Epileptic activity as a tool in neurobiology.
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Biomedical subjects
Publications and source records attributed to A Lücke.
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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.
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.
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.
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.
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.
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