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1. Responsiveness within the hand region of the second somatosensory area of cortex (SII) was investigated in the marmoset monkey (Callithrix jacchus) in association with cooling-induced, reversible inactivation of the primary somatosensory area, SI. The aims were to determine whether thalamocortical systems in this primate species are organized according to a serial scheme in which tactile information is conveyed from the thalamus to SI and thence to SII as the next hierarchical level of processing and to establish whether primates are fundamentally different, in this respect, from mammals in which tactile information is conveyed in parallel from the thalamus to both SI and SII. 2. Inactivation of the SI had area was achieved when the temperature at the face of the silver cooling block over this SI region was lowered to < or = 13 degrees C. Inactivation was confirmed by abolition of the SI surface potential evoked by a brief tap stimulus to the hand and by the abolition of responsiveness in single SI neurons located beneath and around the edge of the block. 3. The effect of SI inactivation on SII-evoked potentials was investigated in 20 experiments by simultaneous recording of the SI- and SII-evoked potentials. The SII response was never abolished and was unchanged in the majority (12/20) of experiments. In the remainder, the SII-evoked potentials underwent a reduction in amplitude that was usually < 30% but never > 50%. 4. Tactile responsiveness was examined quantitatively in 47 individual SII neurons of different functional classes before, during, and after the inactivation of SI. Controlled tactile stimuli consisted of trains of sinusoidal vibration or rectangular pulses delivered to the glabrous or hairy skin of the hand. 5. Thirteen of the 47 SII neurons (28%) were unaffected in their response levels in association with SI inactivation. The remaining 34 SII neurons underwent some reduction in responsiveness, but in only 6% (3/47) was responsiveness abolished by SI inactivation. As the same range of functional classes of tactile neurons were represented among the affected and unaffected SII neurons, there was no evidence for a differential susceptibility among SII tactile neurons to the effect of SI inactivation. 6. Where reductions in amplitude of the SII-evoked potential or in response levels of SII neurons were observed, the effects were not attributable to direct spread of cooling from SI to the SII hand area as there was no cooling-induced prolongation of either the evoked potential or spike waveform in SII, an effect that is known to precede cooling-induced reductions in responsiveness. 7. These lines of evidence indicate that reductions in SII responsiveness in association with SI inactivation may be attributable to a loss of a background facilitatory influence rather than to a blockage of a component of peripheral input that comes over a putative serial path to SII via SI. First, as SI was cooled, there was a progressive increase in latency and time course of the SI responses before their disappearan...

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In three experiments, the human blink response to 50-msec 105-dB white noise was markedly reduced by prior stimulation with weak tones, either 20 msec long or coextensive with lead intervals of 30 to 240 msec. Although the inhibitory effect was greater with a 70-dB than with a 60-dB lead tone, it was not affected by increasing the lead-tone duration beyond 20 msec. At lead intervals of 30 and 60 msec, the latency of blink onset was also reduced by prestimulation, and this effect was greater with the longer lead tones. Neither effect was an artifact of responding to the lead tone itself. The simultaneous occurrence of an inhibitory change in magnitude and a facilitatory change in latency, and the differential influence of lead stimulus duration, suggest that the magnitude and latency modifications involve different neural mechanisms with different time constants.