Inhibitory circuits and the nature of their interactions in the XXXX motor cortex a pharmacological TMS study.

@entity1 @entity851 @entity3175 @entity1246 @entity1162 @entity1772
Inhibitory circuits are crucial in modulating corticospinal output in the primary motor cortex (M1). Relatively little is known about how these inhibitory circuits interact. Here we measured three forms of inhibition in M1 by paired-pulse transcranial magnetic stimulation: @entity851 ( @entity851 ), @entity1162 ( @entity1162 ) and @entity851 ( @entity851 ). We specifically tested their interactions under pharmacological challenge with a single oral dose of @entity3175 , a positive allosteric modulator of the @entity1246 type A receptor ( @entity1246 A R), or @entity1772 , a specific agonist at the @entity1246 type B receptor ( @entity1246 B R). Motor evoked potentials were recorded bilaterally from the first dorsal interosseous muscle in eight right-handed healthy volunteers. @entity3175 enhanced @entity851 , and @entity1772 produced a trend towards enhanced @entity1162 , corroborating the view that @entity851 reflects inhibition mediated by the @entity1246 A R, and @entity1162 very likely reflects inhibition mediated by the @entity1246 B R. The pharmacology of @entity851 was inconclusive and warrants further investigation. Findings strongly suggest that @entity851 , @entity1162 and @entity851 recruit three distinct inhibitory circuits in the @entity1 M1. The interactions between @entity851 and @entity851 , @entity1162 and @entity851 , and @entity1162 and @entity851 were all negative, that is @entity851 suppressed @entity851 , and @entity1162 suppressed both @entity851 and @entity851 . @entity3175 partially restored @entity851 in the presence of @entity1162 , while all other interactions remained unaffected by @entity3175 or @entity1772 . It will be argued that the negative interactions between @entity851 and @entity851 , @entity1162 and @entity851 , and @entity1162 and @entity851 are most likely due to presynaptic @entity1246 B R-mediated autoinhibition.
