D2 receptor block abolishes theta burst stimulation-induced neuroplasticity in the human motor cortex

Katia Karina Monte-Silva (1) , Diane Ruge (1) , James Teo (1) , Walter Paulus (1) , John C Rothwell (1) , Michael A Nitsche (1)

1 Department of Neurology

Dopamine (DA) is a neurotransmitter with an important influence on learning and memory that is thought to be caused by its modulatory effect on plasticity at central synapses, which depend on activation of D1 and D2 receptors. Transcranial methods of brain stimulation (transcranial magnetic stimulation, TMS; transcranial direct current stimulation, tDCS) lead to after effects on cortical excitability that are thought to resemble LTP/LTD in reduced preparations. In a previous study we found that blockade of D2 receptors abolished plasticity induced by tDCS but had no effect on the facilitatory plasticity induced by paired associative stimulation (PAS). We postulated that this was because tDCS produces a non-focal plasticity at many synapses, whereas PAS produces focal plasticity at selected synapses. The present study in 12 volunteers examined effects of D2 receptor blockade (sulpiride, 400mg) on the LTP/LTD-like effects of theta burst transcranial magnetic stimulation (TBS) in the human motor cortex. Administration of sulpiride blocked both the excitatory and inhibitory effects of intermittent (iTBS) and continuous TBS (cTBS) respectively. TBS promotes a non-focal plasticity at many synapses. Since the reduced response to TBS following sulpiride resembles its effect on tDCS the results support an effect of DA on plasticity, which might be related to the focality of the plasticity induced

Mots clés: Clinical Pharmacology; Clinical Trials; Dopamine; Neuropharmacology; Plasticity; Dopamine receptor; Sulpiride; Motor Cortex; Transcranial magnetic stimulation; Theta burst stimulation

Katia Karina Monte-Silva, Diane Ruge, James Teo, Walter Paulus, John C Rothwell, et al.. D2 receptor block abolishes theta burst stimulation-induced neuroplasticity in the human motor cortex. Neuropsychopharmacology, 2011, ⟨10.1038/npp.2011.100⟩. ⟨hal-00654470⟩