Abstract
Effects of tetanic bursts (200 Hz, 10 pulses) on field potentials elicited by ventral posterolateral thalamic nucleus (VPL) stimulation were investigated in the feline somatosensory cortex. In the first experiments, field potentials elicited by VPL stimulation (test pulse) were simultaneously recorded in the primary (SI) and the secondary (SII) somatosensory cortex in six animals. Potentiation of field potentials recorded in SII was induced by tetanic stimulation of VPL in all six animals, whereas the same tetanic bursts failed to produce significant changes in SI in four of the six animals. The results suggest that plastic changes in somatosensory processing take place in SII rather than SI. In subsequent experiments, features of the potentiation observed in SII were examined in 20 animals. The field potentials were simultaneously recorded at 16 points placed vertically at 150-μm intervals from the cortical surface. The potentiation of field potentials (to 110–170% of control values) observed at depths between 600 and 1350 μm lasted more than 90 min after tetanic stimulation. Poststimulus histograms of multiple-unit activities revealed a long-lasting increase in the number of unit discharges evoked by VPL stimulation. This change in the number of activated cellsis regarded as a cause of potentiation of SII field potentials. In the last session, the effects of N-methyl- d-aspartate (NMDA) receptor antagonists on the potentiation of SII field potentials were investigated. Cortical intraventricular injection of d-2-amino-5-phosphonovalerate (APV) and dl-2-amino-7-phosphonoheptanoic acid (APH) prevented induction of the potentiation in SII. NMDA receptor activation participates in forming this SII potentiation.
Published Version
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