Commentary: Deficient inhibition in alcohol-dependence: let's consider the role of the motor system

During an instructed-delay choice reaction time task, suppression of the motor evoked potentials (MEP) elicited by transcranial magnetic stimulation (TMS) in the delay period relative to baseline for the forthcoming movement was significantly weaker in subjects with AD than in healthy control subjects, thus suggesting a storage of neural inhibition in AD patients. [...]inhibitory, mainly GABAergic, transmission plays a key role in the neurochemical mechanisms on the basis of intoxication, tolerance and withdrawal (Koob, 2004). Prolonged ethanol exposition leads to a compensatory “upregulation” of NMDA receptors mediated functions, which is thought to play a crucial role in the occurrence of ethanol tolerance and dependence. [...]AD is characterized by a motor cortical hyperexcitability, which can be secondary to an increased glutamatergic action rather than to a reduced GABAergic activity. [...]it is of crucial importance to correctly identify and define the mechanisms of the impaired inhibition in AD, and the role of the concomitant enhanced glutamatergic transmission cannot be overlooked.