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Biomedical subjects

J Bures

Publications and source records attributed to J Bures.

At least 217 records · Page 12Linked to original sources
PubMed1982

Stimulation induced recurrent epileptiform discharges block cortical and subcortical spreading depression in rats.

Blockade of the spread depression [SD] in chemically or electrically stimulated areas of the cerebral cortex was analyzed in a series of experiments performed in 40 curarized, locally anaesthetised rats. Longlasting stimulation of the cerebral cortex (0.5 to 1.7 mA, 6 Hz, 0.1 ms) elicited recurrent episodes of enhanced evoked potentials propagating to remote cortical areas [Co], the caudate nucleus [Cd], the hippocampus [Hi] and the thalamus [Th] and was accompanied by marked slow potential shifts (4-6 mV amplitude, 2-3 min duration, at 2-5 min intervals]. The projected discharge interfered with SD initiation and propagation in all the examined structures. The SD blockade was most pronounced during the episodes and almost absent in the intervals between them. The block was manifested by reduced amplitude and duration of the slow potential of SD. Pentobarbital [20 mg/kg] suppressed the recurrent discharges and eliminated the corresponding SD blockade. Recurrent excitability changes induced by Cd and Th stimulation elicited similar effects but the threshold was higher in Cd and Th than in Co. SD was less effectively blocked by the projected discharge than by stimulation of the same structure, particularly in the vicinity of the recording electrodes, where the blockade could be observed even under pentobarbital. The SD blockade outlasted stimulation by a considerably longer period of time in Th (about 10 min) than in the Cd (about 3 min). The onset of stimulation and the projected episodes sometimes elicited SD waves but SD blockade prevailed with continued stimulation. The present findings support the hypothesis that excessive neural activity increases the potassium clearance and thus prevents the autoregenerative accumulation of potassium ions, mediating SD propagation.

Animals↗
PubMed1982

[Electric phenomena in the pigeon telencephalon during pecking].

Electrographic correlates of pecking were studied in 50 unrestrained pigeons. The motor potentials appeared earlier (40 msec before pecking) in the Wulst than in the neo-, ecto- and archistriatum (18-28 msec before pecking). Out of 280 examined neurons, 83% were activated and 6% inhibited by pecking. The pre- and postpecking histograms indicated a rostrocaudal activation of the telencephalon. The amplitude of evoked responses to flashes changed in the tectum during pecking.

Animals↗
PubMed1982

Electrical stimulation of chemical blockade of vestibular nuclei can serve as the unconditioned stimulus in the conditioned taste aversion paradigm.

Nausea of vestibular origin can be used instead of poisoning in the conditioned taste aversion (CTA) paradigm. In an attempt to establish the forms of vestibular stimulation best suited for inducing CTA in rats, effectiveness of 2 h rotation (Exp. 1) was compared with tonal asymmetry elicited by unilateral microinjection of 5.0 microliters of 25% KCl into the vestibular complex (Exp. 2), by unilateral electrical stimulation of vestibular nuclei (100 Hz, 1 ms, 100-200 microA, 15 min--Exp. 3) or by 10 min polarization of labyrinth through electrodes inserted in the external auditory meati (Exp. 4). Nystagmus, deviation of the head and leaning towards the blocked and away from the stimulated side were typical symptoms. When the above stimuli were applied within 10 min after saccharin drinking, galvanic stimulation was ineffective, but electrical stimulation or chemical blockade of vestibular nuclei elicited marked CTA to saccharin, considerably stronger than CTA induced by rotation. It is concluded that direct interference with the activity of vestibular nuclei elicits CTA more effectively than the stimulation of the labyrinth and is, therefore, well suited for the analytical research into the mechanisms of CTA.

Analysis of Variance↗
PubMed1981

Unit activity changes elicited in amygdala and neocortex of anaesthetized rats by intraperitoneal injection of lithium chloride.

Intraperitoneal injection of 0.15 M LiCl (2% body weight) to anaesthetized rats elicited, after a 6 min latency, discharge of about 50% units i basolateral amygdala (n = 27). The activation lasted for 15 min on the average. Cortical neurones were not affected by the LiCl injection. It is suggested that the amygdalar reaction to LiCl administration may account for the association of the gustatory trace with the visceral signals of poisoning which mediates acquisition of conditioned taste aversion under anaesthesia.

Amygdala↗
PubMed1981

Cerebral [K+]e increase as an index of the differential susceptibility of brain structures to terminal anoxia and electroconvulsive shock.

The time course of the [K+]e increase elicited by terminal anoxia or by electroconvulsive shock (ECS) was compared in various parts of the rat brain. The [K+]e was measured with ion-selective microelectrodes stereotaxically introduced into the target area. Respiration arrest induced in anesthetized rats a slow [K+]e increase to about 6--10 mM followed by an abrupt rise to 30--50 mM (doubling time 5--14 sec) in the neocortex, hippocampus, amygdala, caudate nucleus, and thalamus. In the reticular formation, zona incerta, and lateral hypothalamus the second phase of [K+]e increase was much slower (doubling time 30--50 sec) and lacked the autoregenerative character. Trans-pinnate ECS (50 Hz, 0.5 sec, 80 mA), administered to rats immobilized with gallamine triethiodide, elicited a generalized [K+]e increase of the spreading depression type in neocortex and hippocampus (40 mM) as well as in the caudate nucleus and thalamus (20--30 mM), followed by slow [K+]e decrease (half-time 40--60 sec). Much lower ECS-induced [K+]e increase (to 5--6 mM) was observed in the reticular formation, zona incerta, lateral hypothalamus and, surprisingly, in the amygdala. It is concluded that the autoregenerative [K+]e release of spreading depression type develops in structures with high density of membranes reacting to partial depolarization by increased sodium permeability.

Animals↗
PubMed1981

Reaching-related potentials in caudate nucleus and cerebellum of rats.

Electrical correlates of the lateralized reaching reaction was studied in rats with implanted electrodes. Averaged event-related potentials (ERPs) in the cerebellar dentate nucleus consisted of a negative wave coinciding with reach onset and followed 70 msec later by a positive deflection. The most prominent component of the more variable caudate ERPs was a negative wave culminating 60--120 msec after reach onset. The positive and negative ERP deflections corresponded to inhibitory and excitatory reactions respectively, at the single neuron level.

Action Potentials↗
PubMed1981

Role of olfactory cues in the radial maze performance of rats.

Contribution of the smell of food and odor trails to the performance of rats in a 12-arm radial maze was assessed in 12 rats. Choice accuracy was increased rather than decreased by omission of bait (Experiment 1). Maze arms entered during the first 6 choices in the 12-arm radial maze were randomly re-entered during the subsequent 6 choices in a parallel maze assembled from the same maze segments (Experiment 2). Error incidence increased from 1.33 to 1.94 per trial but remained below chance (3.0) when after 6 choices in radial maze A the rat completed the trial in an identical and similarly located maze B (Experiment 3). It is concluded that odor cues alone do not guide the animal's choice, but that they contribute to the complex sensory information essential for correct performance.

Animals↗
PubMed1981

Correlation analysis of neuronal interaction in the motor cortex of rats during performance of a discrete instrumental reaction.

Unit activity was recorded in 7 rats trained to reach into a narrow feeder for food. Capillary microelectrodes were inserted with a head-mounted microdrive into the motor cortex contralateral to the preferred forepaw. Recordings of pairs of identifiable units were processed with the LINC 8 computer programmed for detection and classification of spikes, compilation of perireach histograms (+/- 512 ms) and construction of auto- (64 ms) and crosscorrelation (+/- 32 ms) histograms. Perireach histograms revealed activity changes (mostly of the excitatory type) in 82% of examined neurons (n = 28). Significant crosscorrelation was found in 8 of 14 pairs of neurons recorded for about 1 h. Most crosscorrelograms showed symmetric inhibitory troughs, lasting for 6 to 15 ms and better expressed in the +/- 512 ms perireach interval than during periods of spontaneous activity. Whereas symmetric crosscorrelograms (n = 6) indicate a shared inhibitory input, asymmetric crosscorrelograms (n = 2) suggest more direct interaction between the recorded neurons. Significant crosscorrelations were found more frequently when both neurons of the pair displayed significant perireach reactions. It is concluded that reaching is accompanied not only by characteristic excitatory and inhibitory reactions of individual neurons but also by modified neural coordination probably due to shared cerebellar and basal ganglia inputs.

Action Potentials↗
PubMed1980

Electrophysiological correlates of the reversed postoptokinetic nystagmus in the rabbit: activity of vestibular and floccular neurons.

Unit activity changes accompanying the optokinetic nystagmus (OKN) and reversed postoptokinetic nystagmus (RPN) in the rabbit were examined in 180 vestibular and floccular neurons. After initial charging of the RPN generator by 60-min optokinetic stimulation, a sequence of 1-min optokinetic stimulation (OKN) followed by 1-min darkness (RPN) and 1-min illumination of the stationary optokinetic drum (L), was cycled while corresponding unit activity changes were recorded during 3--5 cycles and evaluated with a computer. About 50% of vestibular neurons (type A) increased their activity during OKN and/or decreased it during RPN with respect to the L period, whereas 24% (type B) reached in a reciprocal manner. The remaining neurons were either unaffected or responded in an atypical way. Most floccular neurons (75%) were activated during ipsilateral optokinetic stimulation, but were not significantly affected by RPN. It is suggested that the neural trace of RPN develops in the vestibular complex and vestibulocerebellum as a part of the process compensating for the effect of continued optokinetic stimulation.

Animals↗
PubMed1980

Cortical (K+)e and the stimulation induced blockade of spreading depression in the rat cerebral cortex.

Waves of spreading depression (SD) no not penetrate into an electrically stimulated (10 Hz, 0.05 msec, 20-30 V) cortical area of rats. The blockade develops slowly and is proportional to the (K+)e increase in the stimulated cortex. After cessation of stimulation, (K+)e returns to the resting level within 20-30 sec, but the SD blockade continues for 2-3 min. It is suggested that the stimulation induced activation of a metabolic pump disrupts the autoregenerative mechanism of SD propagation by enhancing K+ reabsorption into neurons.

Animals↗
PubMed1980

Blockade of cortical spreading depression in electrically and chemically stimulated areas of cerebral cortex in rats.

Penetration of cortical spreading depression (SD) into epileptic foci established in the cerebral cortex by penicillin or Metrazol and into electrically stimulated cortical regions was studied in anaesthetized rats. SD suppressed the activity of penicillin foci with low rates of interictal discharge (0.3 Hz) but did not invade more active foci (1 Hz) or foci triggered by electrical stimulation (1-3 Hz). Metrazol foci did not block SD propagation unless stimulated at 6-10 Hz. Repetitive direct cortical responses elicited by 0.05-0.1 msec pulses blocked SD propagation when applied at 6-10 Hz for 5-20 min. The SD blockade covered an area 3-5 mm in diameter around the bipolar stimulating electrodes. The block outlasted the stimulation for several minutes but was fully reversible. New stimulation reinstated the SD blockade after a shorter latency and at lower stimulus intensities and rates. Interaction of the blocked cortical area and SD resulted in anomalous SD propagation, characterized by reentry or circle waves, returning through or around the stimulated region to the recovered cortex. The dynamics of the onset and offset of blocking suggests that SD propagation is prevented by enhanced K+ reabsorption which rapidly removes the K+ ions penetrating the stimulated area from the SD wave front. The interactive phenomena, particularly SD circulation around an epileptic focus, may account for periodic changes of ictal and interictal activity found in some types of focal epilepsy.

Animals↗