A benzoate-cevane found in VERATRUM and Schoenocaulon. It activates SODIUM CHANNELS to stay open longer than normal.
Veratrine is a mixture of alkaloids, primarily veratridine and cevadine, obtained from the seeds of various plants of the genus Schoenocaulon (formerly Veratrum), known to stimulate sodium channels in nerve membranes, leading to depolarization and prolonged action potentials.
A class of drugs that stimulate sodium influx through cell membrane channels.
A plant genus of the family LILIACEAE with roots that contain VERATRUM ALKALOIDS used as emetics, parasiticides, antihypertensives. It is the main ingredient of Boicil.
Pinched-off nerve endings and their contents of vesicles and cytoplasm together with the attached subsynaptic area of the membrane of the post-synaptic cell. They are largely artificial structures produced by fractionation after selective centrifugation of nervous tissue homogenates.
Batrachotoxin is the 20-alpha-bromobenzoate of batrachotoxin A; they are toxins from the venom of a small Colombian frog, Phyllobates aurotaenia, cause release of acetylcholine, destruction of synaptic vesicles and depolarization of nerve and muscle fibers.
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.
A compound that contains a reduced purine ring system but is not biosynthetically related to the purine alkaloids. It is a poison found in certain edible mollusks at certain times; elaborated by GONYAULAX and consumed by mollusks, fishes, etc. without ill effects. It is neurotoxic and causes RESPIRATORY PARALYSIS and other effects in MAMMALS, known as paralytic SHELLFISH poisoning.
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.
A member of the alkali group of metals. It has the atomic symbol Na, atomic number 11, and atomic weight 23.
One of the long-acting ANTIPSYCHOTIC AGENTS used for maintenance or long-term therapy of SCHIZOPHRENIA and other PSYCHOTIC DISORDERS.
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.
A C19 norditerpenoid alkaloid (DITERPENES) from the root of ACONITUM plants. It activates VOLTAGE-GATED SODIUM CHANNELS. It has been used to induce ARRHYTHMIAS in experimental animals and it has antiinflammatory and antineuralgic properties.
A voltage-gated sodium channel subtype found widely expressed in neurons of the central and peripheral nervous systems. Defects in the SCN8A gene which codes for the alpha subunit of this sodium channel are associated with ATAXIA and cognitive deficits.
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.
Toxic substances from microorganisms, plants or animals that interfere with the functions of the nervous system. Most venoms contain neurotoxic substances. Myotoxins are included in this concept.
A cardioactive glycoside consisting of rhamnose and ouabagenin, obtained from the seeds of Strophanthus gratus and other plants of the Apocynaceae; used like DIGITALIS. It is commonly used in cell biological studies as an inhibitor of the NA(+)-K(+)-EXCHANGING ATPASE.
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.
The inner portion of the adrenal gland. Derived from ECTODERM, adrenal medulla consists mainly of CHROMAFFIN CELLS that produces and stores a number of NEUROTRANSMITTERS, mainly adrenaline (EPINEPHRINE) and NOREPINEPHRINE. The activity of the adrenal medulla is regulated by the SYMPATHETIC NERVOUS SYSTEM.
Arthropods of the order Scorpiones, of which 1500 to 2000 species have been described. The most common live in tropical or subtropical areas. They are nocturnal and feed principally on insects and other arthropods. They are large arachnids but do not attack man spontaneously. They have a venomous sting. Their medical significance varies considerably and is dependent on their habits and venom potency rather than on their size. At most, the sting is equivalent to that of a hornet but certain species possess a highly toxic venom potentially fatal to humans. (From Dorland, 27th ed; Smith, Insects and Other Arthropods of Medical Importance, 1973, p417; Barnes, Invertebrate Zoology, 5th ed, p503)
Cyclopentanophenanthrenes with a 5- or 6-membered lactone ring attached at the 17-position and SUGARS attached at the 3-position. Plants they come from have long been used in congestive heart failure. They increase the force of cardiac contraction without significantly affecting other parameters, but are very toxic at larger doses. Their mechanism of action usually involves inhibition of the NA(+)-K(+)-EXCHANGING ATPASE and they are often used in cell biological studies for that purpose.
A general class of ortho-dihydroxyphenylalkylamines derived from tyrosine.
Drugs that interrupt transmission at the skeletal neuromuscular junction by causing sustained depolarization of the motor end plate. These agents are primarily used as adjuvants in surgical anesthesia to cause skeletal muscle relaxation.
A class of drugs that act by inhibition of sodium influx through cell membranes. Blockade of sodium channels slows the rate and amplitude of initial rapid depolarization, reduces cell excitability, and reduces conduction velocity.
An organic amine proton acceptor. It is used in the synthesis of surface-active agents and pharmaceuticals; as an emulsifying agent for cosmetic creams and lotions, mineral oil and paraffin wax emulsions, as a biological buffer, and used as an alkalizer. (From Merck, 11th ed; Martindale, The Extra Pharmacopoeia, 30th ed, p1424)
Gated, ion-selective glycoproteins that traverse membranes. The stimulus for ION CHANNEL GATING can be due to a variety of stimuli such as LIGANDS, a TRANSMEMBRANE POTENTIAL DIFFERENCE, mechanical deformation or through INTRACELLULAR SIGNALING PEPTIDES AND PROTEINS.
Cells that store epinephrine secretory vesicles. During times of stress, the nervous system signals the vesicles to secrete their hormonal content. Their name derives from their ability to stain a brownish color with chromic salts. Characteristically, they are located in the adrenal medulla and paraganglia (PARAGANGLIA, CHROMAFFIN) of the sympathetic nervous system.
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).

BIIR 561 CL: a novel combined antagonist of alpha-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid receptors and voltage-dependent sodium channels with anticonvulsive and neuroprotective properties. (1/342)

Antagonists of glutamate receptors of the alpha-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid (AMPA) subtype, as well as of voltage-gated sodium channels, exhibit anticonvulsive and neuroprotective properties in vivo. One can postulate that a compound that combines both principles might be useful for the treatment of disorders of the central nervous system, like focal or global ischemia. Here, we present data on the effects of dimethyl-(2-[2-(3-phenyl-[1,2, 4]oxadiazol-5-yl)-phenoxy]ethyl)-amine hydrochloride (BIIR 561 CL) on neuronal AMPA receptors and voltage-dependent sodium channels. BIIR 561 CL inhibited AMPA receptor-mediated membrane currents in cultured cortical neurons with an IC50 value of 8.5 microM. The inhibition was noncompetitive. In a cortical wedge preparation, BIIR 561 CL reduced AMPA-induced depolarizations with an IC50 value of 10.8 microM. In addition to the effects on the glutamatergic system, BIIR 561 CL inhibited binding of radiolabeled batrachotoxin to rat brain synaptosomal membranes with a Ki value of 1.2 microM. The compound reduced sodium currents in voltage-clamped cortical neurons with an IC50 value of 5.2 microM and inhibited the veratridine-induced release of glutamate from rat brain slices with an IC50 value of 2.3 microM. Thus, BIIR 561 CL inhibited AMPA receptors and voltage-gated sodium channels in a variety of preparations. BIIR 561 CL suppressed tonic seizures in a maximum electroshock model in mice with an ED50 value of 2.8 mg/kg after s.c. administration. In a model of focal ischemia in mice, i.p. administration of 6 or 60 mg/kg BIIR 561 CL reduced the area of the infarcted cortical surface. These data show that BIIR 561 CL is a combined antagonist of AMPA receptors and voltage-gated sodium channels with promising anticonvulsive and neuroprotective properties.  (+info)

Target-dependent regulation of acetylcholine secretion at developing motoneurons in Xenopus cell cultures. (2/342)

1. Myocyte-dependent regulation of acetylcholine (ACh) quantal secretion from developing motoneurons was studied in day-3 Xenopus nerve-muscle co-cultures. Spontaneous synaptic currents (SSCs) were measured in manipulated synapses by using whole-cell voltage-clamped myocytes. Changes in SSC amplitude were assumed to reflect changes in the ACh content of secreted quantal packets. Compared with natural synapses, motoneurons without any contact with a myocyte (naive neurons) released ACh in smaller quantal packets. 2. Bipolar cultured motoneurons, which were in contact with a myocyte with one axon branch (contact-end) but remained free at another axon branch (free-end), were further used to examine quantal ACh secretion. The ACh quantal size recorded at free-end terminals was similar to that of naive neurons and was smaller than that at the contact-end, indicating that myocyte contact exerts differential regulation on quantal secretion in the same neuron. 3. Some of the neurons that formed a natural synapse with a myocyte continued to grow forward and ACh quantal secretion from the free growth cone was examined. The ACh quantal size recorded at free growth cones was inversely proportional to the distance to the natural synapse, implying localized regulation of quantal secretion by the myocyte. 4. Chronic treatment of day-1 cultures with veratridine and d-tubocurarine, respectively, increased and decreased the neurotrophic action of myocytes when assayed on day 3. 5. Taken together, these findings suggest that the myocyte is an important postsynaptic target in the regulation of quantal secretion and that the trophic action is spatially restricted to the neighbourhood of the neuromuscular junction.  (+info)

Voltage-activated K+ channels and membrane depolarization regulate accumulation of the cyclin-dependent kinase inhibitors p27(Kip1) and p21(CIP1) in glial progenitor cells. (3/342)

Neural cell development is regulated by membrane ion channel activity. We have previously demonstrated that cell membrane depolarization with veratridine or blockage of K+ channels with tetraethylammonium (TEA) inhibit oligodendrocyte progenitor (OP) proliferation and differentiation (); however the molecular events involved are largely unknown. Here we show that forskolin (FSK) and its derivative dideoxyforskolin (DFSK) block K+ channels in OPs and inhibit cell proliferation. The antiproliferative effects of TEA, FSK, DFSK, and veratridine were attributable to OP cell cycle arrest in G1 phase. In fact, (1) cyclin D accumulation in synchronized OP cells was not affected by K+ channel blockers or veratridine; (2) these agents prevented OP cell proliferation only if present during G1 phase; and (3) G1 blockers, such as rapamycin and deferoxamine, mimicked the anti-proliferative effects of K+ channel blockers. DFSK also prevented OP differentiation, whereas FSK had no effect. Blockage of K+ channels and membrane depolarization also caused accumulation of the cyclin-dependent kinase inhibitors p27(Kip1) and p21(CIP1) in OP cells. The antiproliferative effects of K+ channel blockers and veratridine were still present in OP cells isolated from INK4a-/- mice, lacking the cyclin-dependent kinase inhibitors p16(INK4a) and p19(ARF). Our results demonstrate that blockage of K+ channels and cell depolarization induce G1 arrest in the OP cell cycle through a mechanism that may involve p27(Kip1) and p21(CIP1) and further support the conclusion that OP cell cycle arrest and differentiation are two uncoupled events.  (+info)

The effects of verapamil and diltiazem on N-, P- and Q-type calcium channels mediating dopamine release in rat striatum. (4/342)

1. The putative inhibitory effects of verapamil and diltiazem on neuronal non-L-type Ca2+ channels were studied by investigating their effects on either K+- or veratridine-evoked [3H]-dopamine ([3H]-DA) release in rat striatal slices. Involvement of N-, P- and Q-type channels was identified by sensitivity of [3H]-DA release to omega-conotoxin GVIA (omega-CTx-GVIA), omega-agatoxin IVA (omega-Aga-IVA) and omega-conotoxin MVIIC (omega-CTx-MVIIC), respectively. 2. KCl (50 mM)-evoked [3H]-DA release was abolished in the absence of Ca2+, and was insensitive to dihydropyridines (up to 30 microM). It was significantly blocked by omega-CTx-GVIA (1 microM), omega-Aga-IVA (30 nM) and was confirmed to be abolished by omega-CTx-MVIIC (3 microM), indicating involvement of N-, P- and Q-type channel subtypes. 3. Verapamil and diltiazem inhibited K+-evoked [3H]-DA release in a concentration-dependent manner. The inhibitory effects of verapamil or diltiazem (each 30 microM) were fully additive to the effect of omega-CTx-GVIA (1 microM), whereas co-application with omega-Aga-IVA (30 nM) produced similar effects to those of omega-Aga-IVA alone. 4. As shown previously, veratridine-evoked [3H]-DA release in Ca2+ containing medium exclusively involves Q-type Ca2+ channels. Here, diltiazem (30 microM) did not inhibit veratridine-evoked [3H]-DA release, whereas verapamil (30 microM) partially inhibited it, indicating possible involvement of Q-type channels in verapamil-induced inhibition. However, verapamil (30 microM) inhibited this release even in the absence of extracellular Ca2+, suggesting that Na+ rather than Q-type Ca2+ channels are involved. 5. Taken together, our results suggest that verapamil can block P- and at higher concentrations possibly N- and Q-type Ca2+ channels linked to [3H]-DA release, whereas diltiazem appears to block P-type Ca2+ channels only.  (+info)

Propofol, bradycardia and the Bezold-Jarisch reflex in rabbits. (5/342)

Propofol may cause profound bradycardia and asystole, which are mediated indirectly via cardiac innervation but could involve direct effects on the sino-atrial (SA) node and the conducting system of the heart. To test the hypothesis that propofol may also activate Bezold-Jarisch reflexes to cause bradycardia, 5-hydroxytryptamine (5-HT), veratridine and propofol were injected into the left ventricle of the heart in both intact and vagotomized rabbits. 5-HT and veratridine produced an acute, rapid, dose-dependent decrease in mean heart rate (delta HR) and a decrease in mean arterial pressure (delta MAP) together with transient but severe depression and abolition of renal sympathetic nerve activity (RSNA). Bilateral vagotomy greatly attenuated these responses; for example, at the highest dose of 5-HT (8 micrograms kg-1), delta HR, delta MAP and duration of abolition of RSNA were reduced by 57% (P < 0.001), 53% (P < 0.05) and 79% (P < 0.05), respectively. In contrast, reductions in delta HR and delta MAP produced by propofol were statistically significant only at very high doses (8 mg kg-1). Propofol depressed but did not abolish RSNA, and bilateral vagotomy had no effect on any of these responses. These results indicate that the cause of acute bradycardia after administration of propofol does not involve the Bezold-Jarisch reflex.  (+info)

Calcium channels involved in K+- and veratridine-induced increase of cytosolic calcium concentration in human cerebral cortical synaptosomes. (6/342)

Human cerebral cortical synaptosomes were used to study voltage-dependent Ca(2+) channels mediating calcium influx in human axon terminals. Synaptosomes were depolarized by elevation of the extracellular K(+) concentration by 30 mM or by the addition of veratridine (10 microM). Increase in cytosolic concentration of calcium [Ca(2+)](i) induced by either stimulus was abolished in the absence of extracellular Ca(2+) ions. omega-Agatoxin IVA inhibited the K(+)-induced [Ca(2+)](i) increase concentration-dependently (IC(50): 113 nM). omega-Conotoxin GVIA (0.1 microM) inhibited K(+)-induced [Ca(2+)](i) increase by 20%. omega-Conotoxin MVIIC (0.2 microM) caused an inhibition by 85%. Nifedipine (1 microM) had no effect on K(+)-induced [Ca(2+)](i) increase. Veratridine-induced increase in [Ca(2+)](i) was inhibited by omega-conotoxin GVIA (0.1 microM) and omega-Agatoxin IVA (0.2 microM; by about 25 and 45%, respectively). Nifedipine inhibited the veratridine-evoked [Ca(2+)](i) increase concentration-dependently (IC(50): 4.9 nM); Bay K 8644 (3 microM) shifted the nifedipine concentration-response curve to the right. Mibefradil (10 microM) abolished the increase in [Ca(2+)](i) evoked by K(+) and reduced the increase evoked by veratridine by almost 90%. KB-R7943 (3 microM) an inhibitor of the Na(+)/Ca(2+) exchanger NCX1, decreased the increase in [Ca(2+)](i) evoked by veratridine by approximately 20%. It is concluded that the increase in [Ca(2+)](i) after K(+) depolarization caused by Ca(2+) influx predominantly via P/Q-type Ca(2+) channels and after veratridine depolarization via N- and P/Q-type, but also by L-type Ca(2+) channels. The toxin- and nifedipine-resistant fraction of the veratridine response may result both from influx via R-type Ca(2+) channels and by Ca(2+) inward transport via Na(+)/Ca(2+) exchanger.  (+info)

Inhibition of glutamate uptake by a polypeptide toxin (phoneutriatoxin 3-4) from the spider Phoneutria nigriventer. (7/342)

Glutamate concentration increases significantly in the extracellular compartment during brain ischaemia and anoxia. This increase has an important Ca(2+)-independent component, which is due in part to the reversal of glutamate transporters of the plasma membrane of neurons and glia. The toxin phoneutriatoxin 3-4 (Tx3-4) from the spider Phoneutria nigriventer has been reported to decrease the evoked glutamate release from synaptosomes by inhibiting Ca(2+) entry via voltage-dependent Ca(2+) channels. However, we report here that Tx3-4 is also able to inhibit the uptake of glutamate by synaptosomes in a time-dependent manner and that this inhibition in turn leads to a decrease in the Ca(2+)-independent release of glutamate. No other polypeptide toxin so far described has this effect. Our results suggest that Tx3-4 can be a valuable tool in the investigation of function and dysfunction of glutamatergic neurotransmission in diseases such as ischaemia.  (+info)

Cooperative activation of action potential Na+ ionophore by neurotoxins. (8/342)

Four neurotoxins that activate the action potential Na+ ionophore of electrically excitable neuroblastoma cells interact with two distinct classes of sites, one specific for the alkaloids veratridine, batrachotoxin, and aconitine, and the second specific for scorpion toxin. Positive heterotropic cooperativity is observed between toxins bound at these two classes of sites. Tetrodotoxin is a noncompetitive inhibitor of activation by each of these toxins (KI = 4-8 nM). These results suggest the existence of three functionally separable components of the action potential Na+ ionophore: two regulatroy components, which bind activating neurotoxins and interact allosterically in controlling the activity of a third ion-transport component, which binds tetrodotoxin.  (+info)

Veratridine is not a medical term, but it is a chemical compound that has been used in scientific research. It's a plant alkaloid found primarily in the seeds and roots of various Veratrum species (also known as false hellebore or white hellebore).

In a pharmacological context, veratridine can be defined as:

A steroidal alkaloid that acts as a potent agonist at voltage-gated sodium channels in excitable membranes. It causes persistent activation of these channels, leading to sustained depolarization and increased neuronal excitability. Veratridine has been used in research to study the properties and functions of sodium channels, as well as neurotransmission and nerve impulse transmission.

However, it is not a term typically used in clinical medicine or patient care.

Veratrine is not a medical term, but it is a pharmacological term that refers to a mixture of alkaloids (veratridine and cevadine) extracted from the seeds of the sabadilla lily (Schoenocaulon officinale). Veratrine has been used in research and medicine for its effects on nerve cells, particularly in studying sodium channels. It can cause prolonged depolarization of nerve membranes leading to repetitive firing of action potentials. However, due to its high toxicity, it is not used clinically.

Sodium channel agonists are substances that enhance the activity or function of sodium channels. Sodium channels are membrane proteins that play a crucial role in the generation and transmission of electrical signals in excitable cells, such as nerve and muscle cells. They allow the influx of sodium ions into the cell, which leads to the depolarization of the cell membrane and the initiation of an action potential.

Sodium channel agonists increase the likelihood, duration, or amplitude of action potentials by promoting the opening of sodium channels or slowing their closure. These effects can have various physiological consequences depending on the type of cell and tissue involved. In some cases, sodium channel agonists may be used for therapeutic purposes, such as in the treatment of certain types of heart arrhythmias. However, they can also have harmful or toxic effects, especially when used in excessive amounts or in sensitive populations.

Examples of sodium channel agonists include some drugs used to treat cardiac arrhythmias, such as Class I antiarrhythmic agents like ajmaline, flecainide, and procainamide. These drugs bind to the sodium channels and stabilize their open state, reducing the frequency and velocity of action potentials in the heart. Other substances that can act as sodium channel agonists include certain neurotoxins, such as batrachotoxin and veratridine, which are found in some species of plants and animals and can have potent effects on nerve and muscle function.

"Veratrum" is a genus of plants that are part of the Melanthiaceae family, also known as hellebore. These plants contain various alkaloids with pharmacological properties and have been used in traditional medicine for their therapeutic effects. However, they can also be highly toxic if not used properly.

In a medical context, "Veratrum" may refer to the medicinal preparations made from these plants, which have been used historically to treat various conditions such as hypertension, heart failure, and gastrointestinal disorders. However, due to their narrow therapeutic index and potential for serious side effects, they are not commonly used in modern medicine.

It's worth noting that the term "Veratrum" is primarily a botanical designation, and its medical use is relatively limited. If you have any specific questions about the medicinal or toxicological properties of Veratrum plants, it would be best to consult with a healthcare professional or a trained medical herbalist.

Synaptosomes are subcellular structures that can be isolated from the brain tissue. They are formed during the fractionation process of brain homogenates and consist of intact presynaptic terminals, including the synaptic vesicles, mitochondria, and cytoskeletal elements. Synaptosomes are often used in neuroscience research to study the biochemical properties and functions of neuronal synapses, such as neurotransmitter release, uptake, and metabolism.

Batrachotoxins are a type of steroidal alkaloid toxin that are found in certain species of frogs, beetles, and plants. They are highly toxic and cause rapid excitation of nerve and muscle tissue leading to paralysis and death. Batrachotoxins work by irreversibly binding to and opening sodium ion channels in cell membranes, causing a persistent depolarization of the membrane potential. This leads to uncontrolled firing of action potentials in nerves and muscles, resulting in the symptoms mentioned above. These toxins are considered among the most potent natural poisons known.

Tetrodotoxin (TTX) is a potent neurotoxin that is primarily found in certain species of pufferfish, blue-ringed octopuses, and other marine animals. It blocks voltage-gated sodium channels in nerve cell membranes, leading to muscle paralysis and potentially respiratory failure. TTX has no known antidote, and medical treatment focuses on supportive care for symptoms. Exposure can occur through ingestion, inhalation, or skin absorption, depending on the route of toxicity.

Saxitoxin (STX) is a potent neurotoxin that inhibits the sodium channels in nerve cells, leading to paralysis and potentially death. It is produced by certain species of marine dinoflagellates and cyanobacteria, and can accumulate in shellfish that feed on these organisms. Saxitoxin poisoning, also known as paralytic shellfish poisoning (PSP), is a serious medical condition that can cause symptoms such as numbness, tingling, and paralysis of the mouth and extremities, as well as respiratory failure and death in severe cases. It is important to note that saxitoxin is not used as a therapeutic agent in medicine and is considered a harmful substance.

Sodium channels are specialized protein structures that are embedded in the membranes of excitable cells, such as nerve and muscle cells. They play a crucial role in the generation and transmission of electrical signals in these cells. Sodium channels are responsible for the rapid influx of sodium ions into the cell during the initial phase of an action potential, which is the electrical signal that travels along the membrane of a neuron or muscle fiber. This sudden influx of sodium ions causes the membrane potential to rapidly reverse, leading to the depolarization of the cell. After the action potential, the sodium channels close and become inactivated, preventing further entry of sodium ions and helping to restore the resting membrane potential.

Sodium channels are composed of a large alpha subunit and one or two smaller beta subunits. The alpha subunit forms the ion-conducting pore, while the beta subunits play a role in modulating the function and stability of the channel. Mutations in sodium channel genes have been associated with various inherited diseases, including certain forms of epilepsy, cardiac arrhythmias, and muscle disorders.

Sodium is an essential mineral and electrolyte that is necessary for human health. In a medical context, sodium is often discussed in terms of its concentration in the blood, as measured by serum sodium levels. The normal range for serum sodium is typically between 135 and 145 milliequivalents per liter (mEq/L).

Sodium plays a number of important roles in the body, including:

* Regulating fluid balance: Sodium helps to regulate the amount of water in and around your cells, which is important for maintaining normal blood pressure and preventing dehydration.
* Facilitating nerve impulse transmission: Sodium is involved in the generation and transmission of electrical signals in the nervous system, which is necessary for proper muscle function and coordination.
* Assisting with muscle contraction: Sodium helps to regulate muscle contractions by interacting with other minerals such as calcium and potassium.

Low sodium levels (hyponatremia) can cause symptoms such as confusion, seizures, and coma, while high sodium levels (hypernatremia) can lead to symptoms such as weakness, muscle cramps, and seizures. Both conditions require medical treatment to correct.

Penfluridol is an antipsychotic medication that belongs to the class of diphenylbutylpiperidines. It is primarily used in the management of chronic schizophrenia and other related psychotic disorders. Penfluridol works by blocking dopamine receptors in the brain, which helps reduce the symptoms of psychosis such as hallucinations, delusions, and disordered thought processes.

The medication is available in oral form and is typically administered once daily due to its long half-life. Common side effects of penfluridol include sedation, dizziness, orthostatic hypotension, weight gain, and extrapyramidal symptoms (EPS), such as Parkinsonism, akathisia, and dystonia. Penfluridol has also been associated with tardive dyskinesia, a potentially irreversible movement disorder, with long-term use.

It is essential to monitor patients on penfluridol therapy for metabolic changes, cardiac function, and the emergence of extrapyramidal symptoms or other side effects. The medication should be used cautiously in elderly patients, those with a history of cardiovascular disease, and individuals with preexisting movement disorders.

Penfluridol is not approved for use in the United States but is available in some other countries as a treatment option for chronic schizophrenia and related psychotic disorders.

Scorpion venoms are complex mixtures of neurotoxins, enzymes, and other bioactive molecules that are produced by the venom glands of scorpions. These venoms are primarily used for prey immobilization and defense. The neurotoxins found in scorpion venoms can cause a variety of symptoms in humans, including pain, swelling, numbness, and in severe cases, respiratory failure and death.

Scorpion venoms are being studied for their potential medical applications, such as in the development of new pain medications and insecticides. Additionally, some components of scorpion venom have been found to have antimicrobial properties and may be useful in the development of new antibiotics.

Aconitine is a toxic alkaloid compound that can be found in various plants of the Aconitum genus, also known as monkshood or wolf's bane. It is a highly poisonous substance that can cause serious medical symptoms, including numbness, tingling, and paralysis of the muscles, as well as potentially life-threatening cardiac arrhythmias and seizures. Aconitine works by binding to sodium channels in nerve cells, causing them to become overactive and leading to the release of large amounts of neurotransmitters.

In medical contexts, aconitine is not used as a therapeutic agent due to its high toxicity. However, it has been studied for its potential medicinal properties, such as its analgesic and anti-inflammatory effects. Despite these potential benefits, the risks associated with using aconitine as a medicine far outweigh any possible advantages, and it is not considered a viable treatment option.

NAV1.6, also known as SCN8A, is a gene that encodes for the α subunit of a voltage-gated sodium channel, specifically Nav1.6. This channel plays a crucial role in the initiation and propagation of action potentials in neurons. It has a predominant expression in the central and peripheral nervous system, including the nodes of Ranvier in myelinated axons.

Nav1.6 voltage-gated sodium channels are responsible for the rapid upstroke of the action potential and contribute to the generation of repetitive firing in some neuronal populations. Mutations in the SCN8A gene have been associated with various neurological disorders, such as epilepsy, intellectual disability, and movement disorders.

In summary, NAV1.6 voltage-gated sodium channels are essential for normal neuronal excitability and function, and their dysfunction can lead to a range of neurological symptoms.

Potassium is a essential mineral and an important electrolyte that is widely distributed in the human body. The majority of potassium in the body (approximately 98%) is found within cells, with the remaining 2% present in blood serum and other bodily fluids. Potassium plays a crucial role in various physiological processes, including:

1. Regulation of fluid balance and maintenance of normal blood pressure through its effects on vascular tone and sodium excretion.
2. Facilitation of nerve impulse transmission and muscle contraction by participating in the generation and propagation of action potentials.
3. Protein synthesis, enzyme activation, and glycogen metabolism.
4. Regulation of acid-base balance through its role in buffering systems.

The normal serum potassium concentration ranges from 3.5 to 5.0 mEq/L (milliequivalents per liter) or mmol/L (millimoles per liter). Potassium levels outside this range can have significant clinical consequences, with both hypokalemia (low potassium levels) and hyperkalemia (high potassium levels) potentially leading to serious complications such as cardiac arrhythmias, muscle weakness, and respiratory failure.

Potassium is primarily obtained through the diet, with rich sources including fruits (e.g., bananas, oranges, and apricots), vegetables (e.g., leafy greens, potatoes, and tomatoes), legumes, nuts, dairy products, and meat. In cases of deficiency or increased needs, potassium supplements may be recommended under the guidance of a healthcare professional.

Neurotoxins are substances that are poisonous or destructive to nerve cells (neurons) and the nervous system. They can cause damage by destroying neurons, disrupting communication between neurons, or interfering with the normal functioning of the nervous system. Neurotoxins can be produced naturally by certain organisms, such as bacteria, plants, and animals, or they can be synthetic compounds created in a laboratory. Examples of neurotoxins include botulinum toxin (found in botulism), tetrodotoxin (found in pufferfish), and heavy metals like lead and mercury. Neurotoxic effects can range from mild symptoms such as headaches, muscle weakness, and tremors, to more severe symptoms such as paralysis, seizures, and cognitive impairment. Long-term exposure to neurotoxins can lead to chronic neurological conditions and other health problems.

Ouabain is defined as a cardiac glycoside, a type of steroid, that is found in the seeds and roots of certain plants native to Africa. It is used in medicine as a digitalis-like agent to increase the force of heart contractions and slow the heart rate, particularly in the treatment of congestive heart failure and atrial fibrillation. Ouabain functions by inhibiting the sodium-potassium pump (Na+/K+-ATPase) in the cell membrane, leading to an increase in intracellular sodium and calcium ions, which ultimately enhances cardiac muscle contractility. It is also known as g-strophanthin or ouabaine.

Calcium is an essential mineral that is vital for various physiological processes in the human body. The medical definition of calcium is as follows:

Calcium (Ca2+) is a crucial cation and the most abundant mineral in the human body, with approximately 99% of it found in bones and teeth. It plays a vital role in maintaining structural integrity, nerve impulse transmission, muscle contraction, hormonal secretion, blood coagulation, and enzyme activation.

Calcium homeostasis is tightly regulated through the interplay of several hormones, including parathyroid hormone (PTH), calcitonin, and vitamin D. Dietary calcium intake, absorption, and excretion are also critical factors in maintaining optimal calcium levels in the body.

Hypocalcemia refers to low serum calcium levels, while hypercalcemia indicates high serum calcium levels. Both conditions can have detrimental effects on various organ systems and require medical intervention to correct.

The adrenal medulla is the inner part of the adrenal gland, which is located on top of the kidneys. It is responsible for producing and releasing hormones such as epinephrine (also known as adrenaline) and norepinephrine (also known as noradrenaline). These hormones play a crucial role in the body's "fight or flight" response, preparing the body for immediate action in response to stress.

Epinephrine increases heart rate, blood pressure, and respiratory rate, while also increasing blood flow to muscles and decreasing blood flow to the skin and digestive system. Norepinephrine has similar effects but is generally less potent than epinephrine. Together, these hormones help to prepare the body for physical activity and increase alertness and focus.

Disorders of the adrenal medulla can lead to a variety of symptoms, including high blood pressure, rapid heart rate, anxiety, and tremors. Some conditions that affect the adrenal medulla include pheochromocytoma, a tumor that causes excessive production of epinephrine and norepinephrine, and neuroblastoma, a cancerous tumor that arises from immature nerve cells in the adrenal gland.

I believe there may be some confusion in your question as "scorpions" are not a medical term, but instead refer to a type of arachnid. If you're asking about a medical condition that might involve scorpions, then perhaps you're referring to "scorpion stings."

Scorpion stings occur when a scorpion uses its venomous stinger to inject venom into another animal or human. The effects of a scorpion sting can vary greatly depending on the species of scorpion and the amount of venom injected, but generally, they can cause localized pain, swelling, and redness at the site of the sting. In more severe cases, symptoms such as numbness, difficulty breathing, muscle twitching, or convulsions may occur. Some species of scorpions have venom that can be life-threatening to humans, especially in children, the elderly, and those with compromised immune systems.

If you are looking for information on a specific medical condition or term, please provide more details so I can give you a more accurate answer.

Cardiac glycosides are a group of naturally occurring compounds that have a toxic effect on the heart. They are found in certain plants, including foxglove and lily of the valley, as well as in some toads and beetles. The most well-known cardiac glycoside is digoxin, which is derived from the foxglove plant and is used as a medication to treat heart failure and atrial arrhythmias.

Cardiac glycosides work by inhibiting the sodium-potassium pump in heart muscle cells, leading to an increase in intracellular calcium levels. This increases the force of heart contractions, which can be beneficial in treating heart failure. However, if the dose is too high, cardiac glycosides can also cause dangerous arrhythmias and even death.

It's important for healthcare professionals to carefully monitor patients taking cardiac glycosides, as the therapeutic and toxic doses are very close together. Additionally, certain medications and medical conditions can interact with cardiac glycosides and increase the risk of toxicity.

Catecholamines are a group of hormones and neurotransmitters that are derived from the amino acid tyrosine. The most well-known catecholamines are dopamine, norepinephrine (also known as noradrenaline), and epinephrine (also known as adrenaline). These hormones are produced by the adrenal glands and are released into the bloodstream in response to stress. They play important roles in the "fight or flight" response, increasing heart rate, blood pressure, and alertness. In addition to their role as hormones, catecholamines also function as neurotransmitters, transmitting signals in the nervous system. Disorders of catecholamine regulation can lead to a variety of medical conditions, including hypertension, mood disorders, and neurological disorders.

Neuromuscular depolarizing agents are a type of muscle relaxant used in anesthesia and critical care medicine. These drugs work by causing depolarization of the post-synaptic membrane at the neuromuscular junction, which is the site where nerve impulses are transmitted to muscles. This results in the binding of the drug to the receptor and the activation of ion channels, leading to muscle contraction.

The most commonly used depolarizing agent is suxamethonium (also known as succinylcholine), which has a rapid onset and short duration of action. It is often used during rapid sequence intubation, where there is a need for immediate muscle relaxation to facilitate endotracheal intubation.

However, the use of depolarizing agents can also lead to several side effects, including increased potassium levels in the blood (hyperkalemia), muscle fasciculations, and an increase in intracranial and intraocular pressure. Therefore, these drugs should be used with caution and only under the close supervision of a trained healthcare provider.

Sodium channel blockers are a class of medications that work by blocking sodium channels in the heart, which prevents the rapid influx of sodium ions into the cells during depolarization. This action slows down the rate of impulse generation and propagation in the heart, which in turn decreases the heart rate and prolongs the refractory period.

Sodium channel blockers are primarily used to treat cardiac arrhythmias, including atrial fibrillation, atrial flutter, and ventricular tachycardia. They may also be used to treat certain types of neuropathic pain. Examples of sodium channel blockers include Class I antiarrhythmics such as flecainide, propafenone, lidocaine, and mexiletine.

It's important to note that sodium channel blockers can have potential side effects, including proarrhythmia (i.e., the development of new arrhythmias or worsening of existing ones), negative inotropy (decreased contractility of the heart muscle), and cardiac conduction abnormalities. Therefore, these medications should be used with caution and under the close supervision of a healthcare provider.

Tromethamine is a chemical compound with the formula (CH2OH)3CNH2. It is also known as tris(hydroxymethyl)aminomethane or THAM. Tromethamine is a tertiary amine that acts as a buffer, maintaining a stable pH in various solutions.

In medical terms, tromethamine is used as a medication to correct acid-base imbalances in the body. It works by binding hydrogen ions and converting them into water and carbon dioxide, which can then be eliminated from the body. Tromethamine is often used in critically ill patients who have severe metabolic acidosis, a condition characterized by an excess of acid in the body that can lead to organ dysfunction and failure.

Tromethamine is available as a sterile solution for injection or as a powder to be reconstituted with sterile water for injection. It may also be used as an additive to intravenous fluids to help maintain a stable pH. Common side effects of tromethamine include local irritation at the injection site, nausea, vomiting, and headache.

Ion channels are specialized transmembrane proteins that form hydrophilic pores or gaps in the lipid bilayer of cell membranes. They regulate the movement of ions (such as sodium, potassium, calcium, and chloride) across the cell membrane by allowing these charged particles to pass through selectively in response to various stimuli, including voltage changes, ligand binding, mechanical stress, or temperature changes. This ion movement is essential for many physiological processes, including electrical signaling, neurotransmission, muscle contraction, and maintenance of resting membrane potential. Ion channels can be categorized based on their activation mechanisms, ion selectivity, and structural features. Dysfunction of ion channels can lead to various diseases, making them important targets for drug development.

Chromaffin cells are specialized neuroendocrine cells that are responsible for the synthesis and release of catecholamines, which are hormones such as adrenaline (epinephrine) and noradrenaline (norepinephrine). These cells are located in the medulla of the adrenal gland and in some autonomic ganglia outside the central nervous system. Chromaffin cells contain secretory granules that stain brown with chromium salts, hence their name. They play a crucial role in the body's response to stress by releasing catecholamines into the bloodstream, which helps prepare the body for the "fight or flight" response.

Membrane potential is the electrical potential difference across a cell membrane, typically for excitable cells such as nerve and muscle cells. It is the difference in electric charge between the inside and outside of a cell, created by the selective permeability of the cell membrane to different ions. The resting membrane potential of a typical animal cell is around -70 mV, with the interior being negative relative to the exterior. This potential is generated and maintained by the active transport of ions across the membrane, primarily through the action of the sodium-potassium pump. Membrane potentials play a crucial role in many physiological processes, including the transmission of nerve impulses and the contraction of muscle cells.

The structure of veratridine has been confirmed by NMR spectroscopy and X-ray crystallography. Veratridine displays an unusual ... Veratridine increases nerve excitability and intracellular Ca2+ concentrations. Veratridine has been isolated from the seeds of ... HPLC purification of veratrine is a preferred method for isolation of veratridine for biological studies. Veratridine is a ... Veratridine has not been reported to have any effect on the acrosome reaction on its own, but it is able to block the ...
They include veratridine, cyclopamine, and jervine. Because of their actions on the cardiovascular, neuromuscular, and ...
Veratrum Veratridine Keeler R F (1971). "Teratogenic compounds of Veratrum californicum (Durand). 13. Structure of muldamine". ...
Veratridine, a related alkaloid Harborne, J. B.; Baxter, H.; Moss, G. P. (1999). Phytochemical Dictionary: A Handbook of ...
It is highly toxic, containing veratridine, cevadine, and other alkaloids. Its seeds were used by pharmacists around the world ... Hare, J. Daniel (1996). "Purification and Quantitative Analysis of Veratridine and Cevadine by HPLC". Journal of Agricultural ...
Site 2 binds lipid-soluble sodium channel activators such as veratridine. Site 3 binds alpha-scorpion and sea anemone toxins, ...
Other toxins that bind to this region include the alkaloids veratridine, batrachotoxin and aconitine. Experiments utilizing ...
"Synergism between toxin-gamma from Brazilian scorpion Tityus serrulatus and veratridine in chromaffin cells". The American ...
... veratridine, and veriloid. Some of the principal toxins have a modified steroid template while others differ in their ... "Insecticidal activity of various 3-acyl and other derivatives of veracevine relative to the veratrum alkaloids veratridine and ... The Action of Protoveratrine and Veratridine in Hypertension". Circulation. 1 (2): 204-213. doi:10.1161/01.CIR.1.2.204. ISSN ...
Veratridine and veratrine Tropane alkaloids such as atropine hormones and neurotransmitters epinephrine (adrenaline) and ...
... plants contain highly toxic steroidal alkaloids (e.g. veratridine) that activate sodium ion channels and cause rapid ...
... veratridine, and grayanotoxin). This binding results in a sodium-ion channel that stays open longer. Aconitine suppresses the ...
Veratridine, aconitine and grayanotoxin-like batrachotoxin-are lipid-soluble poisons which similarly alter the ion selectivity ...
... veratridine MeSH D03.383.066.150 - caprolactam MeSH D03.383.066.200 - dilazep MeSH D03.383.066.400 - meptazinol MeSH D03.383. ... veratridine MeSH D03.549.439.131 - bromocriptine MeSH D03.549.439.262 - ergonovine MeSH D03.549.439.262.538 - methylergonovine ...
Examples include toxins, such as aconitine, veratridine, batrachotoxin, robustoxin, palytoxin and ciguatoxins and insecticides ...
... triflumezopyrim triflumuron trimethacarb triprene triptolide tyclopyrazoflor umifoxolaner valerate vaniliprole veratridine ...
... the rice was found to be inoculated with veratridine, a steroid-derived alkaloid. Despite its nutritional and remedial values, ...
... veratridine The following toxins modify the gating of sodium channels: Peptide-based toxins μ-Conotoxin δ-Atracotoxin Scorpion ...
... veratridine site of voltage-gated sodium channels (IC50 = 1,260 nM), serotonin transporter (Ki = 528 nM), norepinephrine ...
The structure of veratridine has been confirmed by NMR spectroscopy and X-ray crystallography. Veratridine displays an unusual ... Veratridine increases nerve excitability and intracellular Ca2+ concentrations. Veratridine has been isolated from the seeds of ... HPLC purification of veratrine is a preferred method for isolation of veratridine for biological studies. Veratridine is a ... Veratridine has not been reported to have any effect on the acrosome reaction on its own, but it is able to block the ...
VERATRIDINE (CHA). Dipropyl−6,7−ADTN HBr (DOPA). 6986473 (unk). Bromocriptine mesylate (DOPA). R(−)−2,10,11−Trihydroxyap (DOPA) ...
en veratridine Neurofarmacologia. Definition. Alcaloide neurotòxic que fixa els canals de Na+ en posició oberta i provoca una ...
Veratridine Voltage-gated Na+ channel opener. 7569. Verdinexor Selective exportin-1 (XPO1/CRM1) inhibitor. ...
1993) in cortical neurons exposed to depolarizing conditions such as veratridine or kainate. ...
Veratridine, angiotensin receptors and aldosteronogensis in bovine adrenal glomerulosa cells. Clin Exp Hypertens 8: 323-345. ...
Srinivasan, J.; Richens, A.; Davies, J.A. Effects of felbamate on veratridine-and K+-stimulated release of glutamate from mouse ...
Veratridine-induced LDH release can be inhibited by 100 microM riluzole (-90% and by tetrodotoxin (1 microM). Riluzole markedly ... The neuroprotective activity of riluzole has been studied on N-methyl-D-aspartate (NMDA)- or veratridine-induced toxicity in ... Neuroprotective effects of riluzole on N-methyl-D-aspartate or veratridine-induced neurotoxicity in rat hippocampal slices ...
The two most important compounds are the lipophilic alkaloids veratridine and cevadine, with veratridine having greater ... Veratridine prolongs the open state of sodium channels by increasing the probability of channel opening, and then delaying ... When applied to nerve, veratridine causes an increase in the duration of the action potential, repetitive firing, and a ... Depolarization of neurons by veratridine requires the presence of extracellular sodium ions and can stimulate the release of ...
Calcium-Dependent Blockade of Cardiac Cyclic AMP Accumulation by Batrachotoxin and Veratridine JOAN HELLER BROWN ...
The interaction between the activator agents batrachotoxin and veratridine and the gating processes of neuronal sodium channels ...
J. Gleitz, N. Gottner, A. Ameri, and T. Peters, "Kavain inhibits non-stereospecifically veratridine-activated Na+ channels," ...
"Veratrine is a mixture of cevadine, veratridine, cevadilline, and cevine. …These compounds are quite toxic and, thus, can be ...
... such as veratridine, which can alter the pharmacological sensitivity of the assay. Binding assays typically use radiolabeled ...
... toxicity response in neuro-2a cells consisting of the recovery of the cell viability in the presence of ouabain and veratridine ... toxicity response in neuro-2a cells consisting of the recovery of the cell viability in the presence of ouabain and veratridine ...
CTX were assessed by exposing cells to increasing toxin concentrations in presence of the sodium channel activator veratridine ...
Vagal afferent mediated reflex effects of veratridine on contractility in the conscious dog. Barron, K. & Bishop, V. S., 1 Jan ...
Veratridine. ... is a derivative, the 3-veratroate ester, of veracevine, which belongs to the class of C-nor-D-homosteroidal ... 2-Aminoalcohols are an important class of organic ... Veratridine and veratrine Tropane alkaloids such as atropine hormones and ... "Insecticidal activity of various 3-acyl and other derivatives of veracevine relative to the veratrum alkaloids veratridine and ...
Verb definition: A phrase or other construction used as a verb.
Informatics overfancifully chase the nonfigurative regularizer astride an kr; unrepining veratridine throw allow her lustrously ...
The j point is that of veratridine. Provides a developmental approach to medical toxicology high electronegativity, such as ...
Medical terminology that starts with [V] - Medical Dictionary online-medical-dictionary.org
Intrathecal veratridine administration increases minimum alveolar concentration in rats.. Anesth Analg. 107(3):875-8.*PubMed ...
INaL was identified as steady-state current blocked by 10 μM RAN (IRAN) or 0.5 μM tetrodotoxin (TTX) (ITTX). Veratridine (VERA ... INaL was identified as steady-state current blocked by 10 μM RAN (IRAN) or 0.5 μM tetrodotoxin (TTX) (ITTX). Veratridine (VERA ...
zyrtec alercina alerlisin sin receta en farmacias Tyrosamine whenever unsurnamed veratridine - antisensis owing to seventy- ... veratridine acanthoid unlike a zyrtec alercina alerlisin sin receta en farmacias oculist. Amalgamated creping an quadrat sin ...
... where this claim stealing my veratridine. Boniest veratridine, the amphichroic barley-sugar, writhe merchantable choirmaster ... where this www.swanmedical.es claim stealing my veratridine. ...
This graph shows the total number of publications written about "Cevanes" by people in Harvard Catalyst Profiles by year, and whether "Cevanes" was a major or minor topic of these publication ...
Chemical Treatments for Insect Cell Differentiation: The Effects of 20-Hydroxyecdysone and Veratridine on Cultured Spodoptera ... Chemical Treatments for Insect Cell Differentiation: The Effects of 20-Hydroxyecdysone and Veratridine on Cultured Spodoptera ...
RESULTS: Our V. parviflorum samples contained verazine, veratramine, veratridine, and cyclopamine. DISCUSSION: Steroidal ...
Filters: Keyword is Veratridine and Author is Duch, D S [Clear All Filters] ...
  • The interaction between the activator agents batrachotoxin and veratridine and the gating processes of neuronal sodium channels. (aspetjournals.org)
  • Access to toxins and modified forms thereof (including saxitoxin, gonyautoxin, batrachotoxin, and veratridine) through de novo synthesis drives studies to elucidate toxin-receptor interactions and to develop new pharmacologic tools to study ion channel function in primary cells and murine pain models. (stanford.edu)
  • A comparison of the effects of veratridine on tetrodotoxin-sensitive and tetrodotoxin-resistant sodium channels in isolated rat dorsal root ganglion neurons. (guidetomalariapharmacology.org)
  • 2010. Bidirectional modulation of isoflurane potency by intrathecal tetrodotoxin and veratridine in rats. . (cornell.edu)
  • To exemplify potential studies on ion channels, we characterized voltage-gated sodium channels and their inhibition by tetrodotoxin, saxitoxin and lidocaine, as well as their opening by the plant alkaloid veratridine and the food-relevant marine biotoxin ciguatoxin. (uni-konstanz.de)
  • Intrathecal veratridine administration increases minimum alveolar concentration in rats. (cornell.edu)
  • Veratridine is a steroidal alkaloid found in plants of the lily family, specifically the genera Veratrum and Schoenocaulon. (wikipedia.org)
  • Four extracts of F. paulensis exhibited a novel toxicity response in neuro-2a cells consisting of the recovery of the cell viability in the presence of ouabain and veratridine. (lu.se)
  • Application of phenytoin or veratridine indicated a critical role for the persistent sodium current in maintaining depolarization block. (ox.ac.uk)
  • Veratridine increases nerve excitability and intracellular Ca2+ concentrations. (wikipedia.org)
  • This, and later purification procedures, begin with veratrine, a mixture of the alkaloids present in the Veratrum plants, primarily containing cevadine and veratridine. (wikipedia.org)
  • as commercially available veratridine may vary in purity, HPLC purification of veratrine is a preferred method for isolation of veratridine for biological studies. (wikipedia.org)
  • Moreover, veratridine has the effect of turning the membrane potential to a more positive one and also modifies the effect of progesterone on [Ca2+]i and sperm membrane potential. (wikipedia.org)
  • The dried residue is dissolved in sulfuric acid and the sulfate salt of veratridine is precipitated by dropwise addition of a solution of ammonium sulfate. (wikipedia.org)
  • Vinpocetine, in a pharmacologically relevant concentration range (0.4-10 microM)i reduced the increase of [Na+]i induced by veratridine (100 microM). (globinmed.com)
  • Elevation of extracellular KCl concentration (to 15-30 mM) or veratridine (10-20 microm) stimulated Ca2+ -dependent CCK8s release. (silverchair.com)
  • Basal, elevated KCl- or veratridine-evoked CCK8s release was not affected significantly by propofol (12.5-50 microm), pentobarbital (50 and 100 microm), thiopental (20 microm), etomidate (20 microm), ketamine (20 microm), isoflurane (0.6-0.8 mM), or halothane (0.6-0.8 mMm). (silverchair.com)
  • The seeds contain veratridine and cevadine which are considered toxins. (worldatlas.com)
  • Veratridine has been isolated from the seeds of Schoenocaulon officinale and from the rhizomes of Veratrum album. (wikipedia.org)
  • Veratridine, and other Veratrum alkaloids, have the five-membered ring between the second and third six-membered rings. (wikipedia.org)
  • Veratrum nigrum kan de eerste jaren wat problemen hebben met aanslaan en het duurt vaak een jaar of zeven voordat Veratrum nigrum gaat bloeien. (google.com)
  • Veratrum species contain highly toxic steroidal alkaloids (e.g. veratridine) that activate sodium ion channels and cause rapid cardiac failure and death if ingested. (google.com)
  • Veratridine displays an unusual steroidal backbone. (wikipedia.org)
  • Veratridine inhibits sodium channel inactivation by shifting the activation threshold toward a more negative potential. (wikipedia.org)
  • 6. Veratridine modifies the gating of human voltage-gated sodium channel Nav1.7. (nih.gov)
  • Previous in vitro studies reported that exposure to the Na(v) toxins veratridine and α scorpion toxin cause persistent downregulation of Na(v) mRNA in vitro. (nih.gov)
  • The neuroprotective drug vinpocetine prevents veratridine-induced [Na+]i and [Ca2+]i rise in synaptosomes. (globinmed.com)
  • Basal, elevated KCl depolarization-evoked and veratridine-evoked release of CCK8s from synaptosomes purified from rat cerebral cortex was evaluated at 35 degrees C in the absence or presence of extracellular Ca2+. (silverchair.com)
  • The effect of the neuroprotective drug, vinpocetine on the veratridine-evoked [Na+]i and [Ca2+]i rise in isolated nerve terminals was studied. (globinmed.com)
  • Veratridine acts a neurotoxin by increasing nerve excitability. (wikipedia.org)
  • Clinically relevant concentrations of several classes of general anesthetics did not affect basal, KCl-evoked, or veratridine-evoked CCK8s release from isolated rat cortical nerve terminals. (silverchair.com)
  • Veratridine has not been reported to have any effect on the acrosome reaction on its own, but it is able to block the progesterone-induced acrosome reaction. (wikipedia.org)
  • Moreover, veratridine has the effect of turning the membrane potential to a more positive one and also modifies the effect of progesterone on [Ca2+]i and sperm membrane potential. (wikipedia.org)
  • The stimulatory effect on CRF-41 release induced by veratridine (10(-6) M) was inhibited by approximately 50% in the presence of morphine. (nih.gov)
  • Accounts of these efforts date back to 1878, but the first true purification of veratridine is the one carried out in 1953 by Kupchan et al. (wikipedia.org)

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