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Biomedical subjects

J Bures

Publications and source records attributed to J Bures.

At least 253 records · Page 14Linked to original sources
PubMed1977

Development of cortical spreading depression and of its transition to the caudate nucleus in rats.

The development of Leão's spreading depression (SD) of electroencephalographic activity was studied in young rats by recording the accompanying slow potential changes (SPC). The propagation rate of cortical SD increased from 1.65 mm/min on Day 15 to 2.6 mm/min on Day 20; the increase of SPC amplitude and the decrease of SPC duration were less evident over the same period. The SD elicited in the caudate nucleus by microinjections of KCl did not spread to neocortex in 20- and 30-day-old rats and transition occurred in only 5% of KCl applications in 40-day-old rats. Application of a pyrrolopyrimidine derivative (BW 57-271; 5 mg/kg) increased the cortico-caudate SD transition of 100% in rats aged 20 days or older and increased the SPC amplitude in both structures. The development of SD parameters can be ascribed to dendritic growth and to the decrease of extracellular space; the cortico-caudate propagation block can be ascribed to morphological immaturity of the transitional zone.

Age Factors↗
PubMed1977

Spreading depression elicited by thermal effects of ultrasonic irradiation of cerebral cortex in rats.

Cortical spreading depression (CSD) was elicited by focused ultrasonic irradiation (800 kHz) of exposed cerebral cortex in anesthetized rats. With the acoustic output of 0.64 W at the probe-tissue contact (3 mm in diameter), CSD was elicited after 28-sec irradiation in normothermic rats. Reduction of cortical temperature to 31 degrees C increased the threshold irradiation time to 82 sec on the average. Ten- to thirty-sec heating of cerebral cortex with a thermode elicited CSD when surface temperature exceeded 47 degrees C. Histological examination of the cortical areas exposed to threshold irradiation revealed a central coagulation lesion surrounded by edema. It is concluded that the ultrasonic irradiation elicits CSD by dissipated heat. Differences in threshold duration of irradiation in hypothermic and normothermic rats were used to compute the threshold temperature which had to be exceeded in the critical volume of cortex in order to start CSD.

Animals↗
PubMed1977

Differential effects of cortical speading depression on epileptic foci induced by various convulsants.

Interaction between epileptic foci and spreading depression (SD) was studied in the cerebral cortex of rats anesthetized with Nembutal. At comparable discharge rates, picrotoxin and penicillin caused complete and partial SD blockade respectively, strychnine and Metrazol were ineffective and Aldactone facilitated SD. Conversely, the duration of SD-induced blockade of epileptic activity was maximal for Aldactone and minimal for picrotoxin. Treatment of the picrotoxin focus with tetrodotoxin (10(-4)M) reduced the discharge rate and reinstated SD propagation into the focus. [K+]e measured with ion-selective K+ electrodes 1 mm below the cortical surface increased to 8 mM in penicillin foci blocking SD and remained below 5 mM in Aldactone foci. It is concluded that the differential effect of various convulsants on SD propagation depends on the potassium concentration in the depth of the focus rather than on the discharge rate or on the mechanism of the the epileptogenic effect.

Animals↗
PubMed1977

Electrophysiological correlates of optokinetic and reversed postoptokinetic nystagmus in the rabbit.

Six rabbits with implanted electrodes in visual cortex, lateral geniculate body, superior colliculus and the mesodiencephalic nystagmogenic centres were exposed to 90 min optokinetic stimulation, followed by 30 to 60 min observation of reversed postoptokinetic nystagmus (RPN) in darkness. The oculographically recorded nystagmus was used to trigger a LINC 8 computer programmed for perisaccadic EEG averaging and for examination of excitability of visual centres by flashes applied at different intervals after the saccade onset. Whereas optokinetic nystagmus (OKN) was accompanied by marked electrical potentials appearing at all recording sites during and for about 100 msec after the saccade, these potentials were considerably attenuated or absent during RPN. Visual evoked responses to flashes applied during the OKN saccades were considerably smaller than responses to flashes delayed by 130-200 msec. No saccadic suppression was observed when the same visual stimuli were applied during RPN saccades in darkness. It is concluded that eye movements generated in the absence of external stimuli during RPN elicit only weak corollary discharge.

Animals↗
PubMed1976

Piracetam-induced facilitation of interhemispheric transfer of visual information in rats.

The effect of Piracetam (UCB 6215, 2-pyrrolidoneacetamide) on learning mediated by transcommissural information flow was studied in hooded rats. Acquisition of monocular pattern discrimination was faster in drug-treated rats (100 mg/kg, 30 min before training) than in untreated controls. Subsequent relearning with one hemisphere functionally eliminated by cortical spreading depression showed that the strength of the primary engram formed under Piracetam in the hemisphere contralateral to the trained eye remained unaffected but that the secondary trace (in the ipsilateral hemisphere) was considerably improved and almost equalled the primary one (savings increased from 20-30% to 50-60%). Learning with uncrossed optic fibers was unaffected by the drug. Interhemispheric transfer of lateralized visual engrams acquired during functional hemidecortication was facilitated by Piracetam administration preceding the five transfer trials performed with the untrained eye open (imperative transfer). Piracetam was ineffective when the trained eye was open during transfer trials (facultative transfer). After a visual engram had been lateralized by 5 days of monocular overtraining, Piracetam facilitated formation of the secondary engram induced by 3 interocular transfer trials. It is concluded that Piracetam enhances transcommissural encoding mechanisms activated in the initial stage of monocular learning and in some forms of interhemispheric transfer, but does not affect the transcommissural readout. This effect is interpreted as a special case of the Piracetam-induced facilitation of the phylogenetically old mechanisms of redundant information storage which improve liminal or subnormal learning.

Animals↗