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PubMed1980

Migraine headache: signs and symptoms, biochemistry, and current therapy.

The classification, biochemistry, precipitating factors, differential diagnosis, treatment of acute attacks, and prophylactic therapy of migraine headaches are reviewed. The biochemistry of both classic (prodromal symptoms) and common (no prodromal symptoms) migraines is poorly understood, but appears to involve serotonin. Although their clinical importance is not clear, common precipitating factors include coffee, tea, and cola beverages; chocolate, cheese, and alcohol; light stimulation, stress, fasting, lack of sleep, and fever; and reduced estrogen levels. The symptomatic treatment of acute attacks with ergot preparations, isometheptene, flufenamic acid, analgesics and sedatives is reviewed. Prophylactic therapy with methysergide maleate, tricyclic compounds, monoamine oxidase inhibitors, propranolol, and 5-hydroxytryptophan is also discussed.

Acute Disease↗
PubMed1980

Influence of non-steroidal anti-inflammatory compounds on the hepatic tryptophan pyrrolase activity in hypo- and hyperthyroid rats.

Hypothyroid state induced in the rat by thyroparathyroidectomy does not modify the activity of hepatic tryptophan pyrrolase (TPO) while hyperthyroidism, obtained after daily injection of 3, 3', 5-triiodo-L-thyronine, inhibits significantly the liver TPO activity. Treatment with oxametacine, indomethacin, phenylbutazone, flufenamic acid and acetylsalicylic acid, increases the activity of hepatic TPO in hypothyroid state, whereas, in hyperthyroid rats, the same drugs are able to restore the normal enzymatic activity, except for acetylsalicylic acid. During the development of an acute inflammatory process, provoked by carrageenan injection, the treatment with non-steroidal anti-inflammatory agents induces an enhancement of hepatic TPO activity. On the contrary, such enzymatic activity appears unaffected in chronic inflammation induced by cotton-pellet implantation.

Animals↗
PubMed1993

Effect of some steroidal & non-steroidal anti-inflammatory drugs on purified goat brain cathepsin L.

The lysosomal cysteine proteinases have been found to be involved in various inflammatory conditions. Inhibitory effects of certain commonly used anti-inflammatory drugs were observed on lysosomal thiol proteinase cathepsin L. Of the non-steroidal anti-inflammatory drugs tested, phenylbutazone was found to be most potent inhibitor of cathepsin L activity. The half maximal inhibition was achieved at 0.6 mM concentration. The inhibition by phenylbutazone was of non-competitive type, with a ki of 1.3 x 10(-3) M. Flufenamic acid and indomethacin were also inhibitory to cathepsin L activity, giving half maximal inhibitions at 3.5 mM and 4.5 mM concentrations respectively. In contrast, cathepsin L activity was not affected at all by steroidal anti-inflammatory agents. Aspirin was also found to have no effect on cathepsin L activity whereas salicylic acid, its m- and p-analogs exhibited inhibitory effects but to a lesser degree.

Animals↗
PubMed1989

Drug competition for thyroxine binding to transthyretin (prealbumin): comparison with effects on thyroxine-binding globulin.

We examined the effect of 26 drugs on T4 binding to transthyretin (TTR; prealbumin) and T4-binding globulin (TBG) by determining their ability to inhibit [125I]T4 binding to TTR isolated from normal human plasma and to serum diluted 1:10,000, respectively. The hierarchies for drug inhibition of T4 binding differed greatly for these two proteins. Relative to T4, the drugs were much more potent inhibitors of [125I]T4 binding to TTR than to TBG. Compounds of the anthranilic acid class, such as flufenamic, meclofenamic, and mefenamic acids, interacted particularly strongly with TTR. Flufenamic acid was more potent than T4 itself in inhibiting [125I]T4 binding [175 +/- 17% (+/- SD); cf. T4; n = 3; P less than 0.001], while mefenamic acid, diflunisal, and meclofenamic acid were 20-26% as potent as T4 in their interaction with TTR. The reactivity of diclofenac, fenclofenac, indomethacin, sulindac, and the diuretic ethacrynic acid was 0.8-2.1% relative to that of T4. In contrast, furosemide, the drug most highly reactive with TBG, was only 0.11 +/- 0.03% (n = 7) as potent as T4, followed by meclofenamic acid greater than mefenamic acid greater than fenclofenac greater than flufenamic acid greater than diflunisal greater than milrinone. Aspirin and sodium salicylate were, respectively, 0.05% and 0.20% as active as unlabeled T4 as inhibitors of [125I]T4 binding to TTR, but these compounds had only 3-4 x 10(-6)% of the activity of T4 for TBG binding. Diphenylhydantoin had no detectable effect on T4 binding to TTR and was 2.9 x 10(-4)% as reactive as T4 with TBG. Amiodarone did not interact with either binding site. Drug interactions with TTR may be important when this protein becomes a major circulating T4-binding protein, as in patients with complete or partial TBG deficiency, or when serum T4 is markedly elevated. Such interactions may also be important where TTR is the dominant tissue T4-binding protein, as in the choroid plexus. In addition, the drug competitors described here may be useful as probes to further define the structural basis for specific ligand interactions with different classes of T4-binding sites.

Binding Sites↗
PubMed1998

Determination of flufenamic, meclofenamic and mefenamic acids by capillary electrophoresis using beta-cyclodextrin.

The possibility of separating flufenamic, meclofenamic and mefenamic acids by capillary electrophoresis was studied. The best approach involved combining a suitable pH of the carrier electrolyte (pH 12.0) with the host-guest complexation effects of beta-cyclodextrin. A running buffer consisting of 30 mM phosphate buffer (pH 12.0), 2 mM beta-CD and 10% (v/v) acetonitrile was found to provide a very efficient and stable electrophoresis system for the analysis of fenamic acids by capillary zone electrophoresis. Responses were linear from 0.4 to 40 microg/ml for the three drugs with detection limits of about 0.3 ng/ml. Intra- and inter-day precision values of about 1-2% R.S.D. (n = 11) and 3-4% R.S.D. (n = 30), respectively, were obtained. The method is highly robust and no breakdowns of the current or capillary blockings were observed for several weeks. The general applicability of this rapid CZE procedure (migration times less than 12 min) is demonstrated for several practical samples, including serum, urine and pharmaceuticals.

Anti-Inflammatory Agents, Non-Steroidal↗
PubMed1995

Comparison of the effects of fenamates on Ca-activated chloride and potassium currents in rabbit portal vein smooth muscle cells.

1. The perforated patch and conventional whole-cell recording techniques were used to study the action of flufenamic, mefenamic and niflumic acid on calcium-activated chloride and potassium currents in rabbit portal vein smooth muscle cells. 2. In K-conditions at a holding potential of -77 mV flufenamic acid and mefenamic acid decreased the amplitude of spontaneous transient inward currents (STICs, calcium-activated chloride currents, ICl(Ca)) in a concentration-dependent manner. The potency sequence was niflumic > flufenamic > mefenamic acid. 3. At -77 mV 1 x 10(-5) M flufenamic acid increased the STIC exponential decay time constant (tau). At higher concentrations the STIC decay was described by 2 exponentials with an initial decay (tau f) faster than the control tau value and a second exponential (tau s) which had a time constant slower than the control tau value. Low concentrations of mefenamic acid had no effect or decreased the tau value whereas in higher concentrations biphasic currents were recorded. 4. In K-free conditions the inhibitory effect of both flufenamic and mefenamic acid on STIC amplitude was greater at +50 mV compared to -50 mV, showing that the effect of these agents was voltage-dependent. 5. In cells held at 0 mV in K-containing conditions the fenamates reduced both the frequency and amplitude of spontaneous transient outward currents (STOCs, calcium-activated potassium currents, IK(Ca)). The concentration range to produce these effects was higher than that to decrease STIC amplitude and the potency sequence was flufenamic > niflumic > or = mefenamic acid. 6. All these compounds in concentrations greater than 5 x 10(-5) M evoked a 'noisy' potassium current at 0 mV which reached a maximum after approximately 3 min. This current was readily reversible on washout of the drug and could be elicited several times in the same cell. The current-voltage relationship of the fenamate-evoked current exhibited pronounced outward rectification characteristic of IK(Ca). 7. The current evoked by 2 x 10(-4) M flufenamic acid and 5 x 10(-4) M niflumic acid was not affected by 1 x 10(-5) M glibenclamide but was markedly inhibited by 1 x 10(-3) M tetraethylammonium. Furthermore, large currents were activated by flufenamic and niflumic acid in the presence of caffeine and cyclopiazonic acid (an inhibitor of the sarcoplasmic reticulum Ca-ATPase) to deplete intracellular Ca-stores. 8. Conventional whole-cell recording was performed with pipette solutions in which the ability to buffer changes in intracellular calcium was varied by altering the concentration of the calcium chelator (2-aminophenoxy)-ethane-N,N,N',N'-tetraacetic acid (BAPTA). Flufenamic acid (2 x 10(-4) M) and niflumic acid (5 x 10(-4) M) both evoked large outward currents when recordings were made with either 1 x 10(-4) M or 1 x 10(-2) M BAPTA. Furthermore, bathing the cells in nominally calcium-free extracellular solution did not reduce the amplitude of the evoked currents. 9. It is concluded that both flufenamic and mefenamic acid inhibit ICl(Ca) by a mechanism similar to niflumic acid, possibly open channel blockade. Furthermore, at concentrations greater than 5 x 10(-5) M all three fenamates inhibited STOC activity and evoked directly an outward current which resembled IK(Ca).

Animals↗
PubMed2006

A "sample-and-hold" pulse-counting integrator as a mechanism for graded memory underlying sensorimotor adaptation.

The mechanisms behind the induction of cellular correlates of memory by sensory input and their contribution to meaningful behavioral changes are largely unknown. We previously reported a graded memory in the form of sensorimotor adaptation in the electromotor output of electric fish. Here we show that the mechanism for this adaptation is a synaptically induced long-lasting shift in intrinsic neuronal excitability. This mechanism rapidly integrates hundreds of spikes in a second, or gradually integrates the same number of spikes delivered over tens of minutes. Thus, this mechanism appears immune to frequency-dependent fluctuations in input and operates as a simple pulse counter over a wide range of time scales, enabling it to transduce graded sensory information into a graded memory and a corresponding change in the behavioral output. This adaptation is based on an NMDA receptor-mediated change in intrinsic excitability of the postsynaptic neurons involving the Ca2+-dependent activation of TRP channels.

Acclimatization↗
PubMed2003

Comprehensive study of the luminescent properties and lifetimes of Eu(3+) and Tb(3+) chelated with various ligands in aqueous solutions: influence of the synergic agent, the surfactant and the energy level of the ligand triplet.

The formation and the properties of luminescent complexes of europium and terbium with a variety of organic ligands have been investigated in aqueous solutions. The ligands used include model compounds such as thenoyltrifluoroacetone and pyridine-2,6-dicarboxylic acid and organic analytes of biological or pharmaceutical interest. It is shown that the formation and the luminescent properties of these complexes depend at first on several parameters including the pH and the buffer, the synergic agent and the surfactant. In neutral solutions, trioctylphosphine oxide in the presence of Triton X-100 may act as a co-ligand to promote complex formation and protect the complex from radiationless deactivation processes. Working in slightly alkaline solutions in the presence of EDTA and hexadecyltrimethylammonium chloride may induce the deprotonation of a second coordinating group and favour the formation of a new complex with stronger luminescent properties. In both cases, the luminescence lifetimes are then ultimately related to the energy gap between the ligand triplet and the resonance level of the ion and to the number of water molecules coordinated to the lanthanide ion.

Chelating Agents↗
PubMed2000

A cellular mechanism for the transformation of a sensory input into a motor command.

The initiation and control of locomotion largely depend on processing of sensory inputs. The cellular bases of locomotion have been extensively studied in lampreys where reticulospinal (RS) neurons constitute the main descending system activating and controlling the spinal locomotor networks. Ca(2+) imaging and intracellular recordings were used to study the pattern of activation of RS neurons in response to cutaneous stimulation. Pressure applied to the skin evoked a linear input/output relationship in RS neurons until a threshold level, at which a depolarizing plateau was induced, the occurrence of which was associated with the onset of swimming activity in a semi-intact preparation. The occurrence of a depolarizing plateau was abolished by blocking the NMDA receptors that are located on RS cells. Moreover, the depolarizing plateaus were accompanied by a rise in [Ca(2+)](i), and an intracellular injection of the Ca(2+) chelator BAPTA into single RS cells abolished the plateaus, suggesting that the latter are Ca(2+) dependent and rely on intrinsic properties of RS cells. The plateaus were shown to result from the activation of a Ca(2+)-activated nonselective cation current that maintains the cell in a depolarized state. It is concluded that this intrinsic property of the RS neuron is then responsible for the transformation of an incoming sensory signal into a motor command that is then forwarded to the spinal locomotor networks.

Action Potentials↗
PubMed2003

Fulfenamic acid sensitive, Ca(2+)-dependent inward current induced by nicotinic acetylcholine receptors in dopamine neurons.

Nicotinic acetylcholine receptors (nAChRs) exhibit high Ca(2+) permeabilities and the Ca(2+)-influx through the nAChRs may be involved in regulation of a variety of signal processing in the postsynaptic neurons. The mesencephalic dopamine (DA) neurons receive cholinergic inputs from the brainstem and express abundant nAChRs. Here we report that the Ca(2+)-influx induced by a transient pressure application of ACh activates an inward current mediated by nAChRs and subsequently an inward current component that is sensitive to fulfenamic acid (FFA) and phenytoin, presumably a Ca(2+)-activated nonselective cation current in the DA neurons in the midbrain slices of the rat. The FFA- and phenytoin-sensitive current exhibits a negative slope conductance below -40 mV, suggesting its role in significant enhancement of depolarizing responses. In the current clamp recordings with perforated patch clamp configuration, bath application of carbachol markedly enhanced the glutamate-induced depolarization, which led to a long-lasting depolarizing hump. Activation of nAChRs is involved in this process, in cooperation with muscarinic receptors that suppress afterhyperpolarization caused by Ca(2+)-activated K(+)-channels. The long-lasting depolarizing hump was suppressed by FFA. All these results suggested a potential role of the FFA-sensitive current triggered by nAChR activation in marked enhancement of the excitatory synaptic response in DA neurons.

Acetates↗