Kristian S Jensen1, Bob Oranje, Malene Wienberg, Birte Y Glenthøj. 1. Center for Neuropsychiatric Schizophrenia Research, Faculty of Health Sciences, University Psychiatric Center Glostrup, Copenhagen University, Ndr. Ringvej, 2600 Glostrup, Denmark.
Abstract
RATIONALE: Schizophrenia is a disabling illness with deficits in core mental functions such as sensory gating. The P50 amplitude is an (usually auditory) evoked brain potential that, in a so-called double-click paradigm, can be used to quantify sensory gating. Reports on serotonergic modulation of P50 suppression are sparse. OBJECTIVE: The objective of this study was to study the effects of increased serotonergic activity on parameters of P50 suppression in healthy volunteers. MATERIALS AND METHODS: In a double-blind placebo-controlled crossover design, 21 healthy male volunteers received either placebo or a dose of 10 mg of escitalopram (selective serotonin reuptake inhibitor), after which they were tested in a P50 suppression paradigm. Furthermore, an attempt was made to identify the neural generators of the P50 evoked potential. RESULTS: Escitalopram did not affect P50 suppression but was found to increase P50 amplitude to the first (or conditioning) stimulus. Two bilateral sources located in the temporal cortex, two bilaterally located near the eyes, and one in a fronto-central location were identified, the latter correlating positively with the P50 amplitude. CONCLUSIONS: In the current study, escitalopram did not affect P50 suppression in healthy male volunteers, which indicates that sensory gating is not affected by a nonspecific increase in serotonergic activity. Furthermore, a generator with a fronto-central location in the brain (possibly the anterior cingulate) was found to be the primary source of the P50 evoked potential.
RCT Entities:
RATIONALE: Schizophrenia is a disabling illness with deficits in core mental functions such as sensory gating. The P50 amplitude is an (usually auditory) evoked brain potential that, in a so-called double-click paradigm, can be used to quantify sensory gating. Reports on serotonergic modulation of P50 suppression are sparse. OBJECTIVE: The objective of this study was to study the effects of increased serotonergic activity on parameters of P50 suppression in healthy volunteers. MATERIALS AND METHODS: In a double-blind placebo-controlled crossover design, 21 healthy male volunteers received either placebo or a dose of 10 mg of escitalopram (selective serotonin reuptake inhibitor), after which they were tested in a P50 suppression paradigm. Furthermore, an attempt was made to identify the neural generators of the P50 evoked potential. RESULTS:Escitalopram did not affect P50 suppression but was found to increase P50 amplitude to the first (or conditioning) stimulus. Two bilateral sources located in the temporal cortex, two bilaterally located near the eyes, and one in a fronto-central location were identified, the latter correlating positively with the P50 amplitude. CONCLUSIONS: In the current study, escitalopram did not affect P50 suppression in healthy male volunteers, which indicates that sensory gating is not affected by a nonspecific increase in serotonergic activity. Furthermore, a generator with a fronto-central location in the brain (possibly the anterior cingulate) was found to be the primary source of the P50 evoked potential.
Authors: N Klein; J Sacher; T Geiss-Granadia; T Attarbaschi; N Mossaheb; R Lanzenberger; C Pötzi; A Holik; C Spindelegger; S Asenbaum; R Dudczak; J Tauscher; S Kasper Journal: Psychopharmacology (Berl) Date: 2006-09-06 Impact factor: 4.530
Authors: Louise Witten; Jesper Frank Bastlund; Birte Y Glenthøj; Christoffer Bundgaard; Björn Steiniger-Brach; Arne Mørk; Bob Oranje Journal: Neuropsychopharmacology Date: 2015-07-01 Impact factor: 7.853