The P3 in ‘ecstasy’ polydrug users during response inhibition and execution
Alex Gamma, Daniel Brandeis, Ruven Brandeis, Franz X. Vollenweider
Journal of Psychopharmacology September 1, 2005 DOI: 10.1177/0269881105056535 (opens in new tab)
Study at a glance
AI-extracted from the abstract| Characteristics | Case-control study Peer reviewed |
|---|---|
| Sample size | 33 |
| Population | Current ecstasy polydrug users and non-using controls |
| Topics | Cannabis MDMA |
| Keywords | Disinhibition Impulsivity Inhibitory postsynaptic potential Event-related potential Response inhibition Audiology Inhibitory control Electroencephalography Developmental psychology Cognition |
| Citations | 36 |
| Key findings | Ecstasy polydrug users had lower P3 amplitudes at midline electrodes and a less anterior location of NoGo P3 peaks, but the normal switch pattern between response execution and inhibition was preserved. |
Abstract
Substance abuse and associated externalizing disorders are characterized by behavioural disinhibition and low impulse control, with reduced neural inhibition postulated to be the common underlying brain mechanism. The P3 component of event-related potentials (ERPs) is a widely used neurophysiological measure thought to reflect inhibitory brain processes, but as yet has not been assessed in ecstasy users. We recorded ERPs evoked by a Continuous Performance Test (CPT) in 16 current ecstasy polydrug users and 17 controls. The CPT included conditions where a prepared motor response had to be executed (Go) or inhibited (NoGo). Both controls and ecstasy users showed normal, robust patterns of P3 anteriorization and delay in the NoGo compared to the Go condition. Ecstasy users had lower P3 amplitudes at midline electrodes and a less anterior location of NoGo P3 peaks. These effects became weaker after statistically controlling for age, educational level and lifetime cannabis use. While lower P3 amplitudes are consistent with higher levels of neural disinhibition in ecstasy polydrug users, the normal switch pattern between response execution and inhibition, and the less anterior location of the NoGo P3, do not indicate disturbed inhibitory brain mechanisms.