The Impact of the Selective Monoamine Reuptake Inhibitors Reboxetine and Citalopram on Visually-Evoked Event-Related Potentials in Depressed Patients

Abstract

These results show that, in depressed patients, the P3 latency is decreased by antidepressive treatment. Furthermore, the results suggest that P3 latency might depend on the serotonergic rather than the noradrenergic system.

The astroglial protein S100B and visually evoked event-related potentials before and after antidepressant treatment

“…In previous studies, treatment of depressed patients with antidepressive drugs reduced the visually evoked P3 latency and P2 latency (Bange and Bathien 1998;Hetzel et al 2004), whereas the P3 amplitude increased (Gangadhar et al 1993). Even non-drug treatment, i.e.…”

“…The P3 amplitude has been reported to be reduced for the most part (Blackwood et al 1987;Gangadhar et al 1993;Yanai et al 1997), although one study demonstrated unchanged amplitudes (Bange and Bathien 1998). Several recent reports suggest that specific relationships may exist between certain ERP parameters and central cholinergic, noradrenergic, and especially serotonergic functions (Paige et al 1995;Evers et al 1999;Hegerl et al 2001;Mulert et al 2002;Hetzel et al 2004). …”

Discriminating Depression, Physical and Social Anhedonia by Neurotransmitter Related Challenge Tests

“…It may point to a common hyper-responsiveness of the HPA axis, since cortisol responses to the two transmitter related substances citalopram and reboxetin were significantly correlated (r = 0.378, p < 0.05) This could point to hypersensitive receptors of the corticotropin releasing factor (CRF) typical for depression (Reul & Holsboer, 2002), but it may also demonstrate the close functional association of the two transmitters on the brain level (Hetzel et al, 2004;Mongeau et al, 1997). Furthermore, the concept of pharmacotherapy of depression by mixed 5-HT + NA reuptake inhibitors implies that both types of postsynaptic receptors may be upregulated due to low 5-HT and NA production in depression and therefore are both liable to pronounced hormone responses.…”

Monoaminerge Funktion bei depressiven Patienten

“…[51]). Auf der x-Achse findet sich die Behandlungsdauer in Wochen, auf der y-Achse findet sich der Schweregrad der Depression Die Latenz der P3, einem evozierten ereigniskorrelierten Potenzial für aufgabenrelevante seltenere Reize, war bei depressiven Patienten (n=20) im Vergleich zu Gesunden verlängert [12] und korrelierte negativ (r=−0,74; p=0,001; n=19) mit dem Kortisolanstieg im Citalopram-Stimulationstest (d. h. nach serotonerger Stimuation) [11]. Dies bedeutet, dass eine verlän-gerte P3-Latenz bei Depression mit einer verminderten serotonergen Funktion zusammenhängen könnte.…”