The present studies are designed to further characterise the interneuronal pathway mediating the disynaptic reciprocal group I inhibition between flexors and extensors at the wrist and the elbow levels in humans. In the first series of experiments, we compared the electrical threshold of the reciprocal group I inhibition at the wrist and the elbow level after a prolonged vibration aimed at raising the electrical threshold of the antagonistic activated Ia afferents. Prolonged vibration to the 'conditioning' tendon, which raised significantly the electrical threshold of the inhibition at the elbow level, did not alter it at the wrist level. These results suggest that the dominant input to the relevant interneurones is Ia in origin at the elbow level but Ib in origin at the wrist level. In the second series of experiments, using the spatial facilitation method, we compared the effects on the post-stimulus time histograms of single voluntarily activated motor units of two volleys delivered both separately and together to group I afferents in the nerves supplying the homonymous and antagonistic muscles. At the wrist, but not at the elbow level, the peak of homonymous monosynaptic group I excitation was reduced on combined stimulation, although the antagonistic IPSP was just at the threshold. Because the suppression did not involve the initial bins of the peak, it is argued that the suppression is not due to presynaptic inhibition of Ia terminals, but probably reflects convergence between the homonymous and antagonistic volleys onto the interneurones mediating the disynaptic inhibition. Taken together with the previously reported effects of recurrent inhibition on reciprocal inhibition, these results suggest that inhibition between flexors and extensors is differently organised at the elbow (reciprocal Ia inhibition) and the wrist (non-reciprocal group I inhibition) levels. It is argued that the particular connectivity at the wrist level might correspond to some functional requirements at this ball joint.
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http://dx.doi.org/10.1007/s00221-005-0088-9 | DOI Listing |
BMC Psychol
January 2025
Faculty of Psychology, Naval Medical University, Shanghai, China.
Anxiety is known to significantly impair cognitive function, particularly attentional control. While exercise has been demonstrated to alleviate these cognitive deficits, the precise neural mechanisms underlying these effects remain poorly understood. This study examines the effects of exercise on attentional control in individuals with high trait anxiety, based on attentional control theory, which suggests that such individuals have reduced top-down attention.
View Article and Find Full Text PDFJ Nanobiotechnology
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View Article and Find Full Text PDFVirol J
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Division of Biological Science, Faculty of Science, Prince of Songkla University, Hat Yai, Songkhla, 90110, Thailand.
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View Article and Find Full Text PDFBMC Vet Res
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View Article and Find Full Text PDFBMC Oral Health
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