Previous research has provided controversial evidence on the amelioration of visuospatial attention orienting performance induced by nicotine in humans both in studies using smokers as compared to non-smokers, and/or non-smokers to whom nicotine was contingently administered. Similarly, controversial evidence derives from studies on mice administered nicotine while performing the visual attention tasks. Behavioral responses (RTs) and EEG to targets were recorded from 128 scalp sites. Source reconstructions were carried out by means of swLORETA. Although higher (~20ms), benefits of orienting in Sm in the unchallenging condition, as computed by subtracting LC from CC, did not significantly differ from those of nSm. Conversely, orienting costs in the cognitively challenging condition, as obtained by the difference between LCcount and LC, was 40 ms significantly lower than those of the latter group. While the ERP CC-LC difference waves (DW) in the P3 latency range (i.e., 300-500 ms) were of the same magnitude for the two groups, at central/frontal/prefrontal scalp areas the LCcogn-LC P3 DW was significantly larger for nSm than for Sm. swLORETA computed on the LCcount-LC DW in the P3-peak range (i.e., 377-385 msec) for the two groups showed, among others sources, an activation of BA9 and BA46 for Sm, but not nSm. These findings suggest an expansion of the cognitive processing resources, or of working memory capacity, during visual attention orienting, caused by the nicotine, and the crucial role played by the PFC in determining this expansion. These conclusions are supported by haemodynamic studies indicating an activation of BA 9 and 46 areas during a better memory recall performance, and by electrophysiological studies providing evidence for "number" cells in the same areas in monkeys.
Nicotine reduces short-term memory workload costs in visuospatial attentional orienting
Zani A;
2011
Abstract
Previous research has provided controversial evidence on the amelioration of visuospatial attention orienting performance induced by nicotine in humans both in studies using smokers as compared to non-smokers, and/or non-smokers to whom nicotine was contingently administered. Similarly, controversial evidence derives from studies on mice administered nicotine while performing the visual attention tasks. Behavioral responses (RTs) and EEG to targets were recorded from 128 scalp sites. Source reconstructions were carried out by means of swLORETA. Although higher (~20ms), benefits of orienting in Sm in the unchallenging condition, as computed by subtracting LC from CC, did not significantly differ from those of nSm. Conversely, orienting costs in the cognitively challenging condition, as obtained by the difference between LCcount and LC, was 40 ms significantly lower than those of the latter group. While the ERP CC-LC difference waves (DW) in the P3 latency range (i.e., 300-500 ms) were of the same magnitude for the two groups, at central/frontal/prefrontal scalp areas the LCcogn-LC P3 DW was significantly larger for nSm than for Sm. swLORETA computed on the LCcount-LC DW in the P3-peak range (i.e., 377-385 msec) for the two groups showed, among others sources, an activation of BA9 and BA46 for Sm, but not nSm. These findings suggest an expansion of the cognitive processing resources, or of working memory capacity, during visual attention orienting, caused by the nicotine, and the crucial role played by the PFC in determining this expansion. These conclusions are supported by haemodynamic studies indicating an activation of BA 9 and 46 areas during a better memory recall performance, and by electrophysiological studies providing evidence for "number" cells in the same areas in monkeys.I documenti in IRIS sono protetti da copyright e tutti i diritti sono riservati, salvo diversa indicazione.
