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Biomedical subjects

A Lücke

Publications and source records attributed to A Lücke.

36 records · Page 2Linked to original sources
PubMed1996

Effects of glutamate application on the rhythm of low magnesium-induced epileptiform activity in hippocampal slices of guinea-pigs.

The extracellular concentration of glutamate has previously been reported to increase to more than 10-fold the basal level during seizure activity. In the present study, we tested whether localized increases in extracellular glutamate concentration influence the rhythm of epileptiform discharges in the low-magnesium epilepsy model. In hippocampal slices of guinea-pigs, epileptiform activity was induced by omission of magnesium from the bath fluid. Glutamate and its subreceptor agonists N-methyl-D-aspartate (NMDA) and alpha-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid (AMPA) were ejected into different strata of the CA3 and CA1 regions using microiontophoretic and micropressure application. Glutamate, NMDA and AMPA applied to the CA3 region, but not to the CA1 region, induced a short-lasting increase in epileptiform discharge frequency, often followed by a transient reduction. The effect was most pronounced with application into the stratum lacunosum-moleculare of the CA3 region and could only be evoked in slices exceeding 400 microns in thickness. The effects on the rhythm of epileptiform discharges induced by NMDA and AMPA were blocked by their specific receptor antagonists. They were not influenced by application of GABAA and GABAB receptor antagonists. Changes in somatic membrane potential of CA3 pyramidal neurons did not correlate with changes in the rhythm of epileptiform discharges elicited in this region. The transient suppression of epileptiform discharges that followed the increase in discharge frequency was abolished by an adenosine A1 receptor antagonist. We propose that localized increases in extracellular glutamate concentration modify the rhythm of epileptiform discharges due to changes in neuronal network activity.

Animals↗
PubMed1995

Extracellular potassium elevations in the hippocampus of rats with long-term pilocarpine seizures.

Pilocarpine injection into rodents leads to the development of chronic limbic seizures that follow an initial status epilepticus and a seizure-free interval. It has been proposed that a decreased efficacy of the mechanisms that buffer the extracellular concentration of K+ ([K+]o) leads to an increase in seizure susceptibility. Therefore, we analyzed the changes in [K+]o associated with the synchronous activity induced by 4-aminopyridine (4AP) in hippocampal slices obtained from control and pilocarpine-treated rats. At all recording sites (i.e. stratum radiatum of the CA1 and CA3 subfields, and hilus of the dentate gyrus), the amplitude of GABA-mediated synchronous field potentials induced by 4AP, as well as the associated [K+]o increases, were significantly reduced in slices obtained from the pilocarpine-treated rats. In the control group, the field-potential amplitudes reached 1 mV (i.e. 1.7 +/- 0.3 mV in CA1, 0.93 +/- 0.2 mV in CA3, and 1.03 +/- 0.12 mV in the hilus; mean +/- SEM), while the accompanying rises in [K+]o exceeded 4 mM (i.e. 4.17 +/- 0.15 mM in CA1, 4.04 +/- 0.12 mM in CA3, 4.04 +/- 0.11 mM in the hilus) from a baseline of 3.25 mM. The corresponding values in slices from the pilocarpine-treated group were rarely greater than 0.4 mV (i.e. 0.3 +/- 0.09 mV in CA1, 0.27 +/- 0.03 mV in CA3 and 0.38 +/- 0.06 mV in the hilus), and larger than 3.6 mM (i.e. 3.63 +/- 0.04 mM in CA1, 3.64 +/- 0.03 mM in CA3 and 3.60 +/- 0.04 mM in the hilus) from a similar baseline value. With pilocarpine, the rate of occurrence of the GABA-mediated potential significantly decreased from 0.035 to 0.016 s-1. Since the rises in [K+]o decreased rather than increased and their overall duration was unchanged (possibly reflecting cell loss), we conclude that a modification of [K+]o buffering capacity is unlikely to account for the appearance of in vivo seizures in the pilocarpine model of epilepsy.

4-Aminopyridine↗
PubMed1995

Changes of extracellular calcium concentration induced by application of excitatory amino acids in the human neocortex in vitro.

The influence of the glutamate subreceptor agonists N-methyl-D-aspartate (NMDA) and alpha-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid (AMPA) on cortical field potentials and on changes in extracellular free calcium concentration ([Ca2+]o) was tested on human neocortical slices (eleven from nine different patients). The tissue used was a small portion of that which is normally removed for the treatment of a brain tumor. [Ca2+]o and field potentials were measured by Ca(2+)-selective microelectrodes. Local pressure-microejection of NMDA (100 mumol/l)- and AMPA (1 mmol/l)-induced negative field potentials with maximal amplitudes of 0.9 +/- 0.1 mV (11 slices, mean +/- S.E.M.) and 1.0 +/- 0.1 mV (nine slices), respectively. The negative field potentials induced by NMDA were accompanied by monophasic decreases of [Ca2+]o (0.8 +/- 0.1 mmol/l, nine slices). AMPA elicited no (three slices) or only minor decreases of [Ca2+]o (0.2 +/- 0.1 mmol/l, five slices). The responses to the glutamate subreceptor agonists NMDA and AMPA were reversibly depressed by adding their specific antagonists DL-2-amino-5-phosphonovalerate (APV, 100 mumol/l, six slices) and 6-cyano-7-nitroquinoxalin-2,3-dion (CNQX, 5 mumol/l, four slices), respectively. The results correspond to findings in animal experiments and are consistent with the interpretation that in the human neocortex the Ca2+ permeability of channels gated by NMDA is higher than those gated by AMPA.

2-Amino-5-phosphonovalerate↗
PubMed1995

Synchronous potentials and elevations in [K+]o in the adult rat entorhinal cortex maintained in vitro.

Extracellular field-potential recordings and measurements of the extracellular concentration of potassium ([K+]o) were made in layers II and III of the adult rat entorhinal cortex in a slice preparation. Two types of spontaneous, synchronous potentials were induced by the convulsant drug 4-aminopyridine (4AP, 50 microM). The first type was seen in all slices (n = 19) and consisted of a negative-going field potential that lasted 0.5-3.5 s and occurred at rates of 0.013-0.13 Hz. This event was accompanied by an elevation in [K+]o that attained peak values of 4.0-7.6 mM. The second type was reminiscent of ictal epileptiform discharges and was recorded in 6 of 19 slices; it lasted 21-190 s, recurred at 0.001-0.003 Hz and was associated with [K+]o increases that had peak values of 14-17 mM. Whenever such an ictal discharge occurred, it was closely preceded and thus appeared to be initiated by the first type of field potential. Perfusion with N-methyl-D-aspartate (NMDA) receptor antagonist (+/-)-3-(2-carboxy-piperazine-4-yl)propyl-1-phosphonate (CPP; 10 microM) abolished the ictal discharge (n = 4). This pharmacological procedure did not abolish the negative-going potentials that continued to occur during further application of the non-NMDA antagonist 6-cyano-7-nitroquinoxaline-2,3-dione (CNQX; 10 microM; n = 4). These glutamatergic-independent potentials were, however, blocked by the GABBAA-receptor antagonist bicuculline methiodide (10 microM, n= 3). Thus, as in hippocampus, 4AP can induce in the entorhinal cortex a synchronous GABA-mediated potential that is resistant to excitatory amino acid antagonists.(ABSTRACT TRUNCATED AT 250 WORDS)

4-Aminopyridine↗
PubMed1995

Melatonin reduces low-Mg2+ epileptiform activity in human temporal slices.

Seizure susceptibility waxes and wanes in an apparently circadian manner in many epileptic patients. Fluctuations of melatonin concentration with highest levels during the night and lowest levels in the early morning could be involved in this phenomenon. Therefore, the action of melatonin on epileptic activity was tested. The experiments were carried out on human temporal neocortical slices cut from tissue resected for surgical treatment of epilepsy. Autoradiographic studies were performed on parallel slices with 100-120 pmol 2-[125I]iodomelatonin/l in the absence or presence of unlabelled melatonin. High-affinity binding sites of melatonin could be demonstrated in layers II-V of the temporal cortex. The binding was saturable, specific and occurred with low capacity. In electrophysiological studies, epileptiform field potentials were elicited by omission of Mg2+ from the superfusate and recorded from layers II-V. The frequency of occurrence of epileptiform field potentials was reduced to 0.5 of the initial value with application of melatonin (10 and 100 nmol/l) in each case. This effect was reversible upon washing. The findings favour the hypothesis that melatonin depresses epileptiform neuronal activity through specific neocortical receptors.

Autoradiography↗
PubMed1993

Diffusion analysis of valproate and trans-2-en-valproate in agar and in cerebral cortex of the rat.

The diffusion of valproate (VPA) and trans-2-en-valproate were studied in agar gel and in the cerebral cortex of the rat using pressure microejection and VPA-selective microelectrodes. From the agar measurements a free diffusion coefficient for VPA of 6.52 x 10(-6) cm2.s-1 and for trans-2-en-VPA of 5.25 x 10(-6) cm2.s-1 for 37 degrees C was determined. The tortuosity value in the cortex was 1.92 for VPA and 1.67 for trans-2-en-VPA. The tortuosity values suggest that VPA and trans-2-en-VPA diffuse mainly in the extracellular space of the brain.

Agar↗
PubMed1993

Influence of the organic calcium antagonist verapamil on N-methyl-D-aspartate (NMDA) induced cortical field potentials (neocortical slice, guinea pig).

In the present experiments it was tested whether the organic calcium antagonist verapamil has an influence on N-methyl-D-aspartate (NMDA) induced cortical field potentials (CFP) in neocortical slices of guinea pigs. NMDA (1 mumol/l) was applied via a micropipette by pressure pulses. Verapamil (60 mumol/l) was administered by bath application or ejected locally (100 mumol/l) and simultaneously with NMDA. Neither the systemic administration nor the local application of verapamil had an influence on NMDA induced CFP. It is concluded that the antiepileptic effect of verapamil is not mediated via the NMDA receptor.

2-Amino-5-phosphonovalerate↗
PubMed1992

Interneuronal information transfer: recent advances in synaptology.

The elementary mechanisms underlying synaptic transmission are described with respect to the following topics: 1. morphology and bioelectric activity of nerve cells; 2. electrical and chemical synapses; 3. transmitter-operated opening of membrane channels on the basis of allosteric effects; 4. synaptic transmission on the basis of second messengers (adenylate-cyclase-system, phosphoinositol-cycle); 5. interactions of transmitters.

Animals↗
PubMed1990

Decrease of free calcium concentration at the outer surface of identified snail neurons during paroxysmal depolarization shifts.

Changes of free calcium concentration at the outer neuronal surface during paroxysmal depolarization shifts elicited by pentylenetetrazol were measured. Investigations were performed on the identified neuron B3 of the buccal ganglion of Helix pomatia. Extracellular calcium concentration was recorded by calcium-selective microelectrodes. The extracellular calcium concentration steeply decreased with the commencement of paroxysmal depolarization and started to reincrease when the paroxysmal depolarization had reached its plateau level. It is concluded that an influx of calcium ions takes place during paroxysmal depolarization shifts.

Animals↗
PubMed1989

The influence of the convulsant pentylenetetrazol on Ca2+-selective microelectrodes (neutral carrier ETH 1001).

Interference of the epileptogenic drug pentylenetetrazol (PTZ) on the Ca2+-selective microelectrode based on the neutral carrier ETH 1001 is described. It is suggested that tetraphenylborate, a component of the Ca2+-selective membrane, is responsible for this interference. Though the sensitivity of the Ca2+-selective microelectrode to PTZ is low, the error in measurements of the free Ca2+ concentration in biological preparations treated with PTZ has to be considered, since pathological changes in the extracellular Ca2+ concentration also produce relatively small changes in the relative electrode potential.

Animals↗
PubMed1989

Cervicogenic, hemicranial attacks associated with vascular irritation or compression of the cervical nerve root C2. Clinical manifestations and morphological findings.

Sixteen patients suffering from hemicranial attacks are reported. After many years of unsuccessful conservative treatment (mean = 12.4 years), the patients were treated surgically with good results. The radiological or electrophysiological examinations were non-specific or negative. Only vasoactive tests (provoking or relieving pain) or local anesthesia proved helpful in diagnosing and localizing the origin of pain. Intraoperatively, hemicranial attacks were found to be caused by vascular irritation or compression of the cervical nerve root C2. After decompression (n = 6) or dissection (n = 10) of the nerve root and the ganglion, 12 patients were relieved of their pain, 2 had improved relatively, 1 showed only a slight improvement, and in 1 patient no cause was found and no improvement was achieved. Two patients suffered recurrence of pain postoperatively; one had no further complaints after root extirpation following percutaneous thermorhizotomy. Electron microscopic examination of the nerve root and its ganglion revealed focal morphological changes, including proliferation of connective tissue in the endoneurium and the ganglion itself, the formation of onion-bulb-like structures around single axons, discrete signs of myelin damage and axonal degeneration. These morphological changes are possibly the result of a chronic vascular compression.

Adult↗
PubMed1985

[Incomplete central vein occlusion. A clinicopathologic case report].

A 71-year-old patient died 4 weeks after the occurrence of incomplete occlusion of the central retinal vein. Histology of the two bulbi was compared with the photographic and fluorescenceangiographic findings of the fundus. Histologic evaluation showed that the occlusion had been caused by a thickening of the vein wall due to proliferation of fibrocytes and histiocytes just behind the lamina cribrosa. There were no signs of phlebitis or thrombosis.

Aged↗
PubMed1984

[Retinal light damage--summary of experimental and clinical observations].

The article presents a comprehensive review of the literature on light damage to the retina with special reference to clinical aspects. A definition of the different modes of action of light on the retina and a brief summary of current theories on possible mechanisms of light-damage are presented. Experimental studies applying ophthalmological light sources to the primate eye are described as well as investigations on photochemical light-damage to the human eye. Possible implications of these observations for some types of retinal degeneration are discussed. Finally, the importance of considering possible light-hazards in clinical routine is emphasized.

Animals↗
PubMed1984

[Ulcerative herpetic keratitis. Clinical and pathological findings and prognosis of the graft].

Between 1971 and 1982 33 corneae were excised for therapeutic keratoplasty because of ulcerative herpetic keratitis. The histologic findings and the clinical course enabled distinction of a nonreactive form with a rather good prognosis for keratoplasty (62% clear grafts) and an inflammatory form with bad prognosis (20% clear grafts) because of many herpetic recurrences. Perforating keratoplasty and first interventions in particular did better than lamellar keratoplasty or retransplantation. Existence of preoperative corneal vascularization compromised the prognosis of the graft. Preoperative perforation of the ulcer occurred rather often in nonvascularized corneae without compromising the prognosis of the graft.

Adolescent↗
PubMedDate not supplied

Simultaneous and continuous measurement of free concentration of valproate in blood and extracellular space of rat cerebral cortex.

Free concentration of valproate (VPA) was measured simultaneously and continuously in blood and in the extracellular space of cerebral cortex of rats by VPA-selective microelectrodes. Constant amounts of VPA were injected into the femoral vein with differing duration of injection. Immediately after drug application, the concentration of free VPA in blood and brain increased to a peak value, the degree of which increased with the speed of injection. Ten to 15 min after VPA injection, a plateau value was reached. This plateau value was equal in the extracellular space of cortex and in blood. The data indicate that VPA can "freely" cross the blood-brain barrier (BBB).

Animals↗
PubMedDate not supplied

Redox cycle of stable mixed nitroxides formed from carcinogenic aromatic amines.

1. Of the carcinogenic aromatic nitrogenous compounds investigated, 10 out of 11 were found to be biotransformed in rabbit liver microsomal preparations to nitroxide radicals, as detected by ESR spectroscopy; with non-carcinogenic nitrogenous compounds only 2 out of 8 formed nitroxide radicals. 2. The radicals are stable mixed nitroxides formed by covalent binding of the aromatic nitroxide to endogenous constituents of the microsomal membrane with preservation of the nitroxide radical group (spin-trapping). 3. From the high chemical stability and the observed ESR spectra, spin-label-like structures can be deduced. 4. From this and the known one-electron redox properties of spin-labels, a redox cycle catalysing the production of reactive oxygen species and involved in tumour initiation and/or promotion by aromatic nitrogenous compounds is proposed.

Amines↗