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H D Lux

Publications and source records attributed to H D Lux.

At least 109 records · Page 6Linked to original sources
PubMed1981

Stimulation induced changes in extracellular free calcium in normal cortex and chronic alumina cream foci of cats.

Changes in extracellular [Ca2+]0 (delta Ca) were measured with ion selective microelectrodes in the sensorimotor cortex of cats, surrounding alumina cream lesions and in the contralateral homotopic cortex. The lesions were produced by topical application of alumina cream 6 months-6 years prior to experiments. In normal cortex, stimulus induced reactions of [Ca2+]0 were found to be maximal (up to 0.45 mM) in depths of 200-300 micrometers below the cortical surface. At depths of 600 micrometers and more below the cortical surface, [Ca+2]0 usually rose by up to 0.2 mM above baseline. In the vicinity of the chronic lesion as well as in contralateral cortex [Ca2+]0 fell initially during stimulation in all depths. Close to the lesion delta Ca was as high as 0.8 mM and sites of maximal delta Ca were found to be located deeper in the cortex. About 5 mm from the scar as well as in the contralateral homotopic cortex, maximum delta Ca levels were found in a depth of 200-300 micrometers. It is suggested that Ca2+ dependent mechanisms are involved in epileptogenesis in chronic epileptic foci.

Aluminum↗
PubMed1981

Single channel activity associated with the calcium dependent outward current in Helix pomatia.

A recently improved version of the extracellular patch clamp technique (9, 13) was used to record currents from microscopic membrane areas of Helix neurons with predominant Ca2+ dependent outward currents. Current fluctuations in the patches consisted mainly of frequently interrupted, one-sided steps indicating discrete open-closed state changes of single channels with an ohmic conductance of approximately 19 pS. Frequency of occurrence of the elementary events compares with amplitudes of macroscopic currents during depolarizing voltage steps of varied amplitude. Average delays in appearance of the events vary in line with delayed time courses of the cell's outward current.

Animals↗
PubMed1981

The time courses of intracellular free calcium and related electrical effects after injection of CaCl2 into neurons of the snail, Helix pomatia.

Controlled quantities of 100 mM aqueous CaCl2 solutions were pressure injected into voltage-clamped neurons with a resolution of 10(-11) 1. Ca2+-selective microelectrodes monitored the time course of changes in [Ca2+]i. At a membrane potential of -50 mV CaCl2 quantities in the range of 1% of the cell volume induced an inward current, associated with a conductance increase and having an equilibrium potential between -20 and +20 mV, which accompanied the rise in [Ca2+]i. An artifactual origin of the inward current by the injection procedure or by calcium screening of membrane sites could be excluded. The calcium-induced hyperpolarizing conductance, producing an outward current at -50 mV, followed the inward current and reached maximum during the late decline in [Ca2+]i. In most cases its development was separated from the inward current by an intermediate relative decrease of the membrane conductance. Neither of the two transient conductance increases showed a particular dependence on voltage. Renewed Ca2+ injection quickly decreased the calcium-induced hyperpolarizing conductance for several seconds. Ca2+ injections below 0.05% of the cell volume mostly produced pure outward currents or hyperpolarizing responses. Partial substitution of extracellular CaCl2 by NiCl2 decreased the hyperpolarizing response but not the initial inward current. The immediate effects of increased [Ca2+]i are activation of a depolarizing conductance and the partial block of the late hyperpolarizing conductance. The latter is probably produced through intermediate steps after increasing [Ca2+]i.

Animals↗
PubMed1981

Single channel Ca2+ currents in Helix pomatia neurons.

Unitary Ca2+ currents of TEA injected Helix neurons were recorded in the "Giga seal" situation (6,7) from microscopic membrane patches exposed to 50 mM [Ca2+]o, O [Na+]o, 20 mM [TEA+]o and 2.5 microM [TTX]o. Constant field assumptions yield a channel permeability of 2.9 +/- 1.0 x 10(-14) cm3s-1 corresponding to slope conductances of 5 to 15 pS between 0 and -30 mV. Frequency of occurrence of the units strongly increased with depolarization. Mean open time of the Ca2+ channels was about 3 ms without obvious dependence on voltage. A similar open time was seen with [Ba2+]o, yielding about double the current strength when compared with [Ca2+]o.

Animals↗
PubMed1981

On the action of the anticonvulsant 5,5-diphenylhydantoin and the convulsant picrotoxin in crayfish stretch receptor.

1. The effects of the anticonvulsant drug 5,5-diphenylhydantoin (DPH) and the convulsant drug picrotoxin (PTX) on various membrane properties and GABA-ergic inhibition were investigated in the slowly adapting neurone of the isolated crayfish stretch receptor. The soma was penetrated with two micro-electrodes to allow accurate determination of membrane conductances. 2. Neither DPH nor PTX at 10(-4) M had any significant effect on parameters of the anti- or orthodromic action potential or on the amplitude and duration of post-tetanic hyperpolarization. This suggests that the pharmacological properties of the two drugs are unlikely to be mediated by effects on cationic movements in this preparation. 3. DPH increased the amplitude and duration of the inhibitory post-synaptic potential (i.p.s.p.) within the range 10(-9) to 10(-4) M. The response to ionophoretically applied GABA was similarly prolonged. 4. PTX decreased the amplitude of the i.p.s.p. and prolonged its rising phase within the range 10(-8) to 10(-4) M. The response to ionophoretically applied GABA was similarly depressed. 5. A slow component of fluctuations in the resting potential was accentuated by DPH at 10(-4) M and eliminated by PTX 10(-4) M. This may reflect effects on the random opening and closing of inhibitory channels. 6. We conclude that the action of both drugs is post-synaptic and suggest that DPH decreases the probability of closing, and PTX the probability of opening, of the transmitter-activated channels. 7. The lack of any structural similarity between the two drugs suggests that they modify post-synaptic inhibition at separate sites. These sites appear to be interdependent since analysis of the shift in the DPH dose-response curve by PTX and vice versa, showed neither truly non-competitive nor competitive interaction.

Action Potentials↗
PubMed1980

Transient changes in the size of the extracellular space in the sensorimotor cortex of cats in relation to stimulus-induced changes in potassium concentration.

The time course of local changes of the extracellular space (ES) was investigated by measuring concentration changes of repeatedly injected tetramethylammonium (TMA+) and choline (Ch+) ions for which cell membranes are largely impermeable. After stimulus-induced extracellular [K+] elevations the delta [TMA+] and delta [Ch+] signals recorded with nominally K+-selective liquid ion-exchanger microelectrodes increased by up to 100%, thus indicating a reduction of the ES down to one half of its initial size. The shrinkage was maximal at sites where the K+ release into the ES was also largest. At very superficial and deep layers, however, considerable increases in extracellular K+ concentration were not accompanied by significant reductions in the ES. These findings can be explained as a consequence of K+ movement through spatially extended cell structures. Calculations based on a model combining the spatial buffer mechanism of Kuffler and Nicholls (1966) to osmolarity changes caused by selective K+ transport through primarily K+ permeable membranes support this concept. Following stimulation additional iontophoretically induced [K+]0 rises were reduced in amplitude by up to 35%, even at sites where maximal decreases of the ES were observed. This emphasizes the importance of active uptake for K+ clearance out of the ES.

Animals↗
PubMed1980

[Calcium, potassium and chloride: studies on experimental epilepsy].

Convulsive manifestations are synchronized mass-discharges which are caused by a dysfunction of the dynamic equilibrium between excitation and inhibition. This is caused by a change in membrane activity which increases or decreases the effectiveness of neurotransmitters. We showed the effect of ions on membrane activity and epileptic discharges.

Calcium↗
PubMed1979

Stimulus induced and seizure related changes in extracellular potassium concentration in cat thalamus (VPL).

Extracellular potassium activity (ak) and field potentials (fp) were measured in the nucleus ventro-postero-lateralis (VPL) thalami in order to assess the extent of thalamic participation in cortical seizure activity. Small increases (up to 0.7 mmole/l) or decreases (up to 0.2 mmole/l) in ak were induced by electrical stimulation of the contralateral forepaw. These changes in ak were spatially more limited than the simultaneously recorded fp. Similar observations were made during weak electrical stimulation of the somatosensory cortex and during interictal spikes in a cortical penicillin focus. Large and widespread increases in ak to levels of 11.6 mmoles/l and slow negative fps of 8 mV accompanied seizure generation either in a cortical penicillin focus or during intense repetitive electrical stimulation of the cortical surface. Subsequent to such increases ak fell to subnormal levels. The amplitudes and durations of such undershoots were correlated with the amplitudes of the preceding increases in ak. Sometimes thalamic seizures ceases before cortical epileptic episodes. This resulted in a decrease of cortical EEG amplitudes. After ablation of the sensorimotor cortex seizures in forepaw-VPL could be induced by stimulation of the somatosensory cortex. These results further support the conclusion that specific thalamic nuclei participate in seizure generation and may serve as a subcortical route of seizure spread.

Afferent Pathways↗
PubMed1979

Decrease of inhibitory driving force in crayfish stretch reception: a mechanism of the convulsant action of penicillin.

The effect of penicillin on the evoked IPSP was investigated in the isolated crayfish stretch receptor. The IPSP driving force (IPSP reversal potential minus membrane potential) was reduced in a dose-dependent fashion but, when necessary correction was made for the decrease in resting membrane conductance, the synaptic conductance was only slightly reduced. The possibility that a penicillin-induced intracellular acidification was responsible for the decrease in IPSP driving force is considered.

Animals↗
PubMed1978

Ionic changes during experimentally induced seizure activity.

Changes in intra- and extracellular ionic activity and their relation to generation and termination of seizure phenomena can be studied with the help of ion-selective microelectrodes. Transient changes in extracellular potassium activity (aK) of the cortex regularly accompany paroxysmal activity induced by electrical stimulation and pentylenetetrazol injections or occur within active penicillin and aluminum foci. A rise of aK from baseline levels of about 3 mmoles/l up to ceiling levels of 8--12 mmoles/l, followed by subnormal K activity, is typically found during seizure discharge. Extracellular K accumulation during seizures facilitates the spread into extrafocal regions. Ceiling levels of extracellular aK are characterized by pronounced K reabsorption which is probably a limiting mechanism for the rise in extracellular aK. It may be a consequence of a simultaneous rise in intracellular Na activity that an electrogenic Na--K exchange process is involved in the termination of ictal activity. Seizures are also accompanied by significant reductions in extracellular Ca2+ activity (aCa) to as low as 0.7 mmoles/l (resting aCa 1.25 mmoles/l). There is no critical level of lowered aCa at which a seizure ultimately results. However, unlike changes in aK reductions in aCa can precede ictal activity. Thus, a fall of aCa occurs before the onset of paroxysmal periods during cyclical spike driving in a penicillin focus and before seizures induced by pentylenetetrazol. Ca2+-dependent mechanisms may contribute to seizure generation. In addition to changes in aK and aCa, intracellular chloride activity (aCl) can increase during seizure activity, as a result of an impaired chloride extrusion mechanism, which would lead to a reduced efficacy of inhibitory synaptic transmission and, therefore, to facilitation of seizure generation.

Animals↗
PubMed1977

Calcium-dependent depression of a late outward current in snail neurons.

Neuron cell bodies of Helix pomatia were voltage-clamped with a 300-millisecond depolarizing test pulse (pulse II) delivered I second after a depolarizing conditioning pulse (pulse I). The outward current, measured 200 milliseconds after the onset of pulse. II, exhibited a strong depression that was dependent on the presence of pulse. I. The maximum depression of the pulse II outward current occurred when pulse I voltages lay in the range over which calcium influx is inferred to be greatest; depression of the pulse II current subsided as pulse I potentials approached the putative calcium equilibrium potential. In the presence of extracellular [ethylenebis(oxyethylenenitrilo)]tetraacetic acid (EGTA) or D600, the intensity of the pulse II current became largely independent of pulse I, approaching the values of maximal depression seen in normal Ringer solution. On the other hand, lowering the intracellular pH with extracellular carbon dioxide-carbonate buffer had no measurable effect on the outward currents. Other experiments showed that it is primarily the calcium-dependent, outward-current hump of the N-shaped late current-voltage curve that is depressed by presentation of the conditioning pulse. It was concluded that distinct from an early potassium-activating role, calcium entering during a depolarization leads, during a subsequent depolarization, to a depression of the calcium-activated potassium system that persists for many seconds.

Action Potentials↗