS. They play important roles in the transmission of ACTION POTENTIALS and generate a long-lasting hyperpolarization known as the slow afterhyperpolarization.Biological Factors: Endogenously-synthesized compounds that influence biological processes not otherwise classified under ENZYMES; HORMONES or HORMONE ANTAGONISTS.Potassium Channel Blockers: A class of drugs that act by inhibition of potassium efflux through cell membranes. Blockade of potassium channels prolongs the duration of ACTION POTENTIALS. They are used as ANTI-ARRHYTHMIA AGENTS and VASODILATOR AGENTS.Potassium Channels, Calcium-Activated: Potassium channels whose activation is dependent on intracellular calcium concentrations.Potassium Channels: Cell membrane glycoproteins that are selectively permeable to potassium ions. At least eight major groups of K channels exist and they are made up of dozens of different subunits.Tetraethylammonium: A potassium-selective ion channel blocker. (From J Gen Phys 1994;104(1):173-90)Scorpion Venoms: Venoms from animals of the order Scorpionida of the class Arachnida. They contain neuro- and hemotoxins, enzymes, and various other factors that may release acetylcholine and catecholamines from nerve endings. Of the several protein toxins that have been characterized, most are immunogenic.Muscle Relaxation: That phase of a muscle twitch during which a muscle returns to a resting position.Nitroarginine: An inhibitor of nitric oxide synthetase which has been shown to prevent glutamate toxicity. Nitroarginine has been experimentally tested for its ability to prevent ammonia toxicity and ammonia-induced alterations in brain energy and ammonia metabolites. (Neurochem Res 1995:200(4):451-6)Intermediate-Conductance Calcium-Activated Potassium Channels: A major class of calcium-activated potassium channels that were originally discovered in ERYTHROCYTES. They are found primarily in non-excitable CELLS and set up electrical gradients for PASSIVE ION TRANSPORT.4-Aminopyridine: One of the POTASSIUM CHANNEL BLOCKERS, with secondary effect on calcium currents, which is used mainly as a research tool and to characterize channel subtypes.Membrane Potentials: The voltage differences across a membrane. For cellular membranes they are computed by subtracting the voltage measured outside the membrane from the voltage measured inside the membrane. They result from differences of inside versus outside concentration of potassium, sodium, chloride, and other ions across cells' or ORGANELLES membranes. For excitable cells, the resting membrane potentials range between -30 and -100 millivolts. Physical, chemical, or electrical stimuli can make a membrane potential more negative (hyperpolarization), or less negative (depolarization).Vasodilation: The physiological widening of BLOOD VESSELS by relaxing the underlying VASCULAR SMOOTH MUSCLE.Potassium: An element in the alkali group of metals with an atomic symbol K, atomic number 19, and atomic weight 39.10. It is the chief cation in the intracellular fluid of muscle and other cells. Potassium ion is a strong electrolyte that plays a significant role in the regulation of fluid volume and maintenance of the WATER-ELECTROLYTE BALANCE.Mesenteric Arteries: Arteries which arise from the abdominal aorta and distribute to most of the intestines.Guinea Pigs: A common name used for the genus Cavia. The most common species is Cavia porcellus which is the domesticated guinea pig used for pets and biomedical research.Muscle, Smooth: Unstriated and unstriped muscle, one of the muscles of the internal organs, blood vessels, hair follicles, etc. Contractile elements are elongated, usually spindle-shaped cells with centrally located nuclei. Smooth muscle fibers are bound together into sheets or bundles by reticular fibers and frequently elastic nets are also abundant. (From Stedman, 25th ed)Calcium: A basic element found in nearly all organized tissues. It is a member of the alkaline earth family of metals with the atomic symbol Ca, atomic number 20, and atomic weight 40. Calcium is the most abundant mineral in the body and combines with phosphorus to form calcium phosphate in the bones and teeth. It is essential for the normal functioning of nerves and muscles and plays a role in blood coagulation (as factor IV) and in many enzymatic processes.Tetraethylammonium CompoundsAcetylcholine: A neurotransmitter found at neuromuscular junctions, autonomic ganglia, parasympathetic effector junctions, a subset of sympathetic effector junctions, and at many sites in the central nervous system.Glyburide: An antidiabetic sulfonylurea derivative with actions similar to those of chlorpropamide.Cromakalim: A potassium-channel opening vasodilator that has been investigated in the management of hypertension. It has also been tried in patients with asthma. (Martindale, The Extra Pharmacopoeia, 30th ed, p352)Vasodilator Agents: Drugs used to cause dilation of the blood vessels.Tubocurarine: A neuromuscular blocker and active ingredient in CURARE; plant based alkaloid of Menispermaceae.Endothelium-Dependent Relaxing Factors: Paracrine substances produced by the VASCULAR ENDOTHELIUM with VASCULAR SMOOTH MUSCLE relaxation (VASODILATION) activities. Several factors have been identified, including NITRIC OXIDE and PROSTACYCLIN.Nitric Oxide: A free radical gas produced endogenously by a variety of mammalian cells, synthesized from ARGININE by NITRIC OXIDE SYNTHASE. Nitric oxide is one of the ENDOTHELIUM-DEPENDENT RELAXING FACTORS released by the vascular endothelium and mediates VASODILATION. It also inhibits platelet aggregation, induces disaggregation of aggregated platelets, and inhibits platelet adhesion to the vascular endothelium. Nitric oxide activates cytosolic GUANYLATE CYCLASE and thus elevates intracellular levels of CYCLIC GMP.OxadiazolesDequalinium: A topical bacteriostat that is available as various salts. It is used in wound dressings and mouth infections and may also have antifungal action, but may cause skin ulceration.Electric Stimulation: Use of electric potential or currents to elicit biological responses.Action Potentials: Abrupt changes in the membrane potential that sweep along the CELL MEMBRANE of excitable cells in response to excitation stimuli.Patch-Clamp Techniques: An electrophysiologic technique for studying cells, cell membranes, and occasionally isolated organelles. All patch-clamp methods rely on a very high-resistance seal between a micropipette and a membrane; the seal is usually attained by gentle suction. The four most common variants include on-cell patch, inside-out patch, outside-out patch, and whole-cell clamp. Patch-clamp methods are commonly used to voltage clamp, that is control the voltage across the membrane and measure current flow, but current-clamp methods, in which the current is controlled and the voltage is measured, are also used.Endothelium, Vascular: Single pavement layer of cells which line the luminal surface of the entire vascular system and regulate the transport of macromolecules and blood components.Large-Conductance Calcium-Activated Potassium Channels: A major class of calcium activated potassium channels whose members are voltage-dependent. MaxiK channels are activated by either membrane depolarization or an increase in intracellular Ca(2+). They are key regulators of calcium and electrical signaling in a variety of tissues.Muscle Contraction: A process leading to shortening and/or development of tension in muscle tissue. Muscle contraction occurs by a sliding filament mechanism whereby actin filaments slide inward among the myosin filaments.NG-Nitroarginine Methyl Ester: A non-selective inhibitor of nitric oxide synthase. It has been used experimentally to induce hypertension.Indomethacin: A non-steroidal anti-inflammatory agent (NSAID) that inhibits the enzyme cyclooxygenase necessary for the formation of prostaglandins and other autacoids. It also inhibits the motility of polymorphonuclear leukocytes.Nitroprusside: A powerful vasodilator used in emergencies to lower blood pressure or to improve cardiac function. It is also an indicator for free sulfhydryl groups in proteins.Barium Compounds: Inorganic compounds that contain barium as an integral part of the molecule.Dose-Response Relationship, Drug: The relationship between the dose of an administered drug and the response of the organism to the drug.Myography: The recording of muscular movements. The apparatus is called a myograph, the record or tracing, a myogram. (From Stedman, 25th ed)Tetrodotoxin: An aminoperhydroquinazoline poison found mainly in the liver and ovaries of fishes in the order TETRAODONTIFORMES, which are eaten. The toxin causes paresthesia and paralysis through interference with neuromuscular conduction.Bees: Insect members of the superfamily Apoidea, found almost everywhere, particularly on flowers. About 3500 species occur in North America. They differ from most WASPS in that their young are fed honey and pollen rather than animal food.Encyclopedias as Topic: Works containing information articles on subjects in every field of knowledge, usually arranged in alphabetical order, or a similar work limited to a special field or subject. (From The ALA Glossary of Library and Information Science, 1983)Butyrylthiocholine: A sulfur-containing analog of butyrylcholine which is hydrolyzed by butyrylcholinesterase to butyrate and thiocholine. It is used as a reagent in the determination of butyrylcholinesterase activity.Honey: A sweet viscous liquid food, produced in the honey sacs of various bees from nectar collected from flowers. The nectar is ripened into honey by inversion of its sucrose sugar into fructose and glucose. It is somewhat acidic and has mild antiseptic properties, being sometimes used in the treatment of burns and lacerations.Dictionaries, MedicalDictionaries as Topic: Lists of words, usually in alphabetical order, giving information about form, pronunciation, etymology, grammar, and meaning.Dictionaries, Chemical

Acetylcholine-induced membrane potential changes in endothelial cells of rabbit aortic valve. (1/590)

1. Using a microelectrode technique, acetylcholine (ACh)-induced membrane potential changes were characterized using various types of inhibitors of K+ and Cl- channels in rabbit aortic valve endothelial cells (RAVEC). 2. ACh produced transient then sustained membrane hyperpolarizations. Withdrawal of ACh evoked a transient depolarization. 3. High K+ blocked and low K+ potentiated the two ACh-induced hyperpolarizations. Charybdotoxin (ChTX) attenuated the ACh-induced transient and sustained hyperpolarizations; apamin inhibited only the sustained hyperpolarization. In the combined presence of ChTX and apamin, ACh produced a depolarization. 4. In Ca2+-free solution or in the presence of Co2+ or Ni2+, ACh produced a transient hyperpolarization followed by a depolarization. In BAPTA-AM-treated cells, ACh produced only a depolarization. 5. A low concentration of A23187 attenuated the ACh-induced transient, but not the sustained, hyperpolarization. In the presence of cyclopiazonic acid, the hyperpolarization induced by ACh was maintained after ACh removal; this maintained hyperpolarization was blocked by Co2+. 6. Both NPPB and hypertonic solution inhibited the membrane depolarization seen after ACh washout. Bumetanide also attenuated this depolarization. 7. It is concluded that in RAVEC, ACh produces a two-component hyperpolarization followed by a depolarization. It is suggested that ACh-induced Ca2+ release from the storage sites causes a transient hyperpolarization due to activation of ChTX-sensitive K+ channels and that ACh-activated Ca2+ influx causes a sustained hyperpolarization by activating both ChTX- and apamin-sensitive K+ channels. Both volume-sensitive Cl- channels and the Na+-K+-Cl- cotransporter probably contribute to the ACh-induced depolarization.  (+info)

Charybdotoxin and apamin block EDHF in rat mesenteric artery if selectively applied to the endothelium. (2/590)

In rat mesenteric artery, endothelium-derived hyperpolarizing factor (EDHF) is blocked by a combination of apamin and charybdotoxin (ChTX). The site of action of these toxins has not been established. We compared the effects of ChTX and apamin applied selectively to the endothelium and to the smooth muscle. In isometrically mounted arteries, ACh (0.01-10 micrometers), in the presence of indomethacin (2.8 microM) and Nomega-nitro-L-arginine methyl ester (L-NAME) (100 microM), concentration dependently relaxed phenylephrine (PE)-stimulated tone (EC50 50 nM; n = 10). Apamin (50 nM) and ChTX (50 nM) abolished this relaxation (n = 5). In pressurized arteries, ACh (10 microM), applied intraluminally in the presence of indomethacin (2.8 microM) and L-NAME (100 microM), dilated both PE-stimulated (0.3-0.5 microM; n = 5) and myogenic tone (n = 3). Apamin (50 nM ) and ChTX (50 nM) applied intraluminally abolished ACh-induced dilatations. Bath superperfusion of apamin and ChTX did not affect ACh-induced dilatations of either PE-stimulated (n = 5) or myogenic tone (n = 3). This is the first demonstration that ChTX and apamin act selectively on the endothelium to block EDHF-mediated relaxation.  (+info)

Role of K+ channels in A2A adenosine receptor-mediated dilation of the pressurized renal arcuate artery. (3/590)

1. Adenosine A2A receptor-mediated renal vasodilation was investigated by measuring the lumenal diameter of pressurized renal arcuate arteries isolated from the rabbit. 2. The selective A2A receptor agonist CGS21680 dilated the arteries with an EC50 of 130 nM. The CGS21680-induced vasodilation was, on average, 34% less in endothelium-denuded arteries. 3. The maximum response and the EC50 for CGS21680-induced vasodilation in endothelium-intact arteries were not significantly affected by incubation with the K+ channel blockers apamin (100 nM), iberiotoxin (100 nM), 3,4-diaminopyridine (1 mM), glibenclamide (1 microM) or Ba2+ (10 microM). However, a cocktail mixture of these blockers did significantly inhibit the maximum response by almost 40%, and 1 mM Ba2+ alone or 1 mM Ba2+ in addition to the cocktail inhibited the maximum CGS21680-response by 58% and about 75% respectively. 4. CGS21680-induced vasodilation was strongly inhibited when the extracellular K+ level was raised to 20 mM even though the dilator response to 1 microM levcromakalim, a K(ATP) channel opener drug, was unaffected. 5. CGS21680-induced vasodilation was inhibited by 10 microM ouabain, an inhibitor of Na+/K(+)-ATPase, but ouabain had a similar inhibitory effect on vasodilation induced by 30 nM nicardipine (a dihydropyridine Ca2+ antagonist) or 1 microM levcromakalim. 6. The data suggest that K+ channel activation does play a role in A(2A) receptor-mediated renal vasodilation. The inhibitory effect of raised extracellular K+ levels on the A(2A) response may be due to K(+)-induced stimulation of Na+/K(+)-ATPase.  (+info)

Blockade of SK-type Ca2+-activated K+ channels uncovers a Ca2+-dependent slow afterdepolarization in nigral dopamine neurons. (4/590)

Sharp electrode current-clamp recording techniques were used to characterize the response of nigral dopamine (DA)-containing neurons in rat brain slices to injected current pulses applied in the presence of TTX (2 microM) and under conditions in which apamin-sensitive Ca2+-activated K+ channels were blocked. Addition of apamin (100-300 nM) to perfusion solutions containing TTX blocked the pacemaker oscillation in membrane voltage evoked by depolarizing current pulses and revealed an afterdepolarization (ADP) that appeared as a shoulder on the falling phase of the voltage response. ADP were preceded by a ramp-shaped slow depolarization and followed by an apamin-insensitive hyperpolarizing afterpotential (HAP). Although ADPs were observed in all apamin-treated cells, the duration of the response varied considerably between individual neurons and was strongly potentiated by the addition of TEA (2-3 mM). In the presence of TTX, TEA, and apamin, optimal stimulus parameters (0.1 nA, 200-ms duration at -55 to -68 mV) evoked ADP ranging from 80 to 1,020 ms in duration (355.3 +/- 56.5 ms, n = 16). Both the ramp-shaped slow depolarization and the ensuing ADP were markedly voltage dependent but appeared to be mediated by separate conductance mechanisms. Thus, although bath application of nifedipine (10-30 microM) or low Ca2+, high Mg2+ Ringer blocked the ADP without affecting the ramp potential, equimolar substitution of Co2+ for Ca2+ blocked both components of the voltage response. Nominal Ca2+ Ringer containing Co2+ also blocked the HAP evoked between -55 and -68 mV. We conclude that the ADP elicited in DA neurons after blockade of apamin-sensitive Ca2+-activated K+ channels is mediated by a voltage-dependent, L-type Ca2+ channel and represents a transient form of the regenerative plateau oscillation in membrane potential previously shown to underlie apamin-induced bursting activity. These data provide further support for the notion that modulation of apamin-sensitive Ca2+-activated K+ channels in DA neurons exerts a permissive effect on the conductances that are involved in the expression of phasic activity.  (+info)

Differential effects of apamin- and charybdotoxin-sensitive K+ conductances on spontaneous discharge patterns of developing retinal ganglion cells. (5/590)

The spontaneous discharge patterns of developing retinal ganglion cells are thought to play a crucial role in the refinement of early retinofugal projections. To investigate the contributions of intrinsic membrane properties to the spontaneous activity of developing ganglion cells, we assessed the effects of blocking large and small calcium-activated potassium conductances on the temporal pattern of such discharges by means of patch-clamp recordings from the intact retina of developing ferrets. Application of apamin and charybdotoxin (CTX), which selectively block the small and large calcium-activated potassium channels, respectively, resulted in significant changes in spontaneous firings. In cells recorded from the oldest animals [postnatal day 30 (P30)-P45], which manifested relatively sustained discharge patterns, application of either blocker induced bursting activity. With CTX the bursts were highly periodic, short in duration, and of high frequency. In contrast, with apamin the interburst intervals were longer, less regular, and lower in overall spike frequency. These differences between the effects of the two blockers on spontaneous activity were documented by spectral analysis of discharge patterns. Filling cells from which recordings were made with Lucifer yellow revealed that these effects were obtained in all three morphological classes of cells: alpha, beta, and gamma. These findings provide the first evidence that apamin- and CTX-sensitive K+ conductances can have differential effects on the spontaneous discharge patterns of retinal ganglion cells. Remarkably, the bursts of activity obtained after apamin application in more mature neurons appeared very similar to the spontaneous bursting patterns observed in developing neurons. These findings suggest that the maturation of calcium-activated potassium channels, particularly the apamin-sensitive conductance, may contribute to the changes in spontaneous firings exhibited by retinal ganglion cells during the course of normal development.  (+info)

Coordinate regulation of gonadotropin-releasing hormone neuronal firing patterns by cytosolic calcium and store depletion. (6/590)

Elevation of cytosolic free Ca2+ concentration ([Ca2+]i) in excitable cells often acts as a negative feedback signal on firing of action potentials and the associated voltage-gated Ca2+ influx. Increased [Ca2+]i stimulates Ca2+-sensitive K+ channels (IK-Ca), and this, in turn, hyperpolarizes the cell and inhibits Ca2+ influx. However, in some cells expressing IK-Ca the elevation in [Ca2+]i by depletion of intracellular stores facilitates voltage-gated Ca2+ influx. This phenomenon was studied in hypothalamic GT1 neuronal cells during store depletion caused by activation of gonadotropin-releasing hormone (GnRH) receptors and inhibition of endoplasmic reticulum (Ca2+)ATPase with thapsigargin. GnRH induced a rapid spike increase in [Ca2+]i accompanied by transient hyperpolarization, followed by a sustained [Ca2+]i plateau during which the depolarized cells fired with higher frequency. The transient hyperpolarization was caused by the initial spike in [Ca2+]i and was mediated by apamin-sensitive IK-Ca channels, which also were operative during the subsequent depolarization phase. Agonist-induced depolarization and increased firing were independent of [Ca2+]i and were not mediated by inhibition of K+ current, but by facilitation of a voltage-insensitive, Ca2+-conducting inward current. Store depletion by thapsigargin also activated this inward depolarizing current and increased the firing frequency. Thus, the pattern of firing in GT1 neurons is regulated coordinately by apamin-sensitive SK current and store depletion-activated Ca2+ current. This dual control of pacemaker activity facilitates voltage-gated Ca2+ influx at elevated [Ca2+]i levels, but also protects cells from Ca2+ overload. This process may also provide a general mechanism for the integration of voltage-gated Ca2+ influx into receptor-controlled Ca2+ mobilization.  (+info)

Endothelium-derived relaxing, contracting and hyperpolarizing factors of mesenteric arteries of hypertensive and normotensive rats. (7/590)

Differences in the acetylcholine (ACh)-induced endothelium-dependent relaxation and hyperpolarization of the mesenteric arteries of Wistar Kyoto rats (WKY) and stroke-prone spontaneously hypertensive rats (SHRSP) were studied. Relaxation was impaired in preparations from SHRSP and tendency to reverse the relaxation was observed at high concentrations of ACh in these preparations. Relaxation was partly blocked by NG-nitro-L-arginine (L-NOARG, 100 microM) and, in the presence of L-NOARG, tendency to reverse the relaxation was observed in response to higher concentrations of ACh, even in preparations from WKY. The relaxation remaining in the presence of L-NOARG was also smaller in preparations from SHRSP. The tendency to reverse the relaxation observed at higher concentrations of ACh in preparations from SHRSP or WKY in the presence of L-NOARG were abolished by indomethacin (10 microM). Elevating the K+ concentration of the incubation medium decreased relaxation in the presence of both indomethacin and L-NOARG. Relaxation in the presence of L-NOARG and indomethacin was reduced by the application of both apamin (5 microM) and charybdotoxin (0.1 microM). This suggests that the relaxation induced by ACh is brought about by both endothelium-derived relaxing factor (EDRF, nitric oxide (NO)) and hyperpolarizing factor (EDHF), which activates Ca2+-sensitive K+ channels. Electrophysiological measurement revealed that ACh induced endothelium-dependent hyperpolarization of the smooth muscle of both preparations in the presence of L-NOARG and indomethacin; the hyperpolarization being smaller in the preparation from SHRSP than that from WKY. These results suggest that the release of both NO and EDHF is reduced in preparations from SHRSP. In addition, indomethacin-sensitive endothelium-derived contracting factor (EDCF) is released from both preparations; the release being increased in preparations from SHRSP.  (+info)

Integrin-regulated secretion of interleukin 4: A novel pathway of mechanotransduction in human articular chondrocytes. (8/590)

Chondrocyte function is regulated partly by mechanical stimulation. Optimal mechanical stimulation maintains articular cartilage integrity, whereas abnormal mechanical stimulation results in development and progression of osteoarthritis (OA). The responses of signal transduction pathways in human articular chondrocytes (HAC) to mechanical stimuli remain unclear. Previous work has shown the involvement of integrins and integrin-associated signaling pathways in activation of plasma membrane apamin-sensitive Ca2+-activated K+ channels that results in membrane hyperpolarization of HAC after 0. 33 Hz cyclical mechanical stimulation. To further investigate mechanotransduction pathways in HAC and show that the hyperpolarization response to mechanical stimulation is a result of an integrin-dependent release of a transferable secreted factor, we used this response. Neutralizing antibodies to interleukin 4 (IL-4) and IL-4 receptor alpha inhibit mechanically induced membrane hyperpolarization and anti-IL-4 antibodies neutralize the hyperpolarizing activity of medium from mechanically stimulated cells. Antibodies to interleukin 1beta (IL-1beta) and cytokine receptors, interleukin 1 receptor type I and the common gamma chain/CD132 (gamma) have no effect on me- chanically induced membrane hyperpolarization. Chondrocytes from IL-4 knockout mice fail to show a membrane hyperpolarization response to cyclical mechanical stimulation. Mechanically induced release of the chondroprotective cytokine IL-4 from HAC with subsequent autocrine/paracrine activity is likely to be an important regulatory pathway in the maintenance of articular cartilage structure and function. Finally, dysfunction of this pathway may be implicated in OA.  (+info)

apamin definition: Noun (uncountable) 1. (biochemistry) A neurotoxin originally isolated from Apis mellifera, the Western honey bee....
Apamin-sensitive, non-nitric oxide (NO) endothelium-dependent relaxations to bradykinin in the bovine isolated coronary artery: no role for cytochrome P450 and
The results show that SK2 subunits are necessary for the apamin-sensitive component of the ImAHP. In SK1 Δ/Δ or SK3 T/T(dox) mice, the apamin-sensitive component of the ImAHP was not significantly different from control, there were no significant changes in the levels of SK2 mRNA, and SK2 protein levels were not obviously upregulated, suggesting that only SK2 is necessary for the apamin-sensitive component of the ImAHP. This is consistent with previous suggestions based on the pharmacological profile of the current and the high specificity of apamin (Stocker et al., 1999; Sailer et al., 2002).. In heterologous expression studies, mouse and rat SK1 subunits, different from human SK1 subunits, do not form functional homomeric channels in the plasma membrane, but they are incorporated into heteromeric channels with SK2 or SK3 subunits (Benton et al., 2003; Monaghan et al., 2003). These data suggest that SK1 subunits may contribute to the number of functional SK2-containing channels, although the ...
UCL 1530: blocks actions mediated by the small conductance, apamin-sensitive Ca2+-activated K+ channels in cultured sympathetic neurones and isolated hepatocytes; structure given
Apamin is an 18 amino acid peptide neurotoxin found in apitoxin (bee venom). Dry bee venom consists of 2-3% of apamin. Apamin selectively blocks SK channels, a type of Ca2+-activated K+ channel expressed in the central nervous system. Toxicity is caused by only a few amino acids, these are cysteine1, lysine4, arginine13, arginine14 and histidine18. These amino acids are involved in the binding of apamin to the Ca2+-activated K+ channel. Due to its specificity for SK channels, apamin is used as a drug in biomedical research to study the electrical properties of SK channels and their role in the afterhyperpolarizations occurring immediately following an action potential. The first symptoms of apitoxin (bee venom), that are now thought to be caused by apamin, were described back in 1936 by Hahn and Leditschke. Apamin was first isolated by Habermann in 1965 from Apis mellifera, the Western honey bee. Apamin was named after this bee. Bee venom contains many other compounds, like histamine, ...
The purpose of the present study was to examine how apamin interacts with the three cloned subtypes of small-conductance Ca2+-activated K+ channels (hSK1, rSK2 and rSK3). Expression of the SK channel subtypes in Xenopus laevis oocytes resulted in large outward currents (0.5-5 microA) after direct in …
Drosophila nociceptive neurons convert high-intensity stimuli into characteristic fluctuations of firing rates, quiescent periods of which are regulated by hyperpolarization through small conductance Ca2+-activated K+ channels.
Having left the field a while ago, for reasons that I wont go into, suffice it to say I no longer have access to the relevant literature, Ive been drawn quite by accident to consider the recent proposal that the inhibitory junction potential (IJP) recorded in the gastrointestinal smooth muscle has its origin in cells…
Izabela Rutkowska-Wlodarczyk, M. Isabel Aller, Sergio Valbuena, Jean-Charles Bologna, Laurent Prézeau, et al.. (see pages 5171-5179). Kainate receptors (KARs) have the structure of ionotropic glutamate receptors, but unlike AMPA and NMDA receptors, KARs can activate metabotropic signaling as well as passing ionic current. Several metabotropic effects of KARs have been demonstrated, including inhibition of voltage-sensitive calcium channels, inhibition of glutamate and GABA release, and inhibition of the slow afterhyperpolarization current (IAHP). All these effects are blocked by pertussis toxin and involve phospholipase C, suggesting they are mediated by Go proteins, but how KARs activate G-proteins has remained an open question.. To answer this question, Rutkowska-Wlodarczyk et al. performed a proteomic analysis on mouse brain homogenates and identified proteins that interacted with the intracellular C-terminal portion of GluK1b, a KAR subunit. They found 22 proteins that specifically ...
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इस पाक की महिमा का वर्णन भगवान महादेवजी ने पार्वतीजी के समक्ष किया था । नारदजी ने इसे ब्रम्हाजी के श्रीमुख से सुना व अश्विनीकुमारों ने इस पाक का निर्माण किया था । इसके सेवन से बल,बुद्धि,स्मृति,उत्तम वाणी,सौंन्दर्य,सुकुमारता तथा सौभाग्य की प्राप्ति होती है । माताओं के लिए यह खास वरदानस्वरूप है प्रसूति के बाद सेवन से दूध खुलकर आता है तथा संभावित कई व्याधियों से रक्षा होती है ।सर्दियों ...
TY - JOUR. T1 - The contribution of d-tubocurarine-sensitive and Apamin-sensitive K-channels to EDHF-mediated Relaxation of Mesenteric Arteries from eNOS-/- Mice. AU - Chen, Xiaoliang. AU - Li, Yang. AU - Hollenberg, Morley. AU - Triggle, Christopher. AU - Ding, Hong. PY - 2012/5. Y1 - 2012/5. N2 - The nature of the potassium channels involved in determining endothelium-derived hyperpolarizing factor-mediated relaxation was investigated in first-order small mesenteric arteries from male endothelial nitric oxide synthase (eNOS-/-)-knockout and control (+/+) mice. Acetylcholine-induced endothelium-dependent relaxation of small mesenteric arteries of eNOS-/- was resistant to N-nitro-L-arginine and indomethacin and the guanylyl cyclase inhibitor, 1H-(1,2,4) oxadiazolo (4,3-a) quinoxalin-1-one. Apamin and the combination of apamin and iberiotoxin or apamin and charybdotoxin induced a transient endothelium-dependent contraction of small mesenteric arteries from both eNOS-/- and +/+ mice. ...
TY - JOUR. T1 - The effects of apamin in rats with pretrigeminal or high spinal transsection of the central nervous system. AU - Janicki, P.. AU - Gumulka, S. W.. AU - Krzaścik, P.. AU - Habermann, E.. PY - 1985. Y1 - 1985. N2 - P. Janicki, S.W. Gumulka, P. Krzaścik and E. Habermann. The effects of apamin in rats with pretrigeminal or high spinal transsection of the central nervous system. Toxicon 23, 993-996, 1985. - Rats were injected in one lateral cerebral ventricle (i.c.v.) with apamin (100 ng per animal). The resulting desynchronisation pattern in the electrocorticogram (ECoG) and the symptoms of poisoning were monitored before and after transsection at different levels, and following morphine. Apamin acts primarily on the brain stem and spinal cord, i.e. structures possessing a sensory input, and then indirectly on the higher integrating systems. There is no general parallelism between receptor density and locus of action.. AB - P. Janicki, S.W. Gumulka, P. Krzaścik and E. Habermann. ...
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Action potentials in vertebrate neurons are followed by an afterhyperpolarization (AHP) that may persist for several seconds and may have profound consequences for the firing pattern of the neuron. Each component of the AHP is kinetically distinct and is mediated by different calcium-activated potassium channels. The protein encoded by this gene is activated before membrane hyperpolarization and is thought to regulate neuronal excitability by contributing to the slow component of synaptic AHP. This gene is a member of the KCNN family of potassium channel genes. The encoded protein is an integral membrane protein that forms a voltage-independent calcium-activated channel with three other calmodulin-binding subunits. Alternate splicing of this gene results in multiple transcript variants. [provided by RefSeq, May 2013 ...
Forms a voltage-independent potassium channel activated by intracellular calcium. Activation is followed by membrane hyperpolarization. Thought to regulate neuronal excitability by contributing to the slow component of synaptic afterhyperpolarization. The channel is blocked by apamin (By similarity).
Background. Small conductance Ca2+-activated K+ (SK) channels play significant roles in regulating the excitability of cardiomyocytes (CMs). SK channels are unique in that they are gated solely by intracellular Ca2+ and hence, function to integrate intracellular Ca2+ and membrane potentials on a beat-to-beat basis in the heart. Our previous studies revealed that cardiac SK2 channels coupled with L-type Ca2+ channels (LTCCs) through a physical bridge, α-actinin2, suggesting that LTCCs may be functionally coupled with SK2 channels by providing local Ca2+ domain to activate the SK channels. However, a recent study suggested that sarcoplasmic reticulum (SR) Ca2+ release is necessary and sufficient for the activation of cardiac SK channels. The objective of the study is to examine the mechanisms of SK channel activation in native CMs.. Methods and Results. By using a voltage-clamp protocol in rabbit CMs to activate LTCCs followed immediately by a test voltage to monitor the SK currents, we recorded ...
TY - JOUR. T1 - SK channels and NMDA receptors form a Ca2+-mediated feedback loop in dendritic spines. AU - Ngo-Anh, Thu Jennifer. AU - Bloodgood, Brenda L.. AU - Lin, Michael. AU - Sabatini, Bernardo L.. AU - Maylie, James. AU - Adelman, John. PY - 2005/5. Y1 - 2005/5. N2 - Small-conductance Ca2+-activated K+ channels (SK channels) influence the induction of synaptic plasticity at hippocampal CA3-CA1 synapses. We find that in mice, SK channels are localized to dendritic spines, and their activity reduces the amplitude of evoked synaptic potentials in an NMDA receptor (NMDAR)-dependent manner. Using combined two-photon laser scanning microscopy and two-photon laser uncaging of glutamate, we show that SK channels regulate NMDAR-dependent Ca2+ influx within individual spines. SK channels are tightly coupled to synaptically activated Ca2+ sources, and their activity reduces the amplitude of NMDAR-dependent Ca2+ transients. These effects are mediated by a feedback loop within the spine head; during ...
KCNN4 antibody (potassium intermediate/small conductance calcium-activated channel, subfamily N, member 4) for ELISA, WB. Anti-KCNN4 pAb (GTX87069) is tested in Human, Mouse, Rat samples. 100% Ab-Assurance.
The whole-cell current clamp and voltage clamp techniques were used to record the slow Na+ action potentials (APs) and the inward current in cultured single ventricular cells isolated from young (3 day-old) embryonic chicks. The slow Na+ APs had a +Vmax of 21.5 +/- 7.5 V/s (in 10 different single ce …
SKŁAD , CENA , DOSTĘPNOŚĆ. Skład kremu jest bardzo bogaty i zadowoli każdą z Was. Głównym składnikiem produktu pielęgnacyjnego jest bowiem witamina C - "królowa pielęgnacji skóry" i "królowa młodości". Witamina C stymuluje syntezę kolagenu i kwasu hialuronowego, rozjaśnia skórę i niweluje przebarwienia poprzez hamowanie produkcji melaniny, złuszcza naskórek, jest najsilniejszym przeciwutleniaczem, hamuje wypłukiwanie kolagenu i elastyny, przez co utrzymuje skórę jędrną i napiętą, zmniejsza zaczerwienienia skóry, uszczelnia naczynia krwionośne, wzmacnia barierę lipidową skóry, przez co utrzymuje odpowiedni poziom nawilżenia. Łagodzi, koi i regeneruje skórę, działa antybakteryjnie i minimalizuje niedoskonałości skórne, wspomaga ochronę UVA/UVB, wzmacnia odporność skóry. Można by wymieniać bez końca. Działanie witaminy C w kremie LA ROCHE-POSAY zostało wzmocnione dwoma składnikami aktywnymi: mannozą, czyli cukrem przywracającym skórze ...
Nasodrill nosový výplach sprej 1 × 100 ml platné do: 31.10.2016 - najlepšie ceny všetkých výrobkov, akcie a zľavy nájdete na Zlacnene.sk
Heureka.sk vám poradí ako vyberať Doplnky stravy. Vyberajte si Doplnky stravy podľa parametrov a porovnávajte ceny z internetových obchodov na Heuréke.
Semperit Semp Van-Life 195/70 R15 C 104/102 S Letné lacne a SKLADOM. Nakúpte pneu Semperit Semp Van-Life výhodne na E-pneumatiky.sk. Všetky informácie, parametre i energetické štítky.
休日明けとなる今日の読売ジャイアンツは、韓国のSKワイバーンズと練習試合を行った。・★G出場野手雑感①ショート 坂本3打数1安打 盗塁1*バットの先セカンドハーフライナー*強引にレフト前ヒット(その後盗塁)*見切って四球*詰まってセカンドゴ
[ChEMBL Target Description] ID:CHEMBL3381, Name:Small conductance calcium-activated potassium channel protein 3, Description:, Synonyms:
The SK channel was first cloned in 1996 and is known to be responsible for afterhyperpolarization the controls neuronal discharges. It is also known to be present in the atria, but its function in the ventricles was unclear. Studies from the Peng-Sheng Chen Laboratory documented that the SK current is upregulated in failing rabbit ventricles. SK current activation during ventricular fibrillation shortens the APD and is responsible for inducing recurrent VF in failing rabbit ventricles. The lab then performed studies in failing human ventricles to document the presence of SK current upregulation. In the failing ventricles, SK current is important in steepening the action potential duration restitution curve at rapid rates, which help induce VF.. On the other hand, the SK current is also upregulated in failing ventricles during bradycardia and help maintain the repolarization reserve and prevent afterdepolarization and torsades de pointes ventricular arrhythmia. These findings provided new ...
Department of Anatomy and Neurobiology, Washington University School of Medicine, St. Louis, Missouri (A.D.W.); Departments of Microbiology and Molecular Genetics (G.A.G.) and Physiology and Biophysics (K.G.C.), University of California, Irvine, Irvine, California; Molecular and Cellular Physiology Department, Stanford University, Stanford, California (R.A.); Department of Medical Pharmacology and Toxicology, University of California, Davis, Davis, California (H.W.); and Department of Applied Physiology, University Ulm, Ulm, Germany (S.G.) ...
Bee venom is a natural compound produced by the honey bee (Apis mellifera), and has been reported as having the biological and pharmacological activities, including anti-bacterial, anti-viral and anti-inflammation. In the present study, the inhibitory effects of bee venom and its major peptide components on the tumor invasion were demonstrated. It was confirmed the inhibitory effects of bee venom, melittin, and apamin on the EGF-induced invasion of breast cancer cells. Transwell invasion and wound-healing assays showed that bee venom and melittin significantly inhibits the EGF-induced invasion and migration of breast cancer cells. Also, bee venom and melittin reduced the EGF-stimulated F-actin reorganization at the leading edge, but apamin did not affect. Particularly, melittin inhibited the EGF-induced MMP-9 expression via blocking the NF-κB and PI3K/Akt/mTOR pathway. In addition, melittin significantly suppressed the EGF-induced FAK phosphorylation through inhibition of mTOR/p70S6K/4E-BP1 ...
Bee venom is a natural compound produced by the honey bee (Apis mellifera), and has been reported as having the biological and pharmacological activities, including anti-bacterial, anti-viral and anti-inflammation. In the present study, the inhibitory effects of bee venom and its major peptide components on the tumor invasion were demonstrated. It was confirmed the inhibitory effects of bee venom, melittin, and apamin on the EGF-induced invasion of breast cancer cells. Transwell invasion and wound-healing assays showed that bee venom and melittin significantly inhibits the EGF-induced invasion and migration of breast cancer cells. Also, bee venom and melittin reduced the EGF-stimulated F-actin reorganization at the leading edge, but apamin did not affect. Particularly, melittin inhibited the EGF-induced MMP-9 expression via blocking the NF-κB and PI3K/Akt/mTOR pathway. In addition, melittin significantly suppressed the EGF-induced FAK phosphorylation through inhibition of mTOR/p70S6K/4E-BP1 ...
Effective, safe, and tolerable pharmacological treatment for atrial fibrillation (AF) remains an unmet need. The latest medication to reach the market for intravenous cardioversion was the combined sodium and potassium channel inhibitor vernakalant, however not yet available in the United States. Vernakalant terminated ≈50% of episodes of AF lasting ,7 days in randomized controlled studies, with its highest conversion rate during the first few days while after 8 to 45 days of AF, the conversion rate was ,10%, which was not statistically different from that of placebo.1,2. If lasting for ,24 hours, AF promotes further progression of the disease-a phenomenon described as AF begets AF.3 If atrial remodeling continues, AF often progresses to more sustained forms and becomes more resistant to both pharmacological and nonpharmacological treatments, including ablation.4-6 Among contributing factors, an increased influx of calcium seems to promote fibrosis development and remodeling.7. Three subtypes ...
Results: Bee venom inhibited cell invasion and migration, and also suppressed MMP-9 activity and expression, processes related to tumor invasion and metastasis, in PMA-induced MCF-7 cells. Bee venom specifically suppressed the phosphorylation of p38/JNK and at the same time, suppressed the protein expression, DNA binding and promoter activity of NF-κB. The levels of phosphorylated ERK1/2 and c-Jun did not change. We also investigated MMP-9 inhibition by melittin, apamin and PLA2, representative single component of bee venom. We confirmed that PMA-induced MMP-9 activity was significantly decreased by melittin, but not by apamin and phospholipase A2. These data demonstrated that the expression of MMP-9 was abolished by melittin, the main component of bee venom ...
Jogurt smotanový žilinský čučoriedka 125G platné do: 13.12.2006 - najlepšie ceny všetkých výrobkov, akcie a zľavy nájdete na Zlacnene.sk
Hygienici z regionálnych úradov verejného zdravotníctva skontrolovali od 6. do 13. júna oddelenia s nebalenými rizikovými potravinami v 338 supermarketoch, hypermarketoch a obchodných domoch
In these experiments, the extracellular solution contained Ca2+ (2 mM). TTX (1 μM) was present to block voltage-gated Na+ currents, and 4-AP (5 mM) was present to block IA in all experiments. In different sets of experiments, the extracellular solution also contained a blocker of one known type of KCa, so that the effect of haloperidol on the other type of KCa could be tested specifically. For example, the experimental solution in Figure 8A contained apamin (300 nM) in addition to TTX and 4-AP to block SK-type KCa channels. 16 Figure 8A shows outward currents evoked by a voltage command to +30 mV from a holding potential of −70 mV. Under the experimental conditions, the evoked current is expected to consist of the persistent component of the voltage-gated K+ current and KCa flowing through BK-type channels. Haloperidol had little effect on the amplitude of the outward current. This small effect might be expected if the evoked outward current consisted entirely of the persistent component of ...
Atrial fibrillation (AF) is the most common type of arrhythmia. Current pharmacological treatment for AF is moderately effective and/or increases the risk of serious ventricular adverse effects. To avoid ventricular adverse effects, a new target has been considered, the small conductance calcium-activated K+ channels (KCa2.X, SK channels). In the heart, KCa2.X channels are functionally more important in atria compared to ventricles, and pharmacological inhibition of the channel confers atrial selective prolongation of the cardiac action potential and converts AF to sinus rhythm in animal models of AF. Whether antiarrhythmic drugs (AADs) recommended for treating AF target KCa2.X channels is unknown. To this end, we tested a large number of AADs on the human KCa2.2 and KCa2.3 channels to assess their effect on this new target using automated whole-cell patch clamp. Of the AADs recommended for treatment of AF only dofetilide and propafenone inhibited hKCa2.X channels, with no subtype selectivity. ...
1 the alpha(2)-adrenoceptor function in mesenteric arteries of spontaneously hypertensive rats (SHR) was investigated by comparing membrane potential changes in response to adrenergic agonists in preparations from female SHR, Wistar-Kyoto (WKY) and normotensive Wistar rats (NWR).2 Resting membrane potential was found to be less negative in mesenteric arteries from SHR than in those from NWR and WKY. Apamin induced a decrease in the membrane potential of mesenteric artery rings without endothelium from NWR and WKY, but had no effects in those from SHR. Both UK 14,304 and adrenaline, in the presence of prazosin, induced a hyperpolarization that was significantly lower in de-endothelialized mesenteric rings from SHR than in those from NWR and WKY. in mesenteric rings with endothelium, however, similar hyperpolarization was observed in the three strains.3 in NWR mesenteric rings with endothelium the hyperpolarization induced by activation of alpha(2)-adrenoceptors was abolished by apamin, whereas in ...
Sk ra .. budowie sk ry wyr niono podzia na: nask rek, sk r w a ciw , tkank podsk rn oraz przydatki tj. mieszki w osowe, gruczo y, paznokcie. Od zewn trz sk r pokrywa warstwa lipidowa i z uszczona keratyna. Unaczynienie sk ry odgrywa podstawow rol w termoregulacji ustroju. W sk rze w a ciwej oraz na j... Sk ra w a ciwa i tkanka podsk rna .. budowana jest z kom rek i w kien cznotkankowych, zawiera naczynia, zako czenia nerwowe oraz przydatki sk ry. W jej obr bie wyr niono warstw brodawkow i znajduj c si ni ej warstw siateczkow . Podstaw budowy s : w kna kolagenowe, retikulinowe oraz spr yste nadaj ce sk rze spr ysto i wyt... ...
Uchwała nr XXXI/471/2013 Rady Miasta Wisła z dnia 31 października 2013r. w sprawie określenia warunków i trybu składania deklaracji oraz informacji w podatkach i opłatach lokalnych za pomocą środków komunikacji elektronicznej . Tekst pierwotny. Największa bezpłatna baza aktów prawnych.
MGI protein superfamily detail pages represent the protein classification set for a homeomorphic superfamily from the Protein Information Resource SuperFamily (PIRSF) site.. Mouse superfamily members are shown with links to their corresponding HomoloGene Classes. Note that pseudogenes are included in PIRSF families but not in orthology sets used here. You can select a given mouse superfamily member and download (or forward to NCBI BLAST) FASTA formatted protein sequences of that mouse gene and its mouse, human and rat homologs, as defined in the corresponding HomoloGene Class. The numbers of mouse, human and rat genes in the HomoloGene Class are shown. You can also "Select all" mouse superfamily members to obtain their protein sequences and the protein sequences for all mouse, human and rat homologs of the mouse superfamily members.. The number of protein sequences returned does not always match the numbers of homologs shown, because the same protein sequence can be associated with multiple ...
human KCNN3 protein: a small conductance calcium-regulated potassium channel; mutations in gene shows a possible association with schizophrenia; RefSeq NM_002249
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Sk ka horn 35 cm - 66854 - D evojas od Central7 - internetov port l. Katalog s vybaven m do koupelny pro z kazn ky, v robce a prodejce.
KCNN3兔多克隆抗体(ab28631)可与人样本反应并经WB, ELISA实验严格验证,被1篇文献引用。所有产品均提供质保服务,中国75%以上现货。
Tytu : Parametry barwy sk ry a fototyp sk ry wg Fitzpatricka w szacowaniu ryzykawyst pienia nowotwor w sk ry u cz owieka (na przyk adzie populacji polskiej) ...
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CLEVELAND, Jan. 20, 2016 /PRNewswire/ -- Harrington Discovery Institute at University Hospitals announces 2016 grant funding to 10 physician-scientists....
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ATP-elicited delayed K+ current was not inhibited by a cocktail of K+ channel blockers (4-AP, TEA, apamin, charybdotoxin, glibenclamide). The amplitude of the delayed K+ current decreased after the reduction of extracellular pH from 7.4 to 6.5. These two characteristics suggest that this current could be carried by the TASK subfamily of twin-pore potassium channels (K2P). Purinergic agonists including dATP, but not ADP, activated the delayed K+ current, indicating that P2Y11 is the likely receptor involved in its activation. The PKC activator phorbol ester 12,13-didecanoate stimulated this current. In addition, the PKC inhibitor Gö 6850 partially inhibited it. Real-time quantitative PCR showed that the genes encoding TASK-1 and TASK-2 are expressed. Conclusion ...
Now, what happens when we stick this pipette into a bath solution that has your typical extracellular saline, made to mimic extracellular fluid (i.e., mostly sodium chloride)? Well, the chemical gradients favor the pipette constituents diffusing into the bath, and the bath constituents diffusing into the pipette. But remember, the aspartate is big, so it doesnt diffuse as quickly as any of the other ionic species. That slower diffusion of the anion leaves a net negative charge in the pipette. This charge separation across the junction between two solutions is THE LIQUID JUNCTION POTENTIAL!!!11!!!1 ...
Most medicines cant get through the blood-brain barrier, but certain peptides in animal venoms can navigate across it to inflict damage. Now, researchers are capitalizing on venomous sneak attacks by developing a strategy based on a bee-venom peptide, apamin, to deliver medications to the brain. The researchers will present their work today at the 253rd National Meeting & Exposition of the American Chemical Society.
4J9Z: Unstructured to structured transition of an intrinsically disordered protein peptide in coupling Ca2+-sensing and SK channel activation.
Resveratrol has been reported to stimulate BKCa currents in human vascular endothelial cells and human cardiac fibroblasts [24, 51], which might be associated with its cardioprotective effect. The present study demonstrated that resveratrol could stimulate the activities of BKCa channels in cortical neurons. In fact, BKCa channel is considered to be one of the intrinsic molecular determinants for the control of neuronal excitability in the central nervous system and play a role in the etiology of some neurological diseases. Recent studies have demonstrated the implication of BKCa channels in Fragile X Syndrome (FXS) pathology [22]. In fact, a selective BKCa channel opener molecule (BMS-204352) rescues a broad spectrum of behavioral impairments (social, emotional and cognitive) in an animal model of FXS [17]. Resveratrol might be also beneficial to patients with FXS.. BKCa channels also play an important role in seizure etiology. Loss-of-function BKCa channel mutations can lead to temporal lobe ...
1 The aim of this study was to examine whether sodium nitroprusside (SNP)-induced relaxation of rat fundus longitudinal smooth muscle involves ryanodine-sensitive Ca2+ release. 2 SNP (300 nM-30 microM) elicited concentration-dependent relaxation of precontracted (1 microM carbachol) rat fundus, an effect almost abolished by the selective guanylyl cyclase inhibitor, 1H-[1,2,4]oxadiazolo[4,3-a]quinoxaline-1-one (ODQ, 10 microM). 3 SNP-mediated relaxations were almost abolished by 10 microM ryanodine. 4 SNP-mediated relaxations were also reduced by either 1 microM apamin (a selective small conductance Ca(2+)-sensitive K+ channel, SKCa, inhibitor) or the selective L-type Ca2+ channel inhibitor, nicardipine (3 microM). 5 SNP-induced relaxations were insensitive to 1 mM tetraethylammonium chloride (an inhibitor of large-conductance Ca(2+)-sensitive K+ channels) and 1 microM glibenclamide (an ATP-sensitive K+ channel inhibitor). 6 These data suggest that SNP-mediated fundus relaxation occurs via a ...
How is intermediate-conductance K+ channel abbreviated? i-K+ stands for intermediate-conductance K+ channel. i-K+ is defined as intermediate-conductance K+ channel rarely.
One of the most characteristic features of pyramidal cells in the prefrontal cortex (PFC) is that they present a slow afterhyperpolarizing current (IsAHP) that plays a critical role in the regulation of neuronal excitability. This current is modulated by receptors acting via GΑq/11 G proteins, thus it is thought that neurotransmitters regulate neuronal excitability through the inhibition of this current. IsAHP is known to be mediated by calcium-activated potassium channels, however, neither the identity of the channel underlying this current nor its mechanism of activation are yet well understood. Recent reports have questioned a direct role of calcium in the activation of the channels underlying the IsAHP in hippocampus, suggesting the neuronal calcium sensor (NCS) protein hippocalcin as one of the plausible proteins involved in the triggering of IsAHP; therefore, one of the aims of this work will be to examine the role of hippocalcin and other NCS proteins in the development of IsAHP in pyramidal
Characterisation and interaction between β₂ adrenoceptor (AR) and the large conductance calcium-activated potassium (BK_C_a) channel in human myometrium during pregnancy ...
Progressive renal fibrosis is a common outcome of almost all forms of renal damage, including diabetic nephropathy. Fibrosis leads to chronic kidney failure and, eventually, dialysis or transplantation (1-3). Although much is known about the molecular background and mediators that prompt fibroblasts or transdifferentiated kidney cells to release collagen and matrix (4-6), the search for a unique event that initiates the process remains inconclusive. Targeting this putative key signal would enable researchers to "switch off" fibrosis and, perhaps, the progressive loss of renal function that plagues millions of individuals worldwide (1-6). The intermediate/small-conductance Ca2+-activated K+ channel (KCa3.1; KCNN4; SK4) is one intriguing candidate for such function because it promotes fibrogenesis in target tissue by altering the membrane potential of cells, thus enhancing extracellular Ca2+ entry (7,8). Subsequent Smad2/3 or mitogen-activated protein kinase (MEK)-dependent phosphorylation ...
With just-suprathreshold current pulses, FS cells often displayed a considerable delay before the first spike, whereas GIN cells did not (cf. Fig. 2, C and D, top panels). In addition, GIN cells often displayed an afterdepolarization (ADP) following low-frequency action potentials (Fig. 2C, inset; cf. Halabisky et al. 2006). At higher levels of stimulus current, spike frequency adaptation was evident in GIN cells (Fig. 2D, bottom), but not in FS cells (Fig. 2D, bottom). Finally, at higher stimulus currents, the peak of the first action potential in GIN cells was the most positive in the train and the trough of the first afterhyperpolarization (AHP) was the most negative (Fig. 2C, bottom). By contrast, the action potential heights and AHP magnitudes of FS cells changed little under similar conditions (Fig. 2D, bottom). The firing of GIN cells also differed from that of RS cells, whose second action potential peak was substantially more negative than the first and whose first AHP was the most ...
I basically do what you have described in your blog, with slight differences. I use a seperate bath, filled with my internal and connect it via an agarbridge (3M KCl) to my recording chamber. In the start configuration I have the internal in the pipette, the recording chamber and my ground-bath. Once the pipette makes contact with the internal in the recording chamber I use the pipette offset. BTW when entering my amp is in i=0 mode, to make sure there is no command voltage interfering. In the next step I exchange the internal in the recording chamber for my aCSF solution, dip the pipette in and read the potential. In my last step I exchange the aCSF for my internal solution to check for reversion of the potential to 0 mV, but instead the potential increases. Not to forget, I exchange the agarbridge every time I change the solution for a fresh one. As ground I use a Ag/AgCl pellet connected with the bath by an agarbridge ...
Výživný ATODERM Préventive 200ml od Biodermy. Ku každému nákupu vzorka zdarma a vernostné body. Expedujeme do 24 hod. + doprava zdarma.
Pi4 competes with apamin, another SK-channel toxin. IC50 is 0.5 ± 0.2 µM. Scorpion venoms can be toxic for mammals, insects, ...
... apamin, and MCD peptide. Melittin is the main toxin of bee venom, and it damages red blood cells and white blood cells. Apamin ...
However, Tamapin displaces Apamin in binding assays and is therefore a stronger toxin with respect to Apamin. SK 1 and SK 3 are ... Its sequence similarity to other toxins that can compete with the binding site of apamin is much lower. It is 31 amino acids ... Despite completely different sequences, Apamin (a bee venom toxin) and Tamapin share at least in part, the same binding sites ... Tamapin-2 can also compete very effectively with apamin for binding to synaptosomes. The target of Tamapin is the small ...
Gmachl, M; Kreil, G (1995). "The precursors of the bee Venom Constituents Apamin and MCD Peptide Are Encoded by two Genes in ... In addition to MCD peptide, melittin and apamin have also been identified in this venom and are also described as voltage- ... Although the MCD peptide sequence shows similarity with apamin, they have different toxic properties. MCD peptide belongs to a ...
In addition, SK channels (SK1-SK3) but not SK4 (IK) are sensitive to blockade by the bee toxin apamin, and the scorpion venoms ... Experiments using apamin have shown that specifically blocking SK channels can increase learning and long-term potentiation. In ... Blatz AL, Magleby KL (1986). "Single apamin-blocked Ca-activated K+ channels of small conductance in cultured rat skeletal ...
This toxin shows similarity in its physiological activity and binding specificity to apamin, but both toxins show no structural ... potent inhibitor of apamin binding from Leiurus quinquestriatus hebraeus venom". J. Biol. Chem. 263 (21): 10192-7. PMID 2839478 ...
"Tetraethylammonium blockade of apamin-sensitive and insensitive Ca2+-activated K+ channels in a pituitary cell line." J. ... Inhibition of the electrogenic Na,K pump and Na,K-ATPase activity by tetraethylammonium, tetrabutylammonium, and apamin. ...
Jäger H, Adelman JP, Grissmer S (2000). "SK2 encodes the apamin-sensitive Ca2+-activated K+ channels in the human leukemic T ... 2004). "Calcium-dependent regulation of secretion in biliary epithelial cells: the role of apamin-sensitive SK channels". ...
"Characterization of a new peptide from Tityus serrulatus scorpion venom which is a ligand of the apamin-binding site". FEBS ...
Unlike other toxins from the same family HsTx1 does not seem to affect the apamin-sensitive calcium-dependent potassium channel ...
It has a high affinity for the 125I-apamin acceptor-binding sites of the rat synaptosomal membranes (Ki = 1.45±0.22 nM) and ... Taicatoxin has an inhibitory effect by reducing the affinity of 125I-apamin for its acceptor and not by alteration of the ... 50 nM of taicatoxin blocks the apamin-sensitive after-hyperpolarizing slow tail K+ currents in rat chromaffin cells, but not ... blocks affinity-labeling of a 33-kDa 125I-apamin-binding polypeptide. Other neurotoxins that act on the calcium channels are ...
... termini and is readily blocked by apamin. The gene for KCa2.3, KCNN3, is located on chromosome 1q21. KCa2.3 is found in the ...
Apamin increases cortisol production in the adrenal gland Adolapin, contributing 2-5% of the peptides Phospholipase A2 amounts ...
When the stimulus strength was reduced below the action potential threshold, apamin, a neurotoxin, was added to assess the ...
V. crabro venom contains neurotransmitters such as dopamine, serotonin, and noradrenalineneurotoxin apamin, as well as enzymes ...
On the other hand, TmTx does not seem to inhibit [125I] apamin binding to synaptic membranes in the rat brain or ionomycin- ...
This channel, the apamin sensitive, small conductance SK2 potassium channel, is activated by calcium that is likely released ...
... (MTX) blocks various K+ -channels: Apamin-sensitive small conductance Ca2+ - activated K+ channels (SK) Intermediate ...
... apamin MeSH D20.888.065.115.580 --- melitten MeSH D20.888.065.830 --- scorpion venoms MeSH D20.888.065.830.150 --- ...
... induced relaxation by binding to and thereby opening their apamin-sensitive small conductance (SK) Calcium-activated potassium ...
... apamin MeSH D23.946.833.065.115.580 --- melitten MeSH D23.946.833.065.830 --- scorpion venoms MeSH D23.946.833.065.830.150 --- ...
... is an 18 amino acid peptide neurotoxin found in apitoxin (bee venom). Dry bee venom consists of 2-3% of apamin. Apamin ... Apamin is an element in bee venom. You can come into contact with apamin through bee venom, so the symptoms that are known are ... Apamin was first isolated by Habermann in 1965 from Apis mellifera, the Western honey bee. Apamin was named after this bee. Bee ... Apamin is the only neurotoxin acting purely on the central nervous system. The symptoms of apamin toxicity are not well known, ...
Symptoms of mild cinchonism (which may occur from standard therapeutic doses of quinine) include flushed and sweaty skin, ringing of the ears (tinnitus), blurred vision, impaired hearing, confusion, reversible high-frequency hearing loss, headache, abdominal pain, rashes, drug-induced lichenoid reaction (lichenoid photosensitivity),[1] vertigo, dizziness, dysphoria, nausea, vomiting and diarrhea. Large doses of quinine may lead to severe (but reversible) symptoms of cinchonism: skin rashes, deafness, somnolence, diminished visual acuity or blindness, anaphylactic shock, and disturbances in heart rhythm or conduction, and death from cardiotoxicity (damage to the heart). Quinine may also trigger a rare form of hypersensitivity reaction in malaria patients, termed blackwater fever, that results in massive hemolysis, hemoglobinemia, hemoglobinuria, and kidney failure.[citation needed] Most symptoms of cinchonism (except in severe cases) are reversible and disappear once quinine is withdrawn. ...
... is a condition or a process in which an organism becomes chemically harmed severely (poisoned) by a toxic substance or venom of an animal.[1] Acute poisoning is exposure to a poison on one occasion or during a short period of time. Symptoms develop in close relation to the degree of exposure. Absorption of a poison is necessary for systemic poisoning (that is, in the blood throughout the body). In contrast, substances that destroy tissue but do not absorb, such as lye, are classified as corrosives rather than poisons. Furthermore, many common household medications are not labeled with skull and crossbones, although they can cause severe illness or even death. In the medical sense, toxicity and poisoning can be caused by less dangerous substances than those legally classified as a poison. Toxicology is the study and practice of the symptoms, mechanisms, diagnosis, and treatment of poisoning. Chronic poisoning is long-term repeated or continuous exposure to a poison where symptoms do not ...
... can be measured by its effects on the target (organism, organ, tissue or cell). Because individuals typically have different levels of response to the same dose of a toxic substance, a population-level measure of toxicity is often used which relates the probabilities of an outcome for a given individual in a population. One such measure is the LD50. When such data does not exist, estimates are made by comparison to known similar toxic things, or to similar exposures in similar organisms. Then, "safety factors" are added to account for uncertainties in data and evaluation processes. For example, if a dose of a toxic substance is safe for a laboratory rat, one might assume that one tenth that dose would be safe for a human, allowing a safety factor of 10 to allow for interspecies differences between two mammals; if the data are from fish, one might use a factor of 100 to account for the greater difference between two chordate classes (fish and mammals). Similarly, an extra protection ...
The ATP-dependent K+ channel antagonist glibenclamide (10 mu M) and the Ca2+-activated K+ channel antagonists apamin (0.1 mu M ...
Apamin is an 18 amino acid peptide neurotoxin found in apitoxin (bee venom). Dry bee venom consists of 2-3% of apamin. Apamin ... Apamin is an element in bee venom. You can come into contact with apamin through bee venom, so the symptoms that are known are ... Apamin was first isolated by Habermann in 1965 from Apis mellifera, the Western honey bee. Apamin was named after this bee. Bee ... Apamin is the only neurotoxin acting purely on the central nervous system. The symptoms of apamin toxicity are not well known, ...
apamin definition: Noun (uncountable) 1. (biochemistry) A neurotoxin originally isolated from Apis mellifera, the Western honey ... How would you define apamin? Add your definition here.. Please enable JavaScript to view the comments powered by Disqus.. ...
Apamin for your research needs. Find product specific information including CAS, MSDS, protocols and references. ...
1DU9: SOLUTION STRUCTURE OF BMP02, A NATURAL SCORPION TOXIN WHICH BLOCKS APAMIN-SENSITIVE CALCIUM-ACTIVATED POTASSIUM CHANNELS ...
The purpose of the present study was to examine how apamin interacts with the three cloned subtypes of small-conductance Ca2+- ... Apamin Interacts With All Subtypes of Cloned Small-Conductance Ca2+-activated K+ Channels Pflugers Arch. 2001 Jan;441(4):544-50 ... These results show that apamin binds to and blocks all three subtypes of cloned SK channels, and the distinct values for IC50 ... In all three cases the Ca2+-activated K+ currents could be totally inhibited by 500 nM apamin. Dose-response curves revealed a ...
A NATURAL SCORPION TOXIN WHICH BLOCKS APAMIN-SENSITIVE CALCIUM-ACTIVATED POTASSIUM CHANNELS, 25 STRUCTURES ... SOLUTION STRUCTURE OF BMP02, A NATURAL SCORPION TOXIN WHICH BLOCKS APAMIN-SENSITIVE CALCIUM-ACTIVATED POTASSIUM CHANNELS, 25 ... which had been demonstrated to be a weak blocker of apamin-sensitive calcium-activated potassium channels. Two-dimensional NMR ... which had been demonstrated to be a weak blocker of apamin-sensitive calcium-activated potassium channels. Two-dimensional NMR ...
Inhibition of apamin-sensitive K+ current by hypoxia in adult rat adrenal chromaffin cells. ... Adrenomedullary chromaffin cell Apamin Hypoxia Hypoxic depolarization Small-conductance Ca2+-activated K+ current Whole-cell ... suggesting that an apamin-sensitive component of whole-cell currents is suppressed during hypoxia. In contrast to I SK(Ca), Ca ... Apamin, however, eliminated the hypoxia-induced depolarization (400 nM) (7/8), suggesting that hypoxic depolarization is ...
... J Mol ... Apamin, a toxin in the bee venom, that was previously reported by our group to block the slow Ca2+ APs (Bkaily et al., 1985) ... This channel is highly sensitive to apamin and shares few characteristics with the Ca2+ channel and the TTX-sensitive fast Na+ ...
... non-peptidic blockers of the apamin-sensitive Ca2+-activated K+ channel. JOURNAL OF MEDICINAL CHEMISTRY , 43 (3) pp. 420-431. ... non-peptidic blockers of the apamin-sensitive Ca2+-activated K+ channel ... non-peptidic blockers of the apamin-sensitive Ca2+-activated K+ channel. ...
apamin ligand page. Quantitative data and detailed annnotation of the targets of licensed and experimental drugs. ... N- or C-terminal chimeric constructs permit functional channels that are insensitive to apamin [10]. Heteromeric channels are ... formed between KCa2.1 and 2.2 subunits that show intermediate sensitivity to apamin [2]. ...
The effects of apamin in rats with pretrigeminal or high spinal transsection of the central nervous system. / Janicki, P.; ... Apamin acts primarily on the brain stem and spinal cord, i.e. structures possessing a sensory input, and then indirectly on the ... Apamin acts primarily on the brain stem and spinal cord, i.e. structures possessing a sensory input, and then indirectly on the ... Apamin acts primarily on the brain stem and spinal cord, i.e. structures possessing a sensory input, and then indirectly on the ...
Apamin-sensitive Ca2+-activated K+ channels in astrocytes may be one of the pathways by which glial cells redistribute K+ in ... Apamin, an 18-amino acid bee venom peptide, is a specific blocker of a class of Ca2+ activated K+ channels. Mono 125I- ... proteolytic fragment of the 86-kDa chain but an associated subunit which is only accessible to photolabeling in certain apamin ... Apamin, an 18-amino acid bee venom peptide, is a specific blocker of a class of Ca2+ activated K+ channels. Mono 125I- ...
apamin ligand page. Quantitative data and detailed annnotation of the targets of licensed and experimental drugs. ...
Crystallization and preliminary X-ray diffraction data of the Fab fragment of a monoclonal antibody against apamin, a bee venom ... Fab fragments of anti-apamin monoclonal antibodies have been purified to homogeneity and crystallized. The crystals belong to ...
Tag: apamin. Optimizing the removal of an Acm protecting group. Disulfide rich peptides have gained significant attention ... Author Elizabeth DentonTags Acm, apamin, bee, branch, branches, cysteine, cystine, disulfide, peptide cleavage, solid phase ...
Apamin-sensitive, non-nitric oxide (NO) endothelium-dependent relaxations to bradykinin in the bovine isolated coronary artery ... Apamin-sensitive, non-nitric oxide (NO) endothelium-dependent relaxations to bradykinin in the bovine isolated coronary artery ... Both the high [K(+)](o)/apamin-sensitive relaxation to BK, and the relaxation to the K(ATP) channel-opener, levcromakalim (0.6 ... or apamin (0.3 microM). Ouabain (1 microM), an inhibitor of Na(+)/K(+)-ATPase, decreased the sensitivity to BK without ...
15N Chemical Shifts of Backbone Amides in Bovine Pancreatic Trypsin Inhibitor and Apamin. In: Journal of the American Chemical ... 15N Chemical Shifts of Backbone Amides in Bovine Pancreatic Trypsin Inhibitor and Apamin. Journal of the American Chemical ... 15N Chemical Shifts of Backbone Amides in Bovine Pancreatic Trypsin Inhibitor and Apamin. / Glushka, John; Lee, Maria; Coffin, ... 15N chemical shifts of backbone amides were measured at natural abundance for apamin and bovine pancreatic trypsin inhibitor ...
Apamin exaggerated the bursts and increased the firing rate.C, Example of a cell with the trimodal pattern of activity. Apamin ... A, Firing rate of a Purkinje neuron that fired tonically in the absence of apamin (black trace). Apamin was applied selectively ... Apamin had no effect on the other four cells. When two-thirds of the dendritic tree was exposed to apamin, the average firing ... Bath application of apamin increased the firing rate and reduced the pattern duration. Apamin did not prevent the cell from ...
Effect of CTX Plus Apamin. A combined treatment with CTX plus apamin (each at 50 nmol/L) did not reduce raloxifene-induced ... Raloxifene-induced dilatations were unaffected by treatment with CTX plus apamin, a recipe widely used to block K+-dependent ... Acetylcholine, phenylephrine, l-NAME, apamin, and CTX were purchased from Sigma (St. Louis, Mo.). ICI 182,780, 1400W, LY 294002 ... CTX plus apamin (n=4) (C), and by wortmannin or LY294002 (n=4 to 5) (D). Results are means±SEM of n experiments. The ...
... View/. Open. ... Bar Graphs show re-contraction of arteries in response to L-NAME or charybdotoxin plus apamin (C+A) in arteries with ... When either L-NAME (10-4M) or charybdotoxin (10-7M) plus apamin (5x10-7M) were added after acetylcholine the vasodilatation was ... with charybdotoxin plus apamin respectively). This approach relies on each of these drugs being selective for endothelial ...
B) Graph of mAHP amplitudes after CTL or CTL + apamin (CTL, n = 8 cells; CTL + apamin, n = 5 cells). *P , 0.05, Students t ... Scale is the same as in (A). (F) Graph of mAHP amplitudes after RG108 or RG108 + apamin (RG108, n = 10 cells; RG108 + apamin, n ... Table 4 Single AP waveform characteristics of neurons exposed to CTL versus CTL + apamin and RG108 versus RG108 + apamin in Fig ... apamin (RG108, n = 19 cells; RG108 + apamin, n = 4 cells). (B, D, F, and H) Graphs show means ± SEM from cells pooled from at ...
Apamin does not inhibit human cardiac Na+ current, L-type Ca2+ current or other major K+ currents.. Yu CC; Ai T; Weiss JN; Chen ... Amiodarone inhibits apamin-sensitive potassium currents.. Turker I; Yu CC; Chang PC; Chen Z; Sohma Y; Lin SF; Chen PS; Ai T; ... Apamin-sensitive calcium-activated potassium currents in rabbit ventricles with chronic myocardial infarction.. Lee YS; Chang ... Apamin induces early afterdepolarizations and torsades de pointes ventricular arrhythmia from failing rabbit ventricles ...
100 nM apamin (Ap); 100 nM charybdotoxin (CBX); 100 nM apamin plus 100 nM charybdotoxin (Ap + CBX); or 100 nM apamin plus 50 nM ...
1-EBIO or CyPPA effect could be prevented by SK2 channel blocker apamin. CRD could induce an increase in c-Fos protein ... 1-EBIO or CyPPA effect could be prevented by SK2 channel blocker apamin. CRD could induce an increase in c-Fos protein ... Apamin decreased the amplitude of IAHP in rats that experienced neonatal CRD (p , 0.01, n = 6 neurons per group). (E) Apamin ... which could be blocked by SK2 channel blocker apamin (5 ng/10 μL) (p , 0.05; Figure 4C). Apamin (100 nM) decreased IAHP current ...
  • Furthermore, the specific SK channel blocker apamin increased neuronal excitability but was ineffective after DNMT inhibition. (sciencemag.org)
  • 1-EBIO or CyPPA effect could be prevented by SK2 channel blocker apamin. (frontiersin.org)
  • This response can be partially inhibited by the SK blocker apamin, which inhibits a Ca 2+ -activated K + current in these cells. (pnas.org)
  • The specific SK blocker apamin, but not the IK blocker clotrimazole, reduces both of these effects of 1-EBIO and also diminishes peroxide production after fMLF or IgG-opsonized S. aureus activation of the respiratory burst. (pnas.org)
  • Facilitation of synaptic enhancement by nifedipine likely was attributable to a reduction (∼30%) in the Ca 2+ -dependent K + -mediated afterhyperpolarization (AHP), because the K + channel blocker apamin (1 μ m ) similarly reduced the AHP and promoted synaptic enhancement by 5 Hz stimulation. (jneurosci.org)
  • These responses were reduced by 30% to 50% with apamin, a blocker of Ca 2+ -activated K + channels, and were further inhibited by blockade of ATP-dependent K + channels with glyburide. (ahajournals.org)
  • Dose-response curves revealed a subtype-specific affinity for the apamin-induced inhibition with IC50 values of 704 pM and 196 nM (biphasic) for hSK1, 27 pM for rSK2 and 4 nM for rSK3. (nih.gov)
  • The purpose of the present study was to examine how apamin interacts with the three cloned subtypes of small-conductance Ca2+-activated K+ channels (hSK1, rSK2 and rSK3). (nih.gov)
  • This suppression was eliminated after application of apamin (400 nM), a selective inhibitor of small-conductance Ca 2+ -activated K + current ( I SK(Ca) ) ( n =5), suggesting that an apamin-sensitive component of whole-cell currents is suppressed during hypoxia. (springer.com)
  • 15 N chemical shifts of backbone amides were measured at natural abundance for apamin and bovine pancreatic trypsin inhibitor using heteronuclear multiquantum proton-detected correlated spectroscopy (HMP-COSY). (elsevier.com)
  • In all three cases the Ca2+-activated K+ currents could be totally inhibited by 500 nM apamin. (nih.gov)
  • Apamin increases cortisol production in the adrenal gland Adolapin, contributing 2-5% of the peptides Phospholipase A2 amounts to 10-12% of peptides. (wikipedia.org)
  • Although the MCD peptide sequence shows similarity with apamin, they have different toxic properties. (wikipedia.org)
  • These results show that apamin binds to and blocks all three subtypes of cloned SK channels, and the distinct values for IC50 and Kd suggest that apamin may be useful for determining the expression pattern of SK channel subtypes in native tissue. (nih.gov)
  • Mouse CA1 pyramidal neurons express apamin-sensitive SK2-containing channels in the post-synaptic membrane, positioned close to NMDA-type (N-methyl-D-aspartate) glutamate receptors. (nih.gov)
  • On the other hand, TmTx does not seem to inhibit [125I] apamin binding to synaptic membranes in the rat brain or ionomycin-induced 86Rb+ fluxes in C6 cells in vitro. (wikipedia.org)
  • Apamin-sensitive, non-nitric oxide (NO) endothelium-dependent relaxations to bradykinin in the bovine isolated coronary artery: no role for cytochrome P450 and K+. (mysciencework.com)
  • Therefore, neither cytochrome P(450)-derived metabolites of arachidonic acid nor K(+) appear to mediate the EDHF-like relaxation to BK (i.e the non-NO, high [K(+)](o)/apamin-sensitive component) in bovine coronary arteries. (mysciencework.com)
  • The effects of 1-EBIO and apamin are independent of the NADPH oxidase pathway, as demonstrated by using a PLB-985 cell line lacking the gp91 phox subunit. (pnas.org)
  • Apamin selectively blocks SK channels, a type of Ca2+-activated K+ channel expressed in the central nervous system. (wikipedia.org)
  • Binding of apamin to SK channels is mediated by amino acids in the pore region as well as extracellular amino acids of the SK channel. (wikipedia.org)
  • We evaluated the role of apamin-sensitive SK channels in the pattern and rate of activity of mouse and rat Purkinje neurons. (jneurosci.org)
  • In contrast, apamin did not block LTD induction using 1 Hz stimulation, suggesting that, in aged rats, the AHP does not influence LTD and LTP induction in a similar way. (jneurosci.org)
  • Consistent with these results, membranes prepared from oocytes expressing the SK channel subtypes bound 125I-labelled apamin with distinct dissociation constants (Kd values) of approx. (nih.gov)
  • This channel is highly sensitive to apamin and shares few characteristics with the Ca2+ channel and the TTX-sensitive fast Na+ channel. (nih.gov)
  • Thus, POA GABAergic neurons express an apamin-sensitive channel that mediates, at least in part, the I AHP , and tempers the excitability of these cells. (elsevier.com)
  • The channel is blocked by apamin. (rcsb.org)
  • Using whole-cell patch clamp electrophysiology, we identified an apamin-sensitive current in PLB-985 cells, consistent with an SK channel. (pnas.org)
  • Pi4 competes with apamin, another SK-channel toxin. (wikipedia.org)
  • Apamin, however, eliminated the hypoxia-induced depolarization (400 nM) (7/8), suggesting that hypoxic depolarization is related to the suppression of I SK(Ca) . From the above results, we conclude that adult AMCs are sensitive to hypoxia, and that I SK(Ca) contributes to the hypoxia-induced suppression of whole-cell outward current and depolarization of the resting membrane potential in adult AMCs. (springer.com)
  • Cytochrome P(450)-derived metabolites may be released at higher BK concentrations to act in parallel with NO and the high [K(+)](o)/apamin-sensitive mechanism. (mysciencework.com)
  • The corresponding I AHP was sensitive to antagonism by CdCl 2 (200 μM), apamin (0.3-1 μM), and dequalinium (3 μM). (elsevier.com)
  • The three-dimensional structure of apamin has been studied with several spectroscopical techniques: HNMR, Circular Dichroism, Raman spectroscopy, FT-IR. (wikipedia.org)