Biomedical subjects

O W Witte

Publications and source records attributed to O W Witte.

14 recordsLinked to original sources

PubMed1992

Oscillatory activity in different motor subsystems in palatal myoclonus. A case report.

In a patient with palatal myoclonus the mutual interaction between voluntary movements and the myoclonic activity was analysed. Amplitude and frequency of myoclonic activity in hand muscles were modulated by flexions and extensions. A 1:1 relationship was found between EMG-bursts in hand muscles and palatal movements. A 1:2 relationship was found between eye and finger movements. Resetting of myoclonus in the abductor digiti minimi muscle occurred after cutaneous ulnar nerve stimulation. It is suggested that feedback plays an important role in the generation of the oscillatory activity in PM in addition to pacemaker activity in brainstem neurons.

Aged↗

PubMed1991

Participation of interneurons in penicillin-induced epileptic discharges.

Interneurons of rat motor cortex in vivo and of rat hippocampal slices were studied during penicillin-induced epileptic discharges. Synchronous with pyramidal cells, they showed transient depolarizations similar to paroxysmal depolarization shifts in pyramidal cells. The transient depolarizations were followed by hyperpolarizing or depolarizing afterpotentials lasting 600 to 1200 ms. During the transient depolarizations and the afterdepolarizations the interneurons discharged with increased frequency. This may contribute to the enlarged and prolonged synaptic inhibitions following interictal discharges in pyramidal cells.

Animals↗

PubMed1991

Afterpotentials following penicillin-induced paroxysmal depolarizations in rat hippocampal CA1 pyramidal cells in vitro.

Epileptic discharges were induced by superfusion of rat hippocampal slices with penicillin. Under these conditions the neurons generated paroxysmal depolarization shifts (PDS) after electrical stimulation of Schaffer collaterals. The PDS were followed by large afterhyperpolarizations lasting about 2 s. The mechanisms causing these afterhyperpolarizations were studied in CA1 pyramidal cells. A late component of the afterhyperpolarizations, which determined their overall duration, was blocked by intracellular application of EGTA and reduced by superfusion with 8-Br-cAMP. In the same neurons these drugs had a comparable effect on afterhyperpolarizations following depolarizing current injections; it was therefore concluded that the late component of the PDS afterhyperpolarizations was caused by a slow Ca2(+)-activated K+ current. An initial fast component of PDS afterhyperpolarizations, which peaked about 60 ms after PDS onset, was reduced by EGTA but not affected by 8-Br-cAMP suggesting that the fast Ca2(+)-activated K+ current also contributed to the PDS afterhyperpolarizations. Superfusion of the slice with the gamma-aminobutyric acid B receptor (GABAB) antagonists phaclofen or 5-aminovalerate reduced the amplitude of the afterhyperpolarizations during the first 1000 ms but did not affect the late Ca2(+)-dependent component, indicating that a GABAB-mediated K+ inhibitory postsynaptic potential (IPSP) contributed to the PDS afterhyperpolarization. Intracellular injection of Cl- revealed that an early part of the afterhyperpolarizations lasting about 500 ms was Cl(-)-dependent. This component was blocked by superfusion of the slices with bicuculline, suggesting that a GABAA-mediated Cl- IPSP contributed to the PDS afterhyperpolarization.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

PubMed1989

Separation of different types of afterpotentials following penicillin-induced paroxysmal depolarization shifts of neurons in the motor cortex of the rat.

Afterpotentials of penicillin-induced paroxysmal depolarization shifts (PDS) of neurones in the motor cortex of the rat in vivo were investigated with intracellular recordings. Following the PDS, 4 different types of afterpotentials were observed: fast afterhyperpolarizations with an average duration of 600 ms, fast afterdepolarizations with an average duration of 700 ms, slow afterhyperpolarizations with an average duration of 1.9 s and slow afterdepolarizations with an average duration of 1.8 s. The fast and slow afterpotentials could occur in various combinations with the exception of a fast afterhyperpolarization followed by a slow afterdepolarization. Neurones displaying afterdepolarizations had higher resting membrane potentials than those displaying afterhyperolarizations, i.e. the polarity of the afterpotential depended on membrane potential. Experiments with intracellular Cl- injection indicated that the fast but not the slow afterpotentials are associated with an increase in membrane Cl- conductance. The slow afterhyperpolarizations are suggested to result from a calcium-dependent or a synaptically generated potassium current.

Animals↗

PubMed1989

Calcium-dependent potassium current following penicillin-induced epileptiform discharges in the hippocampal slice.

Penicillin-induced paroxysmal depolarization shifts (PDS) are followed by prolonged afterhyperpolarizations of about 2 seconds duration. Intracellular injection of EGTA blocked a late component of the afterhyperpolarizations; an early one lasting up to one second was only slightly reduced by EGTA. It is concluded that afterhyperpolarizations following penicillin-induced PDS comprise different components: an initial one lasting up to one second which is not Ca2+-dependent and a slow one lasting up to two seconds which is caused by a Ca2+-dependent K+ current.

Action Potentials↗

PubMed1988

Membrane currents induced by pentylenetetrazol in identified neurons of Helix pomatia.

After systemic application of pentylenetetrazol (PTZ), mammalian as well as molluscan neurons generate epileptic paroxysmal depolarization shifts. For a further analysis of these potential oscillations the membrane currents induced by local application of PTZ onto identified neurons of Helix pomatia were investigated. Different types of responses were obtained at membrane potentials negative and positive to ca. -30 mV. At holding potentials more negative than -30 mV, PTZ as a rule evoked an inward current, sometimes preceded by a brief outward current. In a few experiments only a solitary outward current was found. The amplitudes of the inward and outward currents increased towards more negative potentials. The inward current was associated with a decrease and the outward current with an increase in membrane resistance. Besides these findings pharmacological and ion substitution experiments indicate that the inward current represents an unspecific current. At holding potentials more positive than -30 mV, PTZ evoked a sequence of currents which was the same in all neurons. This stereotyped current sequence consisted of (i) an early inward current, (ii) an intermediate outward current, and (iii) a late long-lasting inward current. The amplitudes of all these components increased towards more positive potentials with the outward current being particularly enhanced. The early inward current and the following outward current were associated with a decrease and the late inward current with an increase of the membrane resistance. Besides these pharmacological and ion substitution experiments suggest that the early inward current represents a mixed sodium and calcium current, the intermediate outward current a calcium activated potassium current. The late inward current is assumed to be due to a decreased potassium conductance. On the basis of the present results, it may be concluded that the unspecific inward current in the negative potential range is involved in the initiation and the calcium dependent potassium current in the termination of spontaneously occurring paroxysmal depolarization shifts.

Animals↗

PubMed1988

Post-hypoxic action (intention) myoclonus: a clinico-electroencephalographic study.

A patient with post-hypoxic action myoclonus classified as reticular reflex myoclonus was subjected to an electrophysiological investigation. The myoclonic movements involved mainly the legs but could also affect the whole body. Somatosensory evoked responses were not increased and electroencephalography (EEG) was normal when the patient was relaxed. Startle, self-paced movement or movement on command induced repetitive myoclonic jerks preceded and accompanied by repetitive small spikes in the EEG with phase reversal in the midline at the vertex or slightly posterior to it, regardless of the limb moved. The central spiking subsided considerably earlier than the myoclonic jerks as shown by polygraphic recordings. The EEG spikes were also provoked by mere imagination of movement and persisted in spite of a dramatic reduction of myoclonic activity after treatment with clonazepam. The observations suggest that the vertex spiking in post-hypoxic action myoclonus indicates synchronous cortical activation, but is not closely coupled with activation of the Betz cells of layer V where the pyramidal pathway originates.

Aorta, Abdominal↗

PubMed1987

Motor cortical epileptic foci in vivo: actions of a calcium channel blocker on paroxysmal neuronal depolarizations.

Focal epileptiform activity was induced by local application of penicillin to the surface of the rat motor cortex. Neurons located within the epileptic focus displayed typical paroxysmal depolarization shifts (PDS). The participation of membrane calcium currents in the generation of PDS was examined by injecting the quaternized calcium entry blocker D890 into single neurons by iontophoresis or by pressure pulses. After intracellular injections of D890, PDS were depressed in amplitude by up to 55%. In a few cases the depression of PDS following intracellular application of D890 was preceded by a transient increase. Similar increases of PDS amplitude were obtained by injections of the calcium chelator EGTA. Control experiments in preparations without epileptic activity revealed that excitatory potentials elicited by thalamic stimulation and Cl(-)-dependent inhibitory postsynaptic potentials evoked by epicortical stimulation were not affected by intracellular D890. In these experiments successful intracellular drug application was verified by monitoring the transient shift of the Cl(-)-equilibrium potential induced by injection of KCl together with D890. It is concluded that in the penicillin-induced epileptic focus of the motor cortex Ca2+ inward currents participate in the generation of neuronal PDS.

Animals↗

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↗