Interactions between short latency afferent inhibition and long interval intracortical inhibition |
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Authors: | Kaviraja Udupa Zhen Ni Carolyn Gunraj and Robert Chen |
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Institution: | (1) Division of Neurology, Department of Medicine, University of Toronto, Toronto, ON, Canada;(2) Division of Brain, Imaging and Behaviour—Systems Neuroscience, Toronto Western Research Institute, University Health Network, MP 13-304, 399 Bathurst Street, Toronto, ON, M5T 2S8, Canada;(3) Division of Brain, Imaging and Behaviour—Systems Neuroscience, Toronto Western Research Institute, University Health Network, 7MC-411, 399 Bathurst Street, Toronto, ON, M5T 2S8, Canada; |
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Abstract: | Peripheral nerve stimulation inhibits the motor cortex and the process has been termed afferent inhibition. Short latency
afferent inhibition (SAI) at interstimulus intervals (ISI) of ~20 ms likely involves central cholinergic transmission and
was found to be altered in Alzheimer’s disease and Parkinson’s disease. Cholinergic and GABAA receptors are involved in mediating SAI. The effects of SAI on other intracortical inhibitory and facilitatory circuits have
not been examined. The objective of the present study is to test how SAI interacts with long interval cortical inhibition
(LICI), a cortical inhibitory circuit likely mediated by GABAB receptors. We studied 10 healthy volunteers. Surface electromyogram was recorded from the first dorsal interosseous muscle.
SAI was elicited by median nerve stimulation at the wrist followed by transcranial magnetic stimulation (TMS) at ISI of N20
somatosensory evoked potential latency + 3 ms. The effects of different test motor-evoked potential (MEP) amplitudes (0.2,
1, and 2 mV) were examined for LICI and SAI. Using paired and triple-pulse paradigms, the interactions between SAI and LICI
were investigated. Both LICI and SAI decreased with increasing test MEP amplitude. Afferent stimulation that produced SAI
decreased LICI. Thus, the present findings suggest that LICI and SAI have inhibitory interactions. |
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