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.
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.
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.
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)
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.
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.
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.
Lists of words, usually in alphabetical order, giving information about form, pronunciation, etymology, grammar, and meaning.
Potassium channels whose activation is dependent on intracellular calcium concentrations.
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.
The commonest and widest ranging species of the clawed "frog" (Xenopus) in Africa. This species is used extensively in research. There is now a significant population in California derived from escaped laboratory animals.
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.
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).
Ion channels that specifically allow the passage of SODIUM ions. A variety of specific sodium channel subtypes are involved in serving specialized functions such as neuronal signaling, CARDIAC MUSCLE contraction, and KIDNEY function.
Abrupt changes in the membrane potential that sweep along the CELL MEMBRANE of excitable cells in response to excitation stimuli.
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.
The hollow, muscular organ that maintains the circulation of the blood.
The study of the generation and behavior of electrical charges in living organisms particularly the nervous system and the effects of electricity on living organisms.
Motion picture study of successive images appearing on a fluoroscopic screen.
The domestic cat, Felis catus, of the carnivore family FELIDAE, comprising over 30 different breeds. The domestic cat is descended primarily from the wild cat of Africa and extreme southwestern Asia. Though probably present in towns in Palestine as long ago as 7000 years, actual domestication occurred in Egypt about 4000 years ago. (From Walker's Mammals of the World, 6th ed, p801)
A syndrome associated with damage to the spinal cord above the mid thoracic level (see SPINAL CORD INJURIES) characterized by a marked increase in the sympathetic response to minor stimuli such as bladder or rectal distention. Manifestations include HYPERTENSION; TACHYCARDIA (or reflex bradycardia); FEVER; FLUSHING; and HYPERHIDROSIS. Extreme hypertension may be associated with a STROKE. (From Adams et al., Principles of Neurology, 6th ed, pp538 and 1232; J Spinal Cord Med 1997;20(3):355-60)
Penetrating and non-penetrating injuries to the spinal cord resulting from traumatic external forces (e.g., WOUNDS, GUNSHOT; WHIPLASH INJURIES; etc.).
A cylindrical column of tissue that lies within the vertebral canal. It is composed of WHITE MATTER and GRAY MATTER.
Four CSF-filled (see CEREBROSPINAL FLUID) cavities within the cerebral hemispheres (LATERAL VENTRICLES), in the midline (THIRD VENTRICLE) and within the PONS and MEDULLA OBLONGATA (FOURTH VENTRICLE).
The physiological widening of BLOOD VESSELS by relaxing the underlying VASCULAR SMOOTH MUSCLE.
A nonapeptide messenger that is enzymatically produced from KALLIDIN in the blood where it is a potent but short-lived agent of arteriolar dilation and increased capillary permeability. Bradykinin is also released from MAST CELLS during asthma attacks, from gut walls as a gastrointestinal vasodilator, from damaged tissues as a pain signal, and may be a neurotransmitter.
Single pavement layer of cells which line the luminal surface of the entire vascular system and regulate the transport of macromolecules and blood components.
That phase of a muscle twitch during which a muscle returns to a resting position.
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.
A second generation selective estrogen receptor modulator (SERM) used to prevent osteoporosis in postmenopausal women. It has estrogen agonist effects on bone and cholesterol metabolism but behaves as a complete estrogen antagonist on mammary gland and uterine tissue.
Arteries which arise from the abdominal aorta and distribute to most of the intestines.
Endogenously-synthesized compounds that influence biological processes not otherwise classified under ENZYMES; HORMONES or HORMONE ANTAGONISTS.
Inferior and external epigastric arteries arise from external iliac; superficial from femoral; superior from internal thoracic. They supply the abdominal muscles, diaphragm, iliac region, and groin. The inferior epigastric artery is used in coronary artery bypass grafting and myocardial revascularization.
The force that opposes the flow of BLOOD through a vascular bed. It is equal to the difference in BLOOD PRESSURE across the vascular bed divided by the CARDIAC OUTPUT.
A structurally diverse group of compounds distinguished from ESTROGENS by their ability to bind and activate ESTROGEN RECEPTORS but act as either an agonist or antagonist depending on the tissue type and hormonal milieu. They are classified as either first generation because they demonstrate estrogen agonist properties in the ENDOMETRIUM or second generation based on their patterns of tissue specificity. (Horm Res 1997;48:155-63)
A dipolar ionic buffer.
The technique of using a microtome to cut thin or ultrathin sections of tissues embedded in a supporting substance. The microtome is an instrument that hold a steel, glass or diamond knife in clamps at an angle to the blocks of prepared tissues, which it cuts in sections of equal thickness.
A strain of albino rat used widely for experimental purposes because of its calmness and ease of handling. It was developed by the Sprague-Dawley Animal Company.
The technique of placing cells or tissue in a supporting medium so that thin sections can be cut using a microtome. The medium can be paraffin wax (PARAFFIN EMBEDDING) or plastics (PLASTIC EMBEDDING) such as epoxy resins.
A strain of albino rat developed at the Wistar Institute that has spread widely at other institutions. This has markedly diluted the original strain.
The middle of the three primitive cerebral vesicles of the embryonic brain. Without further subdivision, midbrain develops into a short, constricted portion connecting the PONS and the DIENCEPHALON. Midbrain contains two major parts, the dorsal TECTUM MESENCEPHALI and the ventral TEGMENTUM MESENCEPHALI, housing components of auditory, visual, and other sensorimoter systems.
A 37-amino acid residue peptide isolated from the scorpion Leiurus quinquestriatus hebraeus. It is a neurotoxin that inhibits calcium activated potassium channels.
A large vessel supplying the whole length of the small intestine except the superior part of the duodenum. It also supplies the cecum and the ascending part of the colon and about half the transverse part of the colon. It arises from the anterior surface of the aorta below the celiac artery at the level of the first lumbar vertebra.

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 - Concomitant SK current activation and sodium current inhibition cause J wave syndrome. AU - Chen, Mu. AU - Xu, Dong Zhu. AU - Wu, Adonis Z.. AU - Guo, Shuai. AU - Wan, Juyi. AU - Yin, Dechun. AU - Lin, Shien-Fong. AU - Chen, Zhenhui. AU - Rubart-von der Lohe, Michael. AU - Everett, Thomas H.. AU - Qu, Zhilin. AU - Weiss, James N.. AU - Chen, Peng Sheng. PY - 2018/11/15. Y1 - 2018/11/15. N2 - The mechanisms of J wave syndrome (JWS) are incompletely understood. Here, we showed that the concomitant activation of small-conductance calcium-activated potassium (SK) current (IKAS) and inhibition of sodium current by cyclohexyl-[2-(3,5-dimethyl-pyrazol-1-yl)-6-methyl-pyrimidin-4-yl]-amine (CyPPA) recapitulate the phenotypes of JWS in Langendorff-perfused rabbit hearts. CyPPA induced significant J wave elevation and frequent spontaneous ventricular fibrillation (SVF), as well as sinus bradycardia, atrioventricular block, and intraventricular conduction delay. IKAS activation by CyPPA ...
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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Pneumatiky od popredných výrobcov Continental, Michelin, Barum a mnoho ďalších, vo veľmi širokej ponuke a rôznych typoch nájdete práve v našej ponuke.
Fingerprint Dive into the research topics of The antidepressant fluoxetine blocks the human small conductance calcium-activated potassium channels SK1, SK2 and SK3. Together they form a unique fingerprint. ...
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 …
The Ca2+-activated Cl channel anoctamin-1 (Ano1; Tmem16A) plays a variety of physiological roles, including epithelial fluid secretion. Ano1 is activated by increases in intracellular Ca2+, but there is uncertainty whether Ca2+ binds directly to Ano1 or whether phosphorylation or additional Ca2+-binding subunits like calmodulin (CaM) are required. Here we show that CaM is not necessary for activation of Ano1 by Ca2+ for the following reasons. (a) Exogenous CaM has no effect on Ano1 currents in inside-out excised patches. (b) Overexpression of Ca2+-insensitive mutants of CaM have no effect on Ano1 currents, whereas they eliminate the current mediated by the small-conductance Ca2+-activated K+ (SK2) channel. (c) Ano1 does not coimmunoprecipitate with CaM, whereas SK2 does. Furthermore, Ano1 binds very weakly to CaM in pull-down assays. (d) Ano1 is activated in excised patches by low concentrations of Ba2+, which does not activate CaM. In addition, we conclude that reversible ...
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
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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 ...
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Blocks small conductance calcium-activated potassium channels (PubMed:12239213). Shows activity on KCa2.2/KCNN2 (IC(50)=0.0243 nM), KCa2.3/KCNN3 (IC(50)=1.7 nM), and KCa2.1/KCNN1 (IC(50)=42 nM) (PubMed:12239213). Induces cell death when tested on Jurkat E6-1 and human mammary breast cancer MDA-MB-231 which constituvely express KCa2.2/KCNN2, but not on human peripheral blood lymphocytes (which do not express KCa2.2/KCNN2) (PubMed:24821061).
Abstract(s) :. (Anglais) Cholecystokinin (CCK) / sulfakinin (SK)-type neuropeptides regulate feeding and 37 digestion in chordates and protostomes (e.g. insects). Here we characterised CCK/SK-type 38 signalling for the first time in a non-chordate deuterostome - the starfish Asterias rubens 39 (phylum Echinodermata). In this species, two neuropeptides (ArCCK1, ArCCK2) derived from 40 the precursor protein ArCCKP act as ligands for a CCK/SK-type receptor (ArCCKR) and are 41 expressed in the nervous system, digestive system, tube feet and body wall. Furthermore, 42 ArCCK1 and ArCCK2 cause dose-dependent contraction of cardiac stomach, tube foot and 43 body wall apical muscle preparations in vitro and injection of these neuropeptides in vivo 44 triggers cardiac stomach retraction and inhibition of the onset of feeding in A. rubens. Thus, an 45 evolutionarily ancient role of CCK/SK-type neuropeptides as inhibitory regulators of feeding- 46 related processes in the Bilateria has been conserved in the ...
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 ...
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TY - JOUR. T1 - Effect of different calcium channel blockers on inhibitory junction potentials and slow waves in porcine ileum. AU - Borderies, J. R.. AU - Goñalons, E.. AU - Angel, F.. AU - Vergara, P.. AU - Jiménez, Marcel. PY - 1997/2/14. Y1 - 1997/2/14. N2 - The effect of several calcium channel blockers was evaluated: (i) on spontaneous electrical and mechanical activities and (ii) on the response to electrical field stimulation. The study was carried out on whole-thickness preparation of porcine ileum. Glass microelectrodes were used to record membrane potential from smooth muscle cells. Resting membrane potential was -60 ± 2 mV (n = 18) and preparations generated spontaneous slow waves. Electrical field stimulation (EFS) was applied using different parameters. The amplitude and duration of inhibitory junction potentials (IJPs) increased with EFS strength. IJPs were abolished by tetrodotoxin (1 μM). Nifedipine (1 μM) did not modify the amplitude or duration of IJPs. The frequency 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. ...
Tamapin is a peptide toxin isolated from the venom of the Indian red scorpion Mesobuthus Tamulus. Tamapin is amidated at its C-terminal tyrosine residue (contrary to recombinant tamapin, Smartox tamapin is amidated). It binds to small conductance Ca2+-activated K+ channels (SK channels) with high affinity and inhibits SK channel-mediated currents in pyramidal neurons of the hippocampus as well as in cell lines expressing distinct SK channel subunits. Tamapin is an excellent toxin to discriminate among SK channel subtypes because it presents different affinities for SK1 (42 nM), SK2 (24 pM) and SK3 (1.7 nM) channels. This toxin is also the most potent SK2 channel blocker characterized so far (IC50 for SK2 channels = 24 pM). ...
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 ...
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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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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。
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CLEVELAND, Jan. 20, 2016 /PRNewswire/ -- Harrington Discovery Institute at University Hospitals announces 2016 grant funding to 10 physician-scientists....
Pi4 competes with apamin, another SK-channel toxin. IC50 is 0.5 ± 0.2 μM. Scorpion venoms can be toxic for mammals, insects, ...
Apamin is a neurotoxin that augments polysynaptic reflexes. MCD peptide destroys mast cells. Feeling only slight pain, Schmidt ... Since many small bees are categorized into a pain level of 1, most toxic polypeptides in bee venom are melittin, apamin, and ...
M. Stocker; M. Krause; P. Pedarzani (1999). "An apamin-sentisitive Ca2+-activated K+ current in hippocampal pyramidal neurons ... Examples of calcium-activated channel blockers include: Charybdotoxin Iberiotoxin Apamin Kaliotoxin, Lolitrem, BKCa-specific ...
Stocker M, Krause M, Pedarzani P (April 1999). "An apamin-sensitive Ca2+-activated K+ current in hippocampal pyramidal neurons ...
Hider RC and Ragnarsson U. A proposal for the structure of apamin. FEBS Letts., 1980; 111, 189-193. Hider RC, Drake AF, Inagaki ...
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". ...
... which act on apamin-sensitive Ca2+-activated K+ channels". European Journal of Biochemistry. 245 (2): 457-64. doi:10.1111/j. ... injection in mice it could very well compete to binding to the SKCa channel with the toxin iodinated apamin. Kv1.3 channels can ...
"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 ...
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 - charybdotoxin MeSH ...
... 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 element in bee venom. You can come into contact with apamin through bee venom, so the symptoms that are known are ... Apamin is an 18 amino acid globular peptide neurotoxin found in apitoxin (bee venom). Dry bee venom consists of 2-3% of apamin ... 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 and its guanidination to an apamin derivative with full neurotoxic activity.". Proceedings of the National Academy of ...
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. ...
In other less formal contexts, an alcohol is often called with the name of the corresponding alkyl group followed by the word "alcohol", e.g., methyl alcohol, ethyl alcohol. Propyl alcohol may be n-propyl alcohol or isopropyl alcohol, depending on whether the hydroxyl group is bonded to the end or middle carbon on the straight propane chain. As described under systematic naming, if another group on the molecule takes priority, the alcohol moiety is often indicated using the "hydroxy-" prefix.[17] Alcohols are then classified into primary, secondary (sec-, s-), and tertiary (tert-, t-), based upon the number of carbon atoms connected to the carbon atom that bears the hydroxyl functional group. (The respective numeric shorthands 1°, 2°, and 3° are also sometimes used in informal settings.[18]) The primary alcohols have general formulas RCH2OH. The simplest primary alcohol is methanol (CH3OH), for which R=H, and the next is ethanol, for which R=CH3, the methyl group. Secondary alcohols are those ...
... 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 ...
Text is available under the Creative Commons Attribution-ShareAlike License; additional terms may apply. By using this site, you agree to the Terms of Use and Privacy Policy. Wikipedia® is a registered trademark of the Wikimedia Foundation, Inc., a non-profit organization ...
... 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 ...
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 is an 18 amino acid globular peptide neurotoxin found in apitoxin (bee venom). Dry bee venom consists of 2-3% of apamin ... 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 ...
An Apamin- and Scyllatoxin-Insensitive Isoform of the Human SK3 Channel. Oliver H. Wittekindt, Violeta Visan, Hiroaki Tomita, ... An Apamin- and Scyllatoxin-Insensitive Isoform of the Human SK3 Channel. Oliver H. Wittekindt, Violeta Visan, Hiroaki Tomita, ... An Apamin- and Scyllatoxin-Insensitive Isoform of the Human SK3 Channel. Oliver H. Wittekindt, Violeta Visan, Hiroaki Tomita, ... An Apamin- and Scyllatoxin-Insensitive Isoform of the Human SK3 Channel Message Subject (Your Name) has forwarded a page to you ...
... 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 ...
フィンガープリント 「Amiodarone Inhibits Apamin-Sensitive Potassium Currents」の研究トピックを掘り下げます。これらがまとまってユニークなフィンガープリントを構成します。 * Apamin ... title = "Amiodarone Inhibits Apamin-Sensitive Potassium Currents",. abstract = "Background:Apamin sensitive potassium current ( ... Background:Apamin sensitive potassium current (IKAS), carried by the type 2 small conductance Ca2+-activated potassium (SK2) ... Turker, I., Yu, C. C., Chang, P. C., Chen, Z., Sohma, Y., Lin, S
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 ...
The drugs tested included apamin (100 nm; n = 5), TTX (300 nm; n = 4), a mixture of NBQX (AMPA antagonist; 5 μm), MK-801 (NMDA ... Consistent with the previous report on SMHs in DA neurons (Seutin et al., 1998), SMOCs were completely eliminated by apamin ( ... C, Summary bar graph depicting the effects of apamin, TTX, and various neurotransmitter antagonists on SMOCs. The SMOC ... Seutin V, Massotte L, Scuvee-Moreau J, Dresse A (1998) Spontaneous apamin-sensitive hyperpolarizations in dopaminergic neurons ...
Apamin and the combination of apamin and iberiotoxin or apamin and charybdotoxin induced a transient endothelium-dependent ... Apamin and the combination of apamin and iberiotoxin or apamin and charybdotoxin induced a transient endothelium-dependent ... Apamin and the combination of apamin and iberiotoxin or apamin and charybdotoxin induced a transient endothelium-dependent ... Apamin and the combination of apamin and iberiotoxin or apamin and charybdotoxin induced a transient endothelium-dependent ...
Wagner, E. J., Rønnekleiv, O. K., & Kelly, M. J. (2001). The noradrenergic inhibition of an apamin-sensitive, small-conductance ... Wagner, Edward J. ; Rønnekleiv, Oline K. ; Kelly, Martin J. / The noradrenergic inhibition of an apamin-sensitive, small- ... Wagner, EJ, Rønnekleiv, OK & Kelly, MJ 2001, The noradrenergic inhibition of an apamin-sensitive, small-conductance Ca2+- ... The corresponding IAHP was sensitive to antagonism by CdCl2 (200 μM), apamin (0.3-1 μM), and dequalinium (3 μM). The β- ...
Single apamin-blocked Ca-activated K+ channels of small conductance in cultured rat skeletal muscle. Nature. 1986 Dec 1;323( ... Single apamin-blocked Ca-activated K+ channels of small conductance in cultured rat skeletal muscle. / Blatz, Andrew L.; ... Blatz, A. L., & Magleby, K. L. (1986). Single apamin-blocked Ca-activated K+ channels of small conductance in cultured rat ... Blatz, Andrew L. ; Magleby, Karl L. / Single apamin-blocked Ca-activated K+ channels of small conductance in cultured rat ...
  • Apamin is an 18 amino acid globular peptide neurotoxin found in apitoxin (bee venom). (wikipedia.org)
  • Dry bee venom consists of 2-3% of apamin. (wikipedia.org)
  • 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. (wikipedia.org)
  • BmP02 is a 28-amino acid residue peptide purified from the venom of the Chinese scorpion Buthus martensi Karsch, which had been demonstrated to be a weak blocker of apamin-sensitive calcium-activated potassium channels. (rcsb.org)
  • Apamin, a toxin in the bee venom, that was previously reported by our group to block the slow Ca2+ APs (Bkaily et al. (nih.gov)
  • Apamin, an 18-amino acid bee venom peptide, is a specific blocker of a class of Ca2+ activated K+ channels. (semanticscholar.org)
  • The large conductance (250 pS) Ca-activated K + channel (BK channel) is not a major contributor to the afterhyperpolarization in non-innervated skeletal muscle and some nerve cells, because apamin, a neurotoxic component of bee venom, abolishes the afterhyperpolarization but does not block BK channels, and 5 mM extracellular tetraethylammonium ion (TEA) blocks BK channels but does not reduce the afterhyperpolarization. (elsevier.com)
  • Apamin from bee venom. (uni-hamburg.de)
  • Apamin , which makes up 3% of venom, destroys nerve tissue. (beeculture.com)
  • [ 6 ] In addition, SK channels(SK1-SK3) are sensitive to blockade by the bee venom apamin , [ 7 ] but SK4 (IK) is not. (thefullwiki.org)
  • If apitoxin were a cosmopolitan, apamin would be the lime juice, as it is the key ingredient that puts the bite into bee venom. (blogspot.com)
  • In other experiments, endothelium independent vasodilation induced by SNP, were also reversed by charybdotoxin plus apamin, but not L-NAME. (herts.ac.uk)
  • 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)
  • 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)
  • We obtained a partial rescue of the cellular variability phenotype when we blocked SK current using the specific blocker apamin. (eneuro.org)
  • The effect of apamin, a small conductance calcium activated potassium (SK) channel blocker, on a mouse model of neurofibromatosis 1. (smcm.edu)
  • iv) prechallenged with inhibitors of various potassium channels (glibenclamide, apamin, charybdotoxin, and tetraethylammonium chloride). (hindawi.com)
  • Neither apamin nor glibenclamide modified relaxation. (portlandpress.com)
  • Neither glibenclamide (Glib) nor apamin treatment elicited any significant effect in both transverse and longitudinal phasic activity. (scirp.org)
  • ATP-elicited delayed K + current was not inhibited by a 'cocktail' of K + channel blockers (4-AP, TEA, apamin, charybdotoxin, glibenclamide). (ingentaconnect.com)
  • Apamin is the smallest neurotoxin polypeptide known, and the only one that passes the blood-brain barrier. (wikipedia.org)
  • Apamin is a neurotoxin that acts as an antagonist at calcium-activated potassium channels (SK channels). (perkinelmer.com)
  • or 100 nM apamin plus 50 nM iberiotoxin (Ap + IBX). (pnas.org)
  • 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. (elsevier.com)
  • However, the combination of scyllatoxin and iberiotoxin did not mimic the inhibitory effect of the apamin/charybdotoxin combination. (elsevier.com)
  • Solutions of nitric oxide (NO) gas also relaxed small mesenteric arteries that had been contracted with cirazoline in a concentration-dependent manner, and the sensitivity to NO was reduced by iberiotoxin and the combination of apamin, scyllatoxin, or tubocurarine with charybdotoxin but not by apamin, charybdotoxin, scyllatoxin, or tubocurarine alone. (elsevier.com)
  • In eNOS+/+ mice, the acetylcholine-induced response was primarily mediated by NO and was sensitive to iberiotoxin and the combination of apamin and charybdotoxin. (elsevier.com)
  • Raloxifene-induced dilatations of female arteries were blunted by N G -nitro- l -arginine methyl ester but unaffected by 1400W, charybdotoxin plus apamin, wortmannin, or LY294002. (ahajournals.org)
  • with charybdotoxin plus apamin respectively). (herts.ac.uk)
  • Bar Graphs show re-contraction of arteries in response to L-NAME or charybdotoxin plus apamin (C+A) in arteries with endothelium, dilated with acetylcholine (Figure B) or without endothelium dilated with SNP (Figure C). This data demonstrates that charybdotoxin and apamin have pharmacological effects independent of the endothelium, at the level of smooth muscle cell function. (herts.ac.uk)
  • We imaged SK channels labeled with fluorophore-tagged apamin and monitored SK channel nanoclustering at the single molecule level by combining atomic force microscopy and toxin (i.e., apamin) pharmacology. (deepdyve.com)
  • The most obvious distinguishing feature of this new isoform was that whereas hSK3 was blocked by apamin ( K d = 0.8 nM), scyllatoxin ( K d = 2.1 nM), and d -tubocurarine ( K d = 33.4 μM), hSK3_ex4 was not affected by apamin up to 100 nM, scyllatoxin up to 500 nM, and d -tubocurarine up to 500 μM. (aspetjournals.org)
  • when SK channels are blocked by the specific antagonists apamin or scyllatoxin, cells fire spontaneously at rates as high as 500 spikes per second. (jneurosci.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)
  • In all three cases the Ca2+-activated K+ currents could be totally inhibited by 500 nM apamin. (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)
  • Heterogeneous upregulation of apamin-sensitive potassium currents in failing human ventricles. (nih.gov)
  • Only SK2 and SK3 are blocked by apamin, whereas SK1 is apamin insensitive. (wikipedia.org)
  • The high sensitivity of MRS 2179 has revealed, for the first time in the human gastrointestinal tract, that a P2Y 1 receptor present in smooth muscle probably mediates this mechanism through a pathway that partially involves apamin-sensitive calcium-activated potassium channels. (physiology.org)
  • 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)
  • Apamin is a specific inhibitor of small conductance K + Ca2+ (SK Ca2+ ). (jci.org)
  • The kinetics of labeled derivatives of apamin were studied in vitro and in vivo in mice by Cheng-Raude et al. (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)
  • IJPf is partially suramin and apamin sensitive, and it is abolished after desensitization with adenosine 5′-β-2-thiodiphosphate (ADPβS) and therefore considered purinergic, possibly through P2 receptors ( 35 ). (physiology.org)
  • the potency of xenin to relax was reduced by apamin and suramin. (aspetjournals.org)
  • The channels that formed from the various subunits displayed differential sensitivity to apamin and tubocurare. (sciencemag.org)
  • The corresponding I AHP was sensitive to antagonism by CdCl 2 (200 μM), apamin (0.3-1 μM), and dequalinium (3 μM). (elsevier.com)
  • Rats were injected in one lateral cerebral ventricle (i.c.v.) with apamin (100 ng per animal). (elsevier.com)
  • as I note in the eighth chapter of Venomous , studies have found that apamin injected into the bodies of rats can alter the activity of dopamine-releasing neurons in their forebrains-which makes apamin one of a limited number of compounds we know of able to slip past the blood-brain barrier, and thus a promising candidate for a drug delivery strategy referred to as Trojan horse transit . (discovermagazine.com)
  • Preliminary research found this derivative of apamin improves upon the original toxin's ability to cross the blood-brain barrier and showed it was able to ferry proteins and even nanoparticles effectively, most likely because it is actively pulled across by transport proteins. (discovermagazine.com)
  • 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)
  • We evaluated the role of apamin-sensitive SK channels in the pattern and rate of activity of mouse and rat Purkinje neurons. (jneurosci.org)
  • 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)
  • By local alterations it is possible to find the amino acids that are involved in toxicity of apamin. (wikipedia.org)
  • This is only a small decrease, which indicates that neither the ε-amino group of lysine4 nor the α-amino group of cysteine1 is essential for the toxicity of apamin. (wikipedia.org)
  • The amino acids that cause toxicity of apamin are cysteine1, lysine4, arginine13, arginine14 and histidine18. (wikipedia.org)
  • 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)
  • Blatz, AL & Magleby, KL 1986, ' Single apamin-blocked Ca-activated K + channels of small conductance in cultured rat skeletal muscle ', Nature , vol. 323, no. 6090, pp. 718-720. (elsevier.com)
  • Previous work has shown the involvement of integrins and integrin-associated signaling pathways in activation of plasma membrane apamin-sensitive Ca 2+ -activated K + channels that results in membrane hyperpolarization of HAC after 0.33 Hz cyclical mechanical stimulation. (rupress.org)
  • Acetylcholine-induced relaxation in eNOS-/- mice was unaffected by charybdotoxin or apamin alone but significantly inhibited by the combination of these agents. (elsevier.com)
  • These data indicate that acetylcholine-induced endothelium-derived hyperpolarizing factor-mediated relaxation in small mesenteric arteries from eNOS-/- involved the activation of tubocurarine and apamin-/charybdotoxin- sensitive K-channels. (elsevier.com)
  • Protease-activated receptors mediate apamin-sensitive relaxation of mouse and guinea pig gastrointestinal smooth muscle. (springer.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 reduced frequency but increased amplitude. (hindawi.com)
  • Apamin selectively blocks SK channels, a type of Ca2+-activated K+ channel expressed in the central nervous system. (wikipedia.org)
  • These amino acids are involved in the binding of apamin to the Ca2+-activated K+ channel. (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)
  • 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)
  • Detection and photoaffinity labeling of the Ca2+-activated K+ channel-associated apamin receptor in cultured astrocytes from rat brain. (semanticscholar.org)
  • article{Seagar1987DetectionAP, title={Detection and photoaffinity labeling of the Ca2+-activated K+ channel-associated apamin receptor in cultured astrocytes from rat brain. (semanticscholar.org)
  • 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 is a polypeptide possessing an amino acid sequence of H-Cys-Asn-Cys-Lys-Ala-Pro-Glu-Thr-Ala-Leu-Cys-Ala-Arg-Arg-Cys-Gln-Gln-His-NH2 (with disulfide bonds between Cys1-Cys11 and Cys3-Cys15). (wikipedia.org)
  • Apamin is very rigid because of the two disulfide bridges and seven hydrogen bonds. (wikipedia.org)
  • 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. (elsevier.com)
  • 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)
  • Apamin potentiated bursting activity and enhanced phasic contraction. (nii.ac.jp)
  • Apamin was separated from the other compounds by gel filtration and ion exchange chromatography. (wikipedia.org)
  • 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. (wikipedia.org)
  • Research suggests that small doses of apamin can affect memory. (blogspot.com)