Journal
JOURNAL OF PSYCHOPHARMACOLOGY
Volume 18, Issue 2, Pages 257-261Publisher
SAGE PUBLICATIONS LTD
DOI: 10.1177/0269881104042631
Keywords
alcohol; electroencephalography; electromyography; GABA; monoamine; NMDA; transcranial magnetic stimulation
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Transcranial magnetic stimulation (TMS) provides new possibilities for studying localized changes in the electrical properties of the human cortex. TMS combined with electromyography (EMG) has revealed that drugs blocking Na+ or Ca2+ channels such as phenytoin, lamotrigin or carbamazepine change the motor threshold without affecting intracortical inhibition or facilitation. Gabaergic agents vigabatrin, Lorazepam, diazepam, baclofen and ethanol do not affect the motor threshold, but increase intracortical inhibition and decrease facilitation. N-methyl-D-aspartate receptor antagonists riluzole, dextromethorphan and memantine have similar effects. Dopamine receptor antagonists such as haloperidol, but not sulpiride, decrease intracortical inhibition and increase intracortical facilitation. Other monoamines, such as serotonin and noradrenaline, may have some modulating effect on the cortical excitability. However, TMS combined with EMG gives only indirect evidence about the excitability of the motor cortex because spinal mechanisms may contribute to the results. Cortical excitability can be studied directly by combining TMS with brain imaging methods such as electroencephalography (EEG). Motor and non-motor areas can be stimulated and subsequent brain activity can be measured. Ethanol has been shown to modulate EEG responses evoked by motor-cortex TMS, the effects being largest at the right prefrontal cortex, meaning that ethanol would have changed the functional connectivity. Furthermore, alcohol decreases amplitudes of EEG responses after the left prefrontal stimulation mainly in anterior parts of the cortex, which may be associated with the decrease of the prefrontal cortical excitability. Taken together, TMS provides a new insight to the actions of central nervous system drugs at the cortical level.
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