The effect of methylphenidate on auditory information processing in healthy volunteers: a combined EEG/MEG study

Abstract

The lack of effect of MPH on either MMN or MMNm suggests no association between catecholaminergic activities and MMN generation. However, our findings imply that MPH may change the neural bases of auditory information processing such as the early stimulus evaluation reflected in the P200 component. Dopamine and noradrenaline neurotransmitter systems could be responsible for the modulation of these processes. The exclusive effect of MPH on the P200 component could have a clinical application.

How Human Electrophysiology Informs Psychopharmacology: from Bottom-up Driven Processing to Top-Down Control

“…Moreover, a study by Leung et al (2007) failed to show any significant effect of dopamine D2 and D1/D2 receptor stimulants bromocriptine and pergolide on MMN generation. Korostenskaja et al (2008) demonstrated no significant effect of methylphenidate, working through DA and noradrenaline systems, on MMN. Finally, tyrosine/phenylalanine depletion did not affect the MMN latencies or amplitudes (Leung et al, 2010).…”

Inhibition of cerebral type 1 cannabinoid receptors is associated with impaired auditory mismatch negativity generation in the ketamine model of schizophrenia

“…In this context, the dopamine D2 receptor antagonist haloperidol has been found to significantly increase the MMN amplitudes in healthy human subjects (Kähkönen et al 2001). However, numerous studies were not able to replicate this finding by using haloperidol Pekkonen et al 2002), the dopamine D2 receptor agonist bromocriptin (Leung et al 2007), the dopamine D1 and D2 receptor agonist pergolide (Leung et al 2007), the dopamine and noradrenaline reuptake inhibitor methylphenidate (Korostenskaja et al 2008) as well as acute dopamine depletion (Leung et al 2010). While the role of dopamine in MMN generation cannot be completely ruled out, these findings support the view that the ketamine-induced alterations of the MMN may be linked primarily to glutamate dysfunction involving NMDA receptors.…”

Cognitive neuroscience of Attention Deficit Hyperactivity Disorder: Current status and working hypotheses

“…It enhances synaptic DA in the striatum by inhibiting reuptake by DA transporters and DA and NE in prefrontal cortex by stimulating receptors. Behaviorally, MPH improves performance on ''cool'' [reviewed in Pietrzak et al, 2006] and ''hot'' (e.g., gambling [Devito et al, 2008]) executive function and lower-level sensory processing (e.g., auditory [Korostenskaja et al, 2008] and visual [Jonkman et al, 1997]). Thus, pharmacological modulation of catecholamines has widespread effects extending to all circuits affected in ADHD.…”