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Biomedical subjects

J Walden

Publications and source records attributed to J Walden.

At least 109 records · Page 6Linked to original sources
PubMed1986

Paroxysmal neuronal depolarizations in the rat motorcortex in vivo: intracellular injection of the calcium agonist BAY K 8644.

Epileptic activity was elicited in the rat's motor cortex by local application of penicillin. At the neuronal level it consisted of typical paroxysmal depolarization shifts. The calcium agonist BAY K 8644 was injected into neurons showing such a discharge pattern. The application of this drug increased amplitude and after depolarization of paroxysmal neuronal depolarizations.

3-Pyridinecarboxylic acid, 1,4-dihydro-2,6-dimethy↗
PubMed1985

Acetylcholine responses in snail neurons: increase and decrease in potassium conductance succeeding inward currents.

In the identified neurons B1 and B3 of the buccal ganglion of Helix pomatia, the initial acetylcholine (ACh) inward current was succeeded by two types of secondary responses. The secondary responses consisted either in an outward current or in a long-lasting inward current or in a combination of both. The secondary outward current was decreased with membrane hyperpolarization, associated with a decrease of membrane resistance and abolished in Ca2+-free Co2+ solution. It is assumed to be a K+ current activated by an influx of Ca2+. The secondary inward current also decreased with membrane hyperpolarization, but was associated with an increase of the membrane resistance and could be mimicked by an injection of Na+ into the cells. It is suggested to be due to a block of K+ channels by intracellular Na+. When the secondary responses appeared combined, the outward current preceded the inward current.

Acetylcholine↗
PubMed1985

Decrease of potassium permeability by intracellular application of sodium ions in snail neurons.

In the identified neurons B1, B2 and B3 of Helix pomatia an intracellular injection of Na+ induced an outward current in 10% and an inward current in 90% of the experiments. The outward current was associated with an increase and the inward current with a decrease of the membrane conductance. Both currents reversed at membrane potentials of between -60 and -70 mV. Inward currents were also elicited by intracellular Li+ or tris-[hydroxymethyl]-aminomethane (Tris+) injection. All inward currents were reduced by extracellular administration of tetraethylammonium or quinine. It is suggested that the outward current represents a calcium-activated potassium current and that the inward current is due to a blockade of potassium channels from the intracellular side.

Animals↗
PubMed1985

Suppression of focal epileptiform discharges by intraventricular perfusion of a calcium antagonist.

Calcium currents were found to participate in the generation of epileptic discharges of single cortical neurones. The present experiments tested whether a systemic administration of a calcium antagonist is able to influence epileptic activity in neuronal populations. Focal interictal epileptiform discharges (FIEDs) were elicited by application of penicillin to the motor cortex of the rat. The calcium antagonist verapamil dissolved in artificial cerebrospinal fluid was applied by intraventricular push-pull perfusion to achieve high concentrations of the drug in cerebral tissue and to avoid alterations of the systemic circulatory system. The application of the calcium antagonist reduced FIEDs in amplitude and in frequency of occurrence. In some experiments the suppression of seizure activity was preceded by a transient enhancement. After termination of the drug perfusion FIEDs were often re-established. Control experiments revealed that perfusion with drug-free cerebrospinal fluid did not change FIEDs. In experiments without epileptic activity, cortical evoked potentials elicited by stimulation of the sciatic nerve tended to increase with perfusion of the calcium antagonist. As a whole, the systemic administration of the calcium antagonist verapamil depressed FIED and exerted an inverse effect on synchronized non-epileptic neuronal activity.

Animals↗
PubMed1985

Acetylcholine responses of identified neurons in Helix pomatia--I. Interactions between acetylcholine-induced and potential-dependent membrane conductances.

The influence of potential-dependent membrane conductances on amplitude and time course of acetylcholine (ACh) responses was studied. The investigations were performed on the identified neurons B1 and B3 of the buccal ganglion of Helix pomatia. The neurons B1 and B3 were depolarized by ACh. The depolarization was accompanied by a decrease of membrane resistance. An inward rectification occurring negative to the resting membrane potential (RMP) reduced the amplitude of the ACh depolarizations. An outward rectification occurring positive to the RMP consisted of two parts and ceiled the ACh responses. The early outward current reduced the amplitude and modified the time course of ACh responses. Local responses or axonal action potentials increased the amplitude of the ACh depolarizations.

Acetylcholine↗
PubMed1985

Acetylcholine responses of identified neurons in Helix pomatia--II. Pharmacological properties of acetylcholine responses.

A pharmacological separation of depolarizing and hyperpolarizing mechanisms involved in the generation of acetylcholine (ACh) depolarizations was attempted in the identified neurons B1 and B3 of the buccal ganglia of Helix pomatia. The selectivity of the drugs employed was assayed in non-identified buccal neurons in which ACh increased a hyperpolarizing Cl- conductance. Voltage clamp techniques were used. Under control conditions the depolarizing ACh currents increased non-linearly with more negative membrane potentials. The hyperpolarizing ACh currents showed a linear potential dependence. The buffer substance Tris (5 mmol/l) depressed the depolarizing ACh currents. The effect was accentuated with more negative membrane potentials. Tris failed to affect hyperpolarizing ACh responses. HEPES (5 mmol/l) did not change depolarizing or hyperpolarizing ACh responses. d-Tubocurarine (0.02-0.2 mmol/l), hexamethonium (0.5-5.0 mmol/l) and atropine (0.1 mmol/l) blocked the depolarizing and hyperpolarizing ACh responses. Arecoline (0.1 mmol/l) had neither an agonistic nor an antagonistic effect on the identified and on the non-identified neurons. It displayed an anticholinesterase activity. Anthracene-9-carbonic acid (0.5 mmol/l) depressed selectively the hyperpolarizing ACh responses. In the neurons B1 and B3 no pharmacologically separable hyperpolarizing ACh responses were detected to be superimposed on the ACh depolarizations.

Acetylcholine↗
PubMed1985

Acetylcholine responses of identified neurons in Helix pomatia--III. Ionic composition of the depolarizing currents induced by acetylcholine.

The ionic composition of the currents underlying the acetylcholine (ACh) depolarizations in the identified neurons B1 and B3 of the buccal ganglia of Helix pomatia was analysed. The equilibrium potential of the ACh responses was -2.8 +/- 0.6 mV (N = 49) and -4.0 +/- 0.7 mV (N = 79; mean +/- SEM) in the neurons B1 and B3, respectively. Replacement of NaCl in the bath solution by sucrose shifted the ACh equilibrium potential into the negative direction. A similar but less pronounced shift occurred when Ca2+ was substituted for Na+. Substitution of Cl- in the bath solution by propionate or an increase of the intracellular Cl- concentration did not affect the ACh equilibrium potential. Changes of K+ concentration in the bath between 1 and 50 mmol/l left the ACh equilibrium potential nearly unaffected when the Na+ concentration was at the control level. With a simultaneous reduction of extracellular Na+ an increase of K+ concentration shifted the ACh equilibrium potential towards more positive potentials. The findings are compatible with calculated K+ permeabilities if a K+ redistribution across the cell membrane is considered. In the neurons B1 and B3, channels operated by ACh are permeable for K+, Na+ and Ca2+, with the relative permeabilities 1.6:1.0:0.1.

Acetylcholine↗
PubMed1984

Continuous measurement of pentylenetetrazol concentration by a liquid ion exchanger microelectrode.

A double-barrelled microelectrode is described, which permits the continuous measurement of the concentration of the epileptogenic agent pentylenetetrazol (PTZ). The electrode is based on the liquid potassium exchanger (Corning No. 477 317) and enables measurements of PTZ concentration in physiological salines down to 1 mM. The electromotive behaviour of the liquid membrane against PTZ cannot directly be described by the Nicolsky-Eisenman formalism. It is suggested that specific interactions of the PTZ molecule with the Corning ligand are involved in the potential generating mechanisms.

Animals↗
PubMed1984

Reduction of calcium currents in identified neurons of Helix pomatia: intracellular injection of D890.

The actions of intracellularly applied D890 on membrane currents of the identified neurons B1, B2 and B3 of Helix pomatia were investigated. The TTX-resistant component of the inward current, the inward currents in Na+-free sucrose solution and in Ca2+-free Ba2+ solution were reduced. In Ca2+-free Co2+ solution the inward current was not affected. The late outward currents were strongly reduced. In solutions containing 20 mmol/l NiCl2 the remaining parts of these currents were blocked only to a lesser extent. The early outward current remained unchanged. It is concluded that intracellularly applied D890 mainly exerts its effects on the calcium current.

Animals↗
PubMed1981

Effects of quinine on membrane potential and membrane currents in identified neurons of Helix pomatia.

In the neurons B1, B2 and B3 of Helix pomatia, a systemic administration of quinine elicited: (1) a depolarization accompanied by an increase in membrane resistance (RM), sometimes preceded by a hyperpolarization associated with a decrease in RM; (2) a diminution in amplitude of action potentials and of afterhyperpolarization; (3) a reversible decrease of the amplitude of the inward current with a shift of the maximum amplitude and of the reversal to more negative potential values; (4) no change in the steady state inactivation curve of the inward current; and (5) a partly irreversible depression of the early outward current and of the late outward currents.

Animals↗
PubMed1977

Kinetics of various 99mTc-Sn-pyrophosphate compounds in the rat. I. In vivo studies.

The kinetic data of two different 99mTc-Sn-pyrophosphate compounds (compound A and B) were evaluated in non-adult rats. Only compound A concentrated in bone. Both compounds dispersed rapidly in the intravascular as well as the extravascular space. The plasma protein bond of both compounds increased with time after injection and impaired both the renal clearance of both compounds and the bone clearance of compound A. The renal clearance of both compounds was somewhat above that of 51Cr-EDTA. It is concluded that compound A and B is mainly excreted by glomerular filtration. About one fourth of the glomerular filtrate of compound B is reabsorbed and accumulated by the tubular cells.

Animals↗
PubMedDate not supplied

A calcium antagonist for the treatment of depressive episodes: single case reports.

Preclinical studies indicate that a disturbed intracellular calcium ion homeostasis is involved in the pathophysiology of affective disorders. Therefore some calcium antagonists were investigated, especially in the treatment of the manic syndrome. In the present study the calcium antagonist nimodipine was used in 10 out-patients with single or recurrent depressive episodes. As a result the mean HAMD scores changed from 26.5 to 9.9 after the individual nimodipine administration. These single case reports suggest an effective new therapy strategy for the treatment of affective dysregulations and give rise to controlled clinical studies with calcium antagonists.

Adult↗
PubMedDate not supplied

An open label study of gabapentin in the treatment of acute mania.

Recent anecdotal single case reports have suggested that the new antiepileptic drug gabapentin might be effective in the treatment of manic episodes and in the prophylaxis of bipolar disorder. In the present open trial, 14 patients with acute mania were treated for up to 21 days with gabapentin in a dose range from 1200 to 4800 mg/day. Six patients were treated with gabapentin as add-on medication and 8 patients were treated with a high dose of gabapentin alone. Gabapentin was both efficacious and safe when applied in combination with other drugs such as lithium and valproic acid. All patients in the add-on group and 4/8 patients on gabapentin monotherapy finished the 21 day protocol. Analysis of the scores of the Bech-Rafaelsen Mania Assessment Scale (BRMAS) of these patients showed that the mean BRMAS score declined from 37.7 to 7.8 on day 21 in the add-on group and from 27.8 to 9.0 in 4/8 patients finishing 21 days in the monotherapy group. It is suggested that gabapentin monotherapy might be useful in selected patients to treat modest but not severe manic states. In addition, gabapentin in conjunction with other effective mood stabilisers seems to be safe and efficacious in the treatment of severe mania.

Acetates↗
PubMedDate not supplied

Sexual function in patients with advanced heart failure.

OBJECTIVES: To determine the effect of low ejection fraction on sexual function and the relation between alterations in sexual function and pertinent clinical, demographic, and psychosocial variables in patients with advanced heart failure. DESIGN: This study was descriptive and correlational in design. SETTING: The setting was an outpatient clinic of a university-affiliated hospital. SUBJECTS: Sixty-two male (82%) and female (18%) patients with advanced heart failure (New York Heart Association [NYHA] class III or IV) were studied. MEASURES: Exercise tolerance and symptom severity were assessed by the 6-minute walk and NYHA classification. Ejection fraction was measured by echocardiography. Alterations in the patients' emotional, social, and sexual function were assessed with the self-report version of the Psychosocial Adjustment to Illness Scale. RESULTS: Approximately three quarters of the patients reported a marked decrease in sexual interest and in the frequency of sexual relations caused by illness, with one quarter having ceased all sexual activity. Half the patients described having experienced marked reductions, after heart failure developed, in the pleasure or satisfaction they normally experienced from sex. Few patients had arguments with their spouses about sex or reported significant marital problems as a result of their illness. A significant relation was documented between patients' sexual function and the results of the 6-minute walk (r = 0.32, p < 0.005), as well as between sexual function and NYHA functional class (r = 0.21, p < 0.05). Sexual function was also related to the patient's social environment (r = 0.59, p < 0.001), psychologic distress (r = 0.38, p < 0.001), and domestic environment (r = 0.29, p < 0.05). No significant differences in sexual function were noted when patients were compared on the basis of differences in ejection fraction, medications, gender, or age. CONCLUSION: Advanced heart failure results in marked changes in libido and in the ability to perform sexually. These changes do not affect the marital relationship negatively, at least in the view of the patient. As patients' symptoms of heart failure become increasingly more severe, physicians and nurses need to counsel patients and their spouses about the changes they may experience in their sexual relationships. Attention needs to focus on ways to cope with the decreasing physical status that accompanies advanced heart failure to minimize negative changes in sexual functioning.

Age Factors↗
PubMedDate not supplied

Trimipramine fails to exert antimanic efficacy: a case of the discrepancy between in vitro rationale and clinical efficacy.

Standard mood stabilizers, such as lithium and haloperidol, and anticonvulsants show effectiveness in a maximum of 60%-70% of acutely manic patients. Obviously, there is a clinical need to evaluate other treatment options. Current pathophysiologic concepts suggest that substances with an ameliorating effect on dopaminergic hyperfunction, serotonergic hypofunction, or GABAergic hypofunction might be useful, as may be substances with calcium-antagonistic effects. In vitro, the antidepressant trimipramine exerts dopamine- and calcium-antagonistic properties. Therefore, we conducted an open trial to screen it for antimanic action. We found no clinical benefit in four acutely manic patients receiving up to 400 mg/d of trimipramine. It is concluded that, at least in the case of trimipramine, the pharmacologic profile is not helpful in predicting potential effectiveness in mania.

Adolescent↗