Riluzole suppresses motor cortex facilitation in correlation to its plasmalevel - A study using transcranial magnetic stimulation

Citation
P. Schwenkreis et al., Riluzole suppresses motor cortex facilitation in correlation to its plasmalevel - A study using transcranial magnetic stimulation, EXP BRAIN R, 135(3), 2000, pp. 293-299
Citations number
29
Categorie Soggetti
Neurosciences & Behavoir
Journal title
EXPERIMENTAL BRAIN RESEARCH
ISSN journal
00144819 → ACNP
Volume
135
Issue
3
Year of publication
2000
Pages
293 - 299
Database
ISI
SICI code
0014-4819(200012)135:3<293:RSMCFI>2.0.ZU;2-1
Abstract
The aim of our study was to measure the effects of the glutamate antagonist riluzole on different parameters of motor excitability, using transcranial magnetic stimulation (TMS) during 7 days of riluzole administration, and t o correlate these effects with riluzole plasma levels. Nine healthy volunte ers received a dose of 100 mg riluzole from day 1 to 7 of the study period. Electrophysiological examinations were performed on day 1 before and 2 h, 5 h and 8 h after riluzole administration, on day 2, day 3 and day 5 before riluzole administration, and on day 8. Plasma samples were taken simultane ously. The excitability of the motor cortex, supraspinal and spinal motor p athways was tested by studying intracortical facilitation and inhibition, t he cortical silent period and motor threshold after TMS, as well as the per ipheral silent period and F-wave amplitudes after electrical peripheral ner ve stimulation. We found a significant reduction of intracortical facilitat ion, which correlated significantly with riluzole plasma levels. To a lesse r extent, intracortical inhibition was enhanced on day I, motor threshold w as increased on day 8 and F-wave amplitudes were reduced. These changes did not correlate with riluzole plasma levels. We conclude that the main effec t of riluzole in vivo is a reduction of intracortical facilitation, which i s closely related to the drug's level in the plasma. The most probable mech anism involves an effect on glutamatergic synaptic transmission.