LONG-TERM CHANGES OF HIGH FREQUENCY COMPONENTS CAUSED BY DIRECT CURRENT STIMULATIONS OVER SOMATOSENSOERY CORTEX
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The multiple unit (of 2 to 10 elements) activity of the somatosensory cortex was studied with the help of autospectral analysis in a rabbit learned with biofeedback technique from changes of the neuronal current discharge frequency. The background activity of neuronal pools is characterized by several basic profiles of frequency spectra. In most neuronal pools, after 4 to 12 min. of stimulation (below-threshold frequency is reinforced), the frequency of neuronal discharges is steadily enhanced, and the number of pain stimulations correspondingly diminishes by 30 to 50% for a few minutes or longer -- the result of learning. The appearance and increase in the autospectra of a relatively higher frequency component (0.35 to 0.6 c/s) during adaptive reorganizations reflects the influence of an effective feedback control; enhancement of the power of oscillations with a 0.05 to 0.07 c/s frequency testifies to a process of search by the system of the state extremum.
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Evoked activity of neurons in the parietal associative cortex in response to adequate and electric stimulations of the thalamic radiation fibers was studied during different phases of sleep. The number of responding neurons decreased during slow--wave and, particularly, during paradoxical sleep. With transition from phase to phase, responsiveness changed mainly in polysensory neurons which gave variable responses with long latencies. Mechanisms of change of responsiveness during the two phases appear to be different. Reliable increase of the inhibitory pause in responses during slow-wave sleep and its decrease during paradoxical sleep may indicate a strengthening of mechanisms of reciprocal inhibition during the first phase, and their weakening during the second phase.
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Somatosensory inputs to the primary sensory cortex (S1) after median nerve stimulation include temporally overlapping parallel processing, as reflected by standard low-frequency somatosensory-evoked potentials (LF-SEPs) and high-frequency SEPs (HF-SEPs), the latter being more sensitive to arousal and to other rapid adaptive changes. Experimental data suggest that cortical HF-SEPs are formed by two successive pre- and postsynaptic components, respectively, generated in the terminal part of thalamo-cortical radiation (early burst) and in specialized neuronal pools within S1 (later burst). In eight healthy subjects, slow (1 Hz) or rapid (10 Hz) repetitive transcranial magnetic stimulations (rTMS), which are known to induce opposite changes on cortical excitability, applied on S1 did not modify LF-SEPs, while HF-SEPs showed a series of dissociate changes in the early and later high-frequency burst, moreover occurring with a different time-course. Slow rTMS caused an immediate and lasting decrease of the later burst activity, coupled with an immediate increase of the earlier part of the burst, suggesting that inhibition of cortical excitability triggered opposite, compensatory effects at subcortical levels; rapid rTMS induced a delayed increase of later HF-SEPs, leaving unaltered the earlier subcortical burst. Findings causally demonstrate that LF- and HF-SEPs reflect two distinct functional pathways for somatosensory input processing, and that early and late high-frequency burst do actually reflect the activity of different generators, as suggested by experimental data. Possible underlying neurophysiological phenomena are discussed.
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Shifts of steady potentials (SP) in the cerebral cortex of rats were studied during formation of stationary excitation foci by low-frequency electric stimulation and application of penicillin. The dynamics of SP shifts reflects summary effect of depolarization and hyperpolarization processes, actively involved in each cycle of excitation. As a result of functional heterogeneity of different cortical areas, a spontaneously appearing wave of spreading depression (SD) may be transformed into a spiral wave, actively influencing the dynamics of excitation resulting from direct stimulation of the cortex. The cause of long-term inhibition of paroxysmal activity foci may be repeated generation of slow negative waves of SD persisting in conditions of rapid restoration of cortical ability to conduct SD.
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Changes in cortical excitability incident to brain cooling have been examined on several occasions, utilizing spontaneous ECG,1-3evoked response4-6or cortical threshold for seizure discharge.7-9However, the effects of cold upon slower components of cortical potentials have not been studied, owing largely, we believe, to the general use of capacity coupled amplifiers which attenuate slow frequencies. In earlier studies from this laboratory direct current (d.c.) recording has been utilized, permitting accurate recording of slow changes in cortical potential. Evoked potentials studied in this fashion have been (1) the direct cortical response recorded from a cortical site immediately adjoining a surface-stimulating electrode; (2) recruiting response to repetitive stimulation of the midline thalamus; (3) evoked response of visual cortex activated by brief shocks to optic nerve or light flashes to retina.10-13Graphically, the usual short-latency, fast component of evoked response is followed by a slower component of longer
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