. Brain mechanisms and learning, a symposium. Psychophysiology; Learning, Psychology of. 426 BRAIN MECHANISMS AND LEARNING primary responses. In Fig. 7 (CRO recording with bipolar electrodes) some of these modifications can be observed, a slight change in the first spike and a marked increase of amplitude in the following deflections which are precisely those which arc most changed by habituation and conditioned learning (Guzman, Alcaraz and Fernandez-Guardiola, 1957; Hernandez-Peon, Guzman, Alcaraz and Fernandez-Guardiola, 1958). Studies made with monopolar electrodes demonstrated that t
. Brain mechanisms and learning, a symposium. Psychophysiology; Learning, Psychology of. 426 BRAIN MECHANISMS AND LEARNING primary responses. In Fig. 7 (CRO recording with bipolar electrodes) some of these modifications can be observed, a slight change in the first spike and a marked increase of amplitude in the following deflections which are precisely those which arc most changed by habituation and conditioned learning (Guzman, Alcaraz and Fernandez-Guardiola, 1957; Hernandez-Peon, Guzman, Alcaraz and Fernandez-Guardiola, 1958). Studies made with monopolar electrodes demonstrated that the ampli- tude of the first positive deflection, currently designed wave i, remained unmodified or increased slightly. Conversely, positive waves 3 and 4 and negative wave 5 showed a constant and appreciable increase. We wish to NORMAL CAT PRETRIGEMINAL CAT NORMAL CAT. Fig. 6 Oscillographic recording of secondary cortical photic responses Stimulus: flash i/second. Monopolar record in the same cat before (normal) and after mid- pontine section. Five responses in each trace. Downward deflection negative. Time calibration 40 msec. Amplitude calibration 100 \iV. Stress once again that these results were obtained with a desynchronized EEG pattern. In rostropontine animals exactly the same changes were seen, but cortical spindles intcrfereci with the regularity observed in the midpontine cat. Since the potentiation described was achieved after total transsection of the brain stem, we assume that it is the result of the elimination of a tonic inhibitory influence originated behind the lesion and as a consequence of the exaltation of facilitating influences situated above the level of the lesion. Regarding the site of action of these ascending inhibitory influences of bulbar origin, nothing definite can be said at the present time. Neverthe- less, on the basis of some anatomical and neurophysiological data, we may. Please note that these images are extracted from scanned page images th
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