26779
document
Modulation of human motor cortex excitability by single doses of amantadine . Amantadine-sulfate has been used for several decades to treat acute influenza A , Parkinson 's disease ( PD ) , and acute or chronic drug-induced dyskinesia . Several mechanisms of actions detected in vivo/in vitro including N-methyl-D-aspartate ( NMDA ) -receptor antagonism , blockage of potassium channels , dopamine receptor agonism , enhancement of noradrenergic release , and anticholinergic effects have been described . We used transcranial magnetic stimulation ( TMS ) to evaluate the effect of single doses of amantadine on human motor cortex excitability in normal subjects . Using a double-blind , placebo-controlled , crossover study design , motor thresholds , recruitment curves , cortical stimulation-induced silent period ( CSP ) , short intracortical inhibition ( ICI ) , intracortical facilitation ( ICF ) , and late inhibition ( L-ICI ) in 14 healthy subjects were investigated after oral doses of 50 and 100 mg amantadine with single and paired pulse TMS paradigms . Spinal cord excitability was investigated by distal latencies and M-amplitudes of the abductor digiti minimi muscle . After intake of amantadine , a significant dose-dependent decrease of ICF was noticed as well as a significant increase of L-ICI as compared to placebo . The effect on ICF and L-ICI significantly correlated with amantadine serum levels . ICI was slightly increased after amantadine intake , but the effect failed to be significant . Furthermore , amantadine had no significant effects on motor thresholds , MEP recruitment curves , CSP , or peripheral excitability . In conclusion , a low dose of amantadine is sufficient in modulating human motor cortex excitability . The decrease of ICF and increase of L-ICI may reflect glutamatergic modulation or a polysynaptic interaction of glutamatergic and GABA-ergic circuits . Although amantadine has several mechanisms of action , the NMDA-receptor antagonism seems to be the most relevant effect on cortical excitability . As L-ICI can be influenced by this type of drug , it may be an interesting parameter for studies of motor learning and use-dependent plasticity .
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Intervention_Pharmacological
amantadine
26781
Intervention_Pharmacological
Amantadine-sulfate
26782
Intervention_Physical
transcranial magnetic stimulation ( TMS )
26783
Intervention_Pharmacological
amantadine
26784
Intervention_Control
placebo-controlled
26785
Intervention_Pharmacological
oral doses of 50 and 100 mg amantadine
26786
Intervention_Pharmacological
single and paired pulse TMS paradigms
26787
Intervention_Pharmacological
amantadine
26788
Intervention_Pharmacological
amantadine
26789
Intervention_Pharmacological
amantadine
26790
Intervention_Pharmacological
amantadine
26791
Intervention_Pharmacological
amantadine
26792
Intervention_Pharmacological
amantadine
26793
Outcome_Physical
Modulation of human motor cortex excitability
26794
Outcome_Physical
N-methyl-D-aspartate
26795
Outcome_Mental
antagonism
26796
Outcome_Physical
cortex
26797
Outcome_Physical
Spinal cord excitability
26798
Outcome_Physical
M-amplitudes
26799
Outcome_Physical
ICF
26800
Outcome_Physical
L-ICI
26801
Outcome_Physical
ICF
26802
Outcome_Physical
L-ICI
26803
Outcome_Physical
ICI
26804
Outcome_Physical
motor thresholds
26805
Outcome_Physical
MEP recruitment curves
26806
Outcome_Physical
CSP
26807
Outcome_Physical
peripheral excitability .
26808
Outcome_Physical
modulating human motor cortex excitability
26809
Outcome_Physical
ICF
26810
Outcome_Physical
L-ICI
26811
Outcome_Physical
cortical excitability
26812
Outcome_Physical
L-ICI
26813
Participant_Condition
normal
26814
Participant_Sample-size
14
26815
Participant_Condition
healthy