PubMed Health⌕ Search

Biomedical subjects

D V Lewis

Publications and source records attributed to D V Lewis.

At least 73 records · Page 4Linked to original sources
PubMed1981

Diphenylhydantoin reduces the outward current of the action potential in Aplysia.

Diphenylhydantoin (DPH) has been shown to prolong the repolarization phase of action potentials in Aplysia and to reduce the spike after hyperpolarization. We voltage-clamped somata of Aplysia giant neurons and measured the action potential currents to determine what alterations might be responsible for the prolonged repolarization and reduced undershoot. DPH did not affect the peak inward current; however, it did reversibly reduce the outward current at concentrations of 38 microM or greater. The data indicate that DPH reduced the voltage sensitive potassium conductance rather than the 'A' current or the calcium activated potassium conductance. These changes in outward current would explain the prolonged action potentials and reduced afterhypolarization seen with DPH in Aplysia.

Animals↗
PubMed1981

Diphenylhydantoin enhances early adaptation in Aplysia giant neurons.

Diphenylhydantoin effect on excitability in the molluscan giant neuron was investigated. This model of neuronal excitability was convenient for investigating drug mechanisms because the giant somata of these neurons have multiple current systems and can be voltage clamped. Current and voltage clamp methods were used to quantitate firing frequency and the slow membrane currents associated with changes in firing rate. Diphenylhydantoin enhanced the early rapid deceleration of firing of the cell in response to depolarizing current and blocked an early show inward current.

Action Potentials↗
PubMed1977

Potassium clearance and reactive gliosis in the alumina gel lesion.

Potassium accumulation or impaired potassium clearance has been hypothesized to contribute to epileptogenesis in gliotic epileptogenic foci. To test this hypothesis, potassium clearance rates following direct cortical stimulation were measured in the cortex of monkeys rendered epileptic by the injection of alumina gel into the motor area. Reactive gliosis at the sites in which potassium clearance was measured was then quantitated histologically and compared with potassium clearance rates. Dense gliosis was associated with slowed potassium clearance, although the base-line potassium level appeared no different in actively epileptogenic areas or gliotic areas compared with normal areas. Possible mechanisms and significance of slowed potassium clearance in the alumina focus are discussed.

Aluminum↗
PubMed1977

The electroencephalogram in pediatric practice: its use and abuse.

Utilized appropriately, the EEG is a helpful diagnostic tool; however, it is currently much abused and much overutilized. Understanding its limitations and its usefulness may lead to less frequent but more appropriate requests for EEGs. Realization that the EEG alone neither diagnoses nor rules out epilepsy and that it is not crucial in the diagnosis or management of "minimal brain damage" should decrease the utilization and abuse of the procedure.

Brain Edema↗
PubMed1976

The contribution of local blood flow to the rapid clearance of potassium from the cortical extracellular space.

The transport of potassium to the blood stream following stimulation of the cortex in cats is evaluated by means of a potassium sensitive microelectrode technique. Potassium levels are measured in cortical veins, the sagittal sinus and the extracellular space during and after both pharmacological and electrical stimulation of the cortex. It is concluded that the potassium transport to the blood stream is not a significant factor in the rapid clearance of potassium from the extracellular space following stimulation.

Animals↗
PubMed1976

NADH fluorescence, [K+]0 and oxygen consumption in cat cerebral cortex during direct cortical stimulation.

NADH fluorescence, sagittal sinus blood flow and sinus hemoglobin saturation were monitored simultaneously during direct cortical stimulation of a wide area of the anterior and mid suprasylvian and marginal gyri. The area monitored flurorometrically was located within the area apparently drained by the sinus, so that the flurometric changes could be correlated with oxygen consumption changes calculated from the sinus flow and saturation values. The onset and peak values of calculated oxygen consumption and NADH fluorescence changes usually occurred within several seconds of one another and high, significant (r greater than 0.9 and P less than 0.01) correlations were found between the maximum changes in both parameters following stimulation. The relation of cortical [K+]0 changes to oxygen consumption changes was also explored; again the magnitude of [K+]0 changes and calculated oxygen consumption changes correlated well. The demonstrated agreement between fluorometric and direct (sinus cannulation) measurements of oxidative metabolism reinforces the interpretation of in situ cortical fluorescence changes as indicative of changes in oxygen consumption rate

Animals↗
PubMed1975

NADH fluorescence and [K+]o changes during hippocampal electrical stimulation.

1. Short (2 s) trains of stimuli were applied to the dorsal hippocampal surface of cats, producing an increase in [K+]o and a decrease in NADH fluorescence (the latter being indicative of an increase in tissue oxygen utilization). 2. The [K+]o rose rapidly during stimulation (delta[K+]o values from 1 to 6 mM) with larger stimulus currents producing larger changes. The time course of the poststimulus decline of [K+]o was an exponential decay function, with T 1/2 values varying from 1.3 to 6.9s, and independent of the magnitude of the delta[K+]o. Consistent undershoots of [K+]o occurred following stimuli causing less than 1 mM change in [K+]o. 3. The maximum depression of fluorescence and the time integral of the fluorescence changes following each stimulus train were both highly correlated with the total increase of [K+]o occurring during the stimulus train. 4. Application of several stimulus trains in close succession resulted in more rapid potassium reuptake following the later trains and an unusually large undershoot after the last train. Concomitantly, there was a progressive decrease in the fluorescence level. 5. When afterdischarges were induced by prolonged (less than 2 s) stimulation, larger and more sustained increases in [K+]o and decreases of fluorescence were observed, and there was some indication that afterdischarges were followed by accelerated reuptake of extracellular potassium.

Animals↗
PubMedDate not supplied

Effects of diisopropyl phosphorofluoridate (DFP) on CA3 and CA1 responses in rat hippocampus.

Diisopropyl phosphorofluoridate (DFP), an insecticide, is a potent anticholinesterase that binds essentially irreversibly to acetylcholinesterase, resulting in severe, acute neurologic pathology, and less severe, but longer-lasting, delayed neuropathy. We report here on the short-term effects of bath-applied DFP on extracellularly recorded responses from CA3 and CA1 of rat hippocampus. Exposure to 10 microM DFP evokes low amplitude, spontaneous bursts in CA3 generally within 10 minutes, and the bursting does not reverse with washing. The CA1 neuronal population usually bursts synchronously with CA3, but the population events are of low amplitude and sometimes not detectable, implying a differential sensitivity to DFP. These effects were partially blocked by the muscarinic antagonist atropine, while the cholinergic antagonist gallamine had little effect. Also, the reversible anticholinesterase physostigmine could, within temporal limits, protect slices from DFP's effects, implicating the cholinergic system as the probable mediator in the first stages of DFP-induced epileptogenesis.

Acetylcholine↗
PubMedDate not supplied

Seizure activity in vitro: a dual focus model.

Recently, we have reported that the exposure of hippocampal slices in vitro to artificial cerebrospinal fluid (ACSF) containing no added magnesium results in ictal-like (ictaform) activity in area CA3 of the hippocampal formation. Other reports describe such activity in slices of entorhinal cortex (EC) under similar conditions. Because of the close interrelationship between the entorhinal area and the hippocampal formation, we have begun to study, in vitro, brain slices which contain both the entorhinal cortex and the hippocampal formation. In these slices, we have found that, in the magnesium-free (0-Mg2+) model, there is good electrical communication between area CA3 and the EC. Simultaneous recordings of the activity in the EC and CA3 showed that, when the circuitry linking the two areas was intact, the EC tended to initiate the ictaform activity and lead CA3. However, late in the event, CA3 could lead EC. Furthermore, interictal-like spontaneous bursting in CA3 led to a disorganized pattern of ictaform activity in EC. Finally, when the EC was separated from the hippocampal formation, both areas were capable of ictaform activity which was temporally unrelated. This model provides the opportunity to explore the relationship between two epileptogenic areas in vitro, and to compare and contrast the morphology of the ictaform activity present in both structures. As such, it may prove valuable in both pharmacological and physiological studies of seizure disorders.

Animals↗
PubMedDate not supplied

The effects of baclofen and pertussis toxin on epileptiform activity induced in the hippocampal slice by magnesium depletion.

Bathing hippocampal slices in artificial cerebrospinal fluid without magnesium elicits repetitive, long ictal-like discharges termed ictaform events. The ictaform events are separated by interictal periods that are initially silent with no interictal bursts. Interictal bursts appear in the later part of the interictal periods and intensify just before the next ictaform event. The GABAB agonist, baclofen, entirely suppressed interictal bursts during the interictal periods and produced a dose-dependent prolongation of the interictal period. Conversely, in slices pretreated with pertussis toxin to reduce the GABAB neurotransmission, interictal bursts were greatly increased, often occupying the entire interictal period, although the total duration of the interictal periods was not affected. Pertussis toxin pretreatment also lengthened the ictaform events. These opposing effects of baclofen and pertussis toxin suggest that GABAB neuro-transmission is important in regulating both the occurrence of interictal bursts in the interictal period, as well as the duration of ictaform events in the low magnesium model of epileptiform activity.

Animals↗