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We examine a specific candidate for temporal coding of information by spike trains, the occurrence of a temporal firing pattern among some number of neurons that repeats more often than expected by chance. Methods for detection of repeating patterns have long been available, but there are no analytic methods for calculating the expected numbers of repeating patterns to enable assignment of significance to the results from the experimental data. The expected numbers can be calculated by Monte-Carlo methods by repeatedly modifying the original data spike trains. Ideally the surrogates produced by such changes should destroy all patterns and cross-correlations but preserve other aspects of the trains such as rate, interval structure etc. We present here a novel variant of the 'dither surrogate' (Date et al. 1998) and use surrogates generated by this algorithm to evaluate repeating pattern significance in data recorded in monkey motor cortex during behavior. Although we can demonstrate high statistical significance for the excess repetition of some spike patterns, it is not obvious that this has physiological meaning or that such patterns are used for information transfer.
EN
The corticothalamic system acts as a complex network in promoting the various oscillatory patterns (slow oscillation, spindles, delta) that characterize the state of quiet sleep. Local synchronizing mechanisms of any of the above-mentioned oscillations occur at the site of their genesis, thalamic or cortical. These mechanisms are assisted by the wide-range, synchronized occurrence of the cortical slow oscillation, which finally produces the coalesced picture of slow-wave sleep EEG. Multisite, simultaneous intracellular and field potential recordings in cat, as well as EEG recordings in human were performed in order to assess the state of synchrony and the propagation of various sleep rhythms in the corticothalamic network.
EN
Locomotive limb movements were studied in 6 dogs before and after unilateral primary somatosensory cortex (SI)lesion. Single limb movement parameters as well as interlimb coordination in lesioned dogs differed significantly from the parameters measured before surgery.Both left limbs showed a proprioceptive deficit and were more flexed during normal posture and during locomotion.This resulted in prolonged stance in the left fore and in the right hind legs.The symptoms were greatly pronounced in the left fore limb compared to a slightly impaired left hindlimb. Due to the proprioceptive deficit, the dogs did not have satisfactory control over the position of the distal part of the front limb which caused frequent stumbling and even falling. The symptoms were transient and fully compensated after 3-4 weeks.
EN
Propagation of signals from the gastro-intestinal system towards the occipital cortex within sleep-wake cycle was investigated in three monkeys used in the study of sleep impairment in a chronic MPTP model of Parkinsonism. The monkeys differed in motor abilities and sleep structure. One animal (M1) was non-motor disabled and had no sleep alterations. The other two monkeys were severely motor affected, but one (M2) had normal sleep cycles; meanwhile, the other (M3) had no complete sleep cycles. To evaluate the level of sleep and to record cortical evoked responses screw electrodes were implanted over the occipital cortex. Two hours before overnight recordings, two hook electrodes were injected intraperitoneally (under light Ketanest anesthesia) and anchored in gut. Using these electrodes, electric stimulation was applied during slow wave sleep, and in wakefulness. Cortical evoked responses to intraperitoneal stimulation were found indeed during sleep in experiments with M1 and M2. These results show that also in primates with normal sleep pattern visceral information is transferred to the cerebral cortex during slow wave sleep.
EN
The aims of this study were (1) to characterize calcium signaling in rat cortex induced by repeated in vitro application of the glutamatergic agonists L-glutamate, NMDA, AMPA and DHPG, (2) to analyze the influence of transient severe hypobaric hypoxia (180 Torr) administered in vivo on calcium responses to stimulation of glutamate receptors by their agonists, and (3) to evaluate the effects of preconditioning with intermittent mild hypobaric hypoxia (360 Torr), 24 h before the severe hypoxia, on these Ca2+ responses. Intracellular Ca2+ dynamics was studied using the fluorescent probes fura-2 and chlortetracycline to monitor free and bound calcium (Cai and Cab), respectively. In control cortical slices, application of L-glutamate, NMDA and AMPA induced concomitant increases in Cai and Cab, reflecting Ca2+ influx and its intracellular accumulation in neurons. DHPG, an agonist of group I mGlu receptors induced a decrease in Cab accompanied by a rise in Cai levels, indicating Ca2+ mobilization. In cortical slices collected 24 h after severe hypoxia, the responses of Cab to glutamate administration were increased, DHPG-induced shifts were reversed, the increase in Cab after the first application of AMPA was reduced, while after the second, Cab rises were potentiated, and the increases in Cab evoked by NMDA application were slightly suppressed. The alterations of responses in Cab to the selective agonists were completely prevented by preconditioning with mild hypoxia. Our results suggest that protection of normal glutamatergic calcium signaling contributes to tolerance to hypoxia induced by preconditioning.
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