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A Araque

Publications and source records attributed to A Araque.

At least 37 records · Page 2Linked to original sources
PubMed1995

Selective block of Ca(2+)-dependent K+ current in crayfish neuromuscular system and chromaffin cells by sea anemone Bunodosoma cangicum venom.

The effects of the nematocyst venom of the sea anemone Bunodosoma cangicum on depolarization-activated currents were studies in opener crayfish muscle fibers and in cultured bovine chromaffin cells. The venom selectively and reversibly blocked the Ca(2+)-dependent K+ current (IK(Ca)) present in crayfish muscle in a dose-dependent manner without affecting voltage-gated Ca2+ or K+ currents. Furthermore, the venom also reduced IK(Ca) in chromaffin cells, without modifying voltage-gated Na+, Ca2+, or K+ currents. Synaptic transmission in crayfish muscle was also affected by the venom. Repetitive excitatory and inhibitory postsynaptic currents (each associated with a presynaptic action potential) were evoked by each nerve stimulus, suggesting that presynaptic IK(Ca) may control the electrical activity of excitatory and inhibitory presynaptic fibers. We conclude that B. cangicum venom includes a toxin that selectively and reversibly blocks Ca(2+)-dependent K+ currents in crayfish muscle and in bovine chromaffin cells, and modifies excitatory and inhibitory synaptic transmission, probably abolishing a similar conductance at the presynaptic fibers.

Animals↗
PubMed1995

Fast, persistent, Ca(2+)-dependent K+ current controls graded electrical activity in crayfish muscle.

The early outward current in opener muscle fibres of crayfish (Procambarus clarkii) was studied using the two-electrode voltage-clamp technique. This current was abolished in Ca(2+)-free and 5 mM Cd2+ solutions, and was blocked by extra- or intracellular tetraethylammonium, indicating that it was a Ca(2+)-dependent K+ current [IK(Ca)]. IK(Ca) was voltage dependent, apamin insensitive and sensitive to charybdotoxin (CTX), which, in addition to its tetraethylammonium sensitivity, suggests that the channels mediating IK(Ca) behave in a BK type manner. IK(Ca) activation was extremely fast, reaching a maximum within 5 ms, and the inactivation was incomplete, stabilizing at a persistent steady-state. IK(Ca) was insensitive to intracellular ethylenebis(oxonitrilo)tetraacetate (EGTA), but was abolished by injection of the faster Ca2+ chelator 1,2-bis(2-aminophenoxy)ethane-N,N,N',N'-tetraacetic acid (BAPTA), suggesting that voltage-dependent Ca2+ channels and those mediating IK(Ca) should be clustered closely on the membrane. Under two-electrode current-clamp recording mode, low amplitude, graded responses were evoked under control conditions, whereas repetitive all-or-none spikes were elicited by application of CTX or after loading the cells with BAPTA. We conclude that IK(Ca) activates extremely quickly, is persistent and is responsible for the generation and control of the low amplitude, graded, active responses of opener muscle fibres.

Animals↗
PubMed1995

Evolution of immunoglobulin A nephropathy into Henoch-Schönlein purpura in an adult patient.

We report the first case of the evolution of immunoglobulin A (IgA) nephropathy into Henoch-Schönlein purpura in an adult patient. A 28-year-old man presented with an episode of gross hematuria and acute renal failure. The serum IgA level was increased and renal biopsy findings were diagnostic of IgA nephropathy. In addition, many renal tubuli were filled by red blood cell casts and presented a marked tubular necrosis. Coincidental with the disappearance of gross hematuria, renal function progressively improved. The patient continued to have microhematuria, normal renal function, and isolated bouts of macroscopic hematuria. Ten years later, the patient developed arthralgias, a purpuric rash in the legs, gross hematuria, and an elevated serum creatinine level. A skin biopsy showed leukocytoclastic vasculitis with IgA deposits. The renal biopsy showed histologic lesions very similar to those observed in the first biopsy 10 years before: mesangial proliferation with mesangial deposition of IgA and tubular necrosis with obstruction of renal tubuli by red blood cell casts. The serum creatinine level returned to normal. Recurrent episodes of purpura associated with macroscopic hematuria persisted during the follow-up, but without worsening of renal function. An interesting feature of our patient was the development of reversible renal failure associated with macroscopic hematuria on two different occasions. Although this complication has been described in IgA nephropathy, it has been rarely reported in Henoch-Schönlein purpura. It is possible that IgA nephropathy and Henoch-Schönlein purpura are different clinical manifestations of the same disease and probably share a common pathogenesis. Our case is a demonstrative example of this hypothesis.

Acute Kidney Injury↗
PubMed1995

Idiopathic dialysis ascites in the nineties: resolution after renal transplantation.

The incidence of idiopathic dialysis ascites seems to have decreased since the introduction of more effective techniques for control of fluid overload and uremia in chronic hemodialysis patients. Most of the patients reported so far had some predisposing factor, such as malnutrition or sustained fluid overload. We report a case of idiopathic dialysis ascites in a young well-nourished woman with an excellent control of fluid overload and in whom biocompatible dialyzer membranes and volumetric controlled ultrafiltration had been used since her onset of chronic dialysis. Extensive studies excluded the existence of an underlying cause for ascites. Ascitic fluid had the characteristics of an exudate, and a peritoneal biopsy specimen showed chronic nonspecific inflammatory changes. Massive ascites persisted for 6 months, requiring repeated paracentesis, until the performance of a successful renal transplantation. Coinciding with the recovery of renal function, a dramatic disappearance of ascites was observed.

Adult↗
PubMed1995

Familial hypomagnesemia with hypercalciuria and nephrocalcinosis.

Very few patients with familial hypomagnesemia, hypercalciuria and nephrocalcinosis have been described. Information about clinical course, familial studies or evolution after renal transplantation is very scant. We have studied eight patients with this syndrome who belong to five different families. The mean age at diagnosis was 15 +/- 7 years (5 to 25 years). The primary clinical data were polyuria-polydipsia (8 cases), ocular abnormalities (5), recurrent urinary tract infections (5) and recurrent renal colics with stone passage (2). Bilateral nephrocalcinosis was observed in all cases. Every patient showed hypomagnesemia (1.1 +/- 0.2 mg/dl) with inappropriately high urinary magnesium (Mg) excretions (70 +/- 17 mg/day), Mg clearances (4.4 +/- 1.2 ml/m) and Mg fractional excretions (16.2 +/- 7.1%). Hypercalciuria was present in every case except in those with advanced renal insufficiency. Serum parathormone levels were abnormally high. Serum calcium (Ca), phosphorus and potassium, and urinary excretions of uric acid and oxalate were normal. Neither chronic oral Mg administration nor thiazide diuretics normalized serum Mg levels or urinary Ca excretions, respectively. Follow-up was 6 +/- 4.5 years. Renal function worsened in every case with six patients starting on chronic dialysis after 4.3 +/- 3.8 years. The progression rate of renal insufficiency correlated with the severity of nephrocalcinosis. Five patients have received a kidney graft, and their serum Mg and urinary Ca have always been within normal values after transplantation. Twenty-six members of four of the affected families were studied: none of them showed hypomagnesemia, renal insufficiency or nephrocalcinosis. However, eleven cases (42%) had hypercalciuria and four of them presented with recurrent renal stones. Two family members had medullary sponge kidneys. In conclusion, progression to renal insufficiency is common in this syndrome; oral Mg and thiazide diuretics are ineffective to correct abnormalities. After kidney graft, tubular handling of Mg and Ca was normal. A striking incidence (42%) of hypercalciuria was found in the familial study.

Adolescent↗
PubMed1995

Cd2+ regulation of the hyperpolarization-activated current IAB in crayfish muscle.

The effects of Cd2+ on the hyperpolarization-activated K(+)-mediated current called IAB (Araque, A., and W. Buño. 1994. Journal of Neuroscience. 14:399-408.) were studied under two-electrode voltage-clamp in opener muscle fibers of the crayfish Procambarus clarkii. IAB was reversibly reduced by extracellular Cd2+ in a concentration-dependent manner, obeying the Hill equation with IC50 = 0.452 +/- 0.045 mM and a Hill coefficient of 1 (determined from the maximal chord conductance of IAB). Cd2+ decreased the IAB conductance (GAB) and shifted its voltage dependence towards hyperpolarized potentials in a similar degree, without affecting the slope of the voltage dependence. The IAB activation time constant increased, whereas the IAB deactivation time constant was not modified by Cd2+. The IAB equilibrium potential (EAB) was unmodified by Cd2+, indicating that the selective permeability of IAB channels was not altered. IAB was unaffected by intracellular Cd2+. The Cd(2+)-regulation of IAB did not depend on [K+]o, and the effects of [K+]o on IAB were unchanged by Cd2+, indicating that Cd2+ did not compete with K+. Therefore, Cd2+ probably bound to a different site to that involved in the K+ permeability pathway. We conclude that Cd2+ affected the gating of IAB channels, interfering with their opening but not with their closing mechanism. The results can be explained by a kinetic model in which the binding of Cd2+ to the IAB channels would stabilize the gating apparatus at its resting position, increasing the energy barrier for the transition from the closed to the open channel states.

Animals↗
PubMed1994

P-type Ca2+ channels mediate excitatory and inhibitory synaptic transmitter release in crayfish muscle.

The toxin fraction (FTX) and peptide omega-Aga-IVA from the venom of the funnel-web spider Agelenopsis aperta, as well as a synthetic analogue of FTX, specifically block the P-type voltage-dependent Ca2+ channel (VDCC). The effects of these toxins on synaptic transmission were studied in the neuromuscular synapses of the crayfish opener muscle, which has a single excitatory and a single inhibitory motoneuron. FTX selectively and reversibly blocked excitatory and inhibitory postsynaptic currents and potentials in a dose-dependent manner. FTX had no effect on (i) resting and postsynaptic membrane conductance, (ii) postsynaptic L-type VDCC, and (iii) both glutamate- and gamma-aminobutyric acid-induced postsynaptic responses. Mean amplitude and frequency of miniature postsynaptic potentials were unchanged by FTX. The postsynaptic VDCC was inhibited by nifedipine, a selective dihydropyridine antagonist of L-type VDCC, whereas synaptic transmission was unaffected. Transmission was also undisturbed by omega-conotoxin, suggesting that N-type VDCCs are not involved. The peptide omega-Aga-IVA blocked excitatory and inhibitory transmission without affecting postsynaptic VDCC. Synaptic transmission was also blocked by synthetic FTX. We conclude that presynaptic P-type VDCCs are involved in both evoked excitatory and inhibitory transmitter release in crayfish neuromuscular synapses.

Animals↗
PubMed1994

Participation of voltage-gated conductances on the response succeeding inhibitory synaptic potentials in the crayfish slowly adapting stretch receptor neuron.

1. We examined the contribution of voltage-gated conductances to inhibitory postsynaptic potential (IPSP) effects under current clamp in silent and spiking slowly adapting stretch receptor neurons (SN1s) in the slow receptor muscle of the crayfish Procambarus. The receptor exemplifies the simplest inhibitory neural circuit, with one presynaptic and one postsynaptic neuron. The effects of synaptic inhibition were compared with the outcome of hyperpolarizing current pulses. Because pulse effects were exclusively due to postsynaptic mechanisms, an estimation of the synaptic or extrasynaptic origin of the results of IPSP was possible. 2. Inhibition by single IPSPs increased gradually with the time elapsed from the preceding spike in 60% of the spiking SN1s. However, early IPSP arrivals were exclusively excitatory in the rest of the cases. Inhibition was restricted to a single expanded SN1 interspike interval, but the early excitation and the postinhibitory rebound lasted several intervals. Rebound was invariably present; it was the only consequence of IPSPs in silent receptors and could be extremely long lasting (> 25 s). 3. The membrane potential of the SN1 neuron was clamped at hyperpolarized values (greater than -65 mV) by prolonged IPSP barrages at high rate (> 20/s). A prominent depolarizing sag and a gradual reduction of the IPSP amplitude were observed with prolonged presynaptic stimulation. There were subthreshold IPSP amplitude oscillations consisting of gradual increases and decreases of the post-IPSP peak depolarization at lower presynaptic rates. IPSP amplitude variations (< or = 10 mV) were primarily due to larger local responses. 4. Essentially all IPSP effects were mimicked by hyperpolarizing pulses. Sag was also evoked by pulses and was accompanied by a gradual conductance increase preceded by a brief initial drop. Sag and rebound were markedly reduced by Cs+ (2 mM) and tetrodotoxin (1 microM) and less by Ba2+ (5 mM) or tetraethylammonium (25 mM) superfusion. Both were somewhat decreased by acetylcholine (30 microM), which also markedly depolarized and accelerated firings, results which were usually reduced by atropine (10 microM). 5. In conclusion, IPSP and hyperpolarizing pulse effects were essentially identical, implying that extrasynaptic membrane properties were decisive. Interestingly, net excitatory consequences were usual, effectively increasing sensitivity and reducing the sensory threshold. Pharmacological evidence is provided suggesting that the hyperpolarization-activated current, IQ, and also probably the K+ M-current, the A-current, and the low-threshold, persistent Na+ conductances participate in sag and rebound genesis.(ABSTRACT TRUNCATED AT 400 WORDS)

Animals↗
PubMed1994

Nicotinic and muscarinic activation of motoneurons in the crayfish locomotor network.

1. We investigated the effects of acetylcholine (Ach) on identified motoneurons (MNs) using an in vitro preparation of the crayfish thoracic nervous system. Discontinuous current-clamp and single electrode voltage-clamp recordings from 50 MNs were performed along with micropipette pressure ejection of Ach (or agonists) close to the recording electrode. 2. Localized ejections of relatively large volumes (500-2,500 pl) of Ach (10(-2) M) or of the muscarinic agonist oxotremorine (Oxo, 10(-2)M) onto the MN neuropile region, usually (90% of the cases) induced a slow, alternating rhythmic activity in antagonistic MNs. In other cases (4 experiments), with similar deliveries of Ach or Oxo, MNs developed the ability to fire rhythmically but only when depolarized by sustained current injection. Pressure ejections of smaller volumes (50-200 pl) of Ach (10(-2)M) close to the recorded MN could give rise to a fast (1-2 s) large amplitude (< or = 20 mV) membrane depolarization (12%), a long-lasting (10 s to several minutes) and small (2-5 mV) depolarization (14%), and a combination of the two (74%). These responses appeared to involve different regions of the neurite because they changed when the drug-ejection pipette was displaced in the neuropile. Moreover, fast and long-lasting depolarizing components resulted from a direct effect of Ach onto the MNs because they persisted under tetrodotoxin (TTX, 10(-6)M) and cobalt (Co2+, 5 x 10(-3) M) superfusion. 3. Whereas the membrane resistance decreased during the fast Ach-induced depolarization, it increased during the long-lasting depolarization. The increase in membrane resistance was more pronounced at depolarized potentials more than -55 mV and involve a reduction in K+ conductance. 4. Superfusion with nicotinic and muscarinic antagonists revealed that the fast Ach-induced depolarization involved nicotinic receptors, muscarinic receptors, or both, whereas the slow depolarization was exclusively muscarinic. 5. The Ach-evoked inward currents were studied under voltage clamp. The fast nicotinic component (Inic) increased with hyperpolarizing holding potentials and decreased with depolarizing potentials, reversing at between 10 and 30 mV. The fast muscarinic current (Ifmus) displayed similar characteristics and reversed at about -10 mV. Whereas both fast components were voltage independent, the long-lasting muscarinic component (Ismus) was voltage dependent. The response grew with membrane depolarization, but when the holding potential was hyperpolarized below resting level, the response declined to disappear at about -60 mV and beyond.(ABSTRACT TRUNCATED AT 400 WORDS)

Acetylcholine↗
PubMed1994

MOTOR NEURONES OF THE CRAYFISH WALKING SYSTEM POSSESS TEA+-REVEALED REGENERATIVE ELECTRICAL PROPERTIES

In crustaceans, some motor neurones (MNs) have been shown to be part of the central pattern generator in the stomatogastric system (Harris-Warrick et al. 1992; Moulins, 1990), the swimmeret system (Heitler, 1978) or the walking system (Chrachri and Clarac, 1990). These MNs induce changes in the central rhythm when depolarized and are conditional oscillators in the stomatogastric ganglion. Moreover, in the walking system, rhythmic activity can be triggered by muscarinic cholinergic agonists (Chrachri and Clarac, 1987). We have recently analyzed the role of muscarinic receptors in crayfish walking leg MNs (D. Cattaert and A. Araque, in preparation) and demonstrated that oxotremorine, a muscarinic agonist, evoked long-lasting depolarizing responses associated with an increased input resistance. The outward current blocked by oxotremorine is likely to be carried by K+, as is the case for the M current (IM) in vertebrates (Brown and Adams, 1980). In most neurones, K+ conductances play a principal role in maintaining the membrane potential at rest: for example, IM is active at the resting membrane potential, thus contributing to its maintenance, and the 'delayed-rectifier' (IK) assists the fast repolarization after an action potential. Some K+ conductances are Ca2+-dependent (IK,Ca) and are activated by an increase in internal Ca2+ concentration. In such cases, Ca2+ currents may result in hyperpolarization of the neurone through activation of IK,Ca. In opposition to these K+ currents, the direct effect of Na+ and Ca2+ conductances is to depolarize the neurone. For example, the persistant Na+ current (INap) that is responsible for the slow subthreshold depolarization termed slow pre-potentials (Gestrelius et al. 1983; Leung and Yim, 1991) participates in the formation of pacemaker depolarization (Barrio et al. 1991) and generates plateau-type responses in control conditions (Barrio et al. 1991; Llinas and Sugimori, 1980). Similarly Ca2+ or non-specific (Na+/Ca2+) conductances generate such events in Aplysia californica burster neurones (Adams and Benson, 1985), crustacean cardiac ganglion (Tazaki and Cooke, 1990), insect neurones (Hancox and Pitman, 1991) and crustacean stomatogastric ganglion (Kiehn and Harris-Warrick, 1992). Since crustacean MNs can participate in rhythm production, such depolarizing conductances may exist in most of them and may contribute to the long-lasting MN depolarizations and spike bursts present during locomotion.

Journal Article↗
PubMed1994

[Effect of pravastatin on hypercholesterolemia associated with proteinuria].

BASIS: Hyperlipidemia associated to nephrotic syndrome has been involved in the deterioration of the renal function in these patients. The reduction in the synthesis of cholesterol with pravastatin, an hydrophilic inhibitor of such synthesis, may improve both the dyslipemia, the renal function and the proteinuria. METHODS: We conducted a controlled open randomized study in 16 patients with proteinuria greater than 2 g/day, creatinine clearance greater than 0.5 ml/s (30 ml/min) and hypercholesterolemia with LDL cholesterol greater than 4.9 mmol/l (190 mg/dl) distributed in two groups. One of these groups received hypolipemiant dietetic treatment and 20-40 mg of pravastatin and the other group, only the dietetic treatment. RESULTS: The patients receiving pravastatin showed a 27% decrease in total plasmatic cholesterol, compared to a 6.7% in the control group (p < 0.01). This decrease was more evident in the LDL cholesterol fraction (44 vs 9%; p < 0.01). No significant modifications were observed in the HDL cholesterol fraction, triglycerides, renal function or proteinuria. Neither clinical nor enzymatiz adverse effects from hepatic or muscular origin were observed.

Female↗
PubMed1994

Electrolyte excretion and sodium intake.

Established essential hypertension is characterized by normal equilibrium between the intake and renal excretion of sodium. Urinary sodium excretion is interrelated with that of other ions, such as potassium and calcium, and that the response of blood pressure to salt ingestion can be conditioned by the simultaneous intake of varying levels of those ions. The authors address three aspects: the correlations between urinary excretion of sodium and calcium and sodium and potassium in a population of untreated essential hypertensive persons, the response of blood pressure during the escape induced by exogenous mineralocorticoid administration in mild essential hypertension, and the effect of intravenous calcium gluconate infusion on sodium excretion and renal function. The first part shows that sodium excretion is closely correlated with that of other ions in essential hypertension, and the second part shows that, to escape from the sodium-retaining effect of a mineralocorticoid, mild hypertensive subjects must have increased blood pressure within or near the cutoff point that defines salt sensitivity. Of interest, the elevation in blood pressure takes place while sympathetic nervous activity is blunted. The third part provides evidence to explain one of the mechanisms by which calcium influences renal function and enhances renal sodium excretion. The intrarenal effects of low doses of calcium are dependent on the renal production of prostaglandins.

Atrial Natriuretic Factor↗
PubMed1994

Novel hyperpolarization-activated K+ current mediates anomalous rectification in crayfish muscle.

The ionic current underlying anomalous rectification in opener muscle fibers of crayfish was studied under two-electrode voltage clamp. Opener muscle fibers showed a mean resting potential (RP) of -64.8 mV and an input resistance of 0.4 M omega. Hyperpolarizing voltage command pulses from a holding potential (H) of -60 mV evoked an instantaneous voltage-independent linear current (IL) followed by a time- and voltage-dependent inward current (IAB) that reached a steady state within 500 msec. The reversal potential of IAB (EAB) was estimated from tail current amplitudes. At an extracellular K+ concentration ([K+]o) of 5.4 mm the mean EAB was -61.8 mV. EAB shifted toward positive potentials by 50.8 mV for a 10-fold increase in [K+]o. The conductance underlying IAB (GAB) increased sigmoidally with hyperpolarization, starting close to the RP, saturating at a GAB,max of about -140 mV, and showing a mean half-activation at -94.4 mV. The activation curve of GAB shifted 53.6 mV toward positive potentials with a 10-fold increase in [K+]o. GAB,max did not increase in raised [K+]o. The activation and deactivation kinetics of IAB were accurately described by single exponentials with similar time constants (< 100 msec). Time constants changed as an exponential function of the membrane potential. IAB, its time course, GAB, and EAB were not modified in the following conditions: (1) Na(+)- and Ca(2+)-free solutions, (2) intracellular EGTA, (3) extracellular (100 mM) or intracellular tetraethylammonium, (4) extracellular Cs+ (up to 50 mM), Rb+ (up to 10 mM), Ba2+ (13.5 mM), or Mn2+ (13.5 mM). However, low extracellular concentrations of Cd2+ or Zn2+ strongly and reversibly reduced both IL and IAB. Therefore, we conclude that anomalous rectification in crayfish muscle is generated by a voltage- and time-dependent K+ current IAB. This current displayed many electrophysiological and pharmacological characteristics that distinguished it from all others mediating anomalous rectification described previously.

Animals↗
PubMed1993

Compressive myelopathy due to dialysis-associated amyloidosis.

A 66-year-old woman presented a spastic quadriparesis due to compression of the cervical cord 6 years after the beginning of chronic hemodialysis. Five years later, she developed a second episode of compressive myelopathy affecting the lumbar spine. On both occasions, surgical laminectomy with removal of fibroligamentous rings that compressed the cord led to a total recovery of the patient. Histological study demonstrated the presence of massive amyloid deposits in the surgically excised material.

Aged↗