Effects of olanzapine on auditory P300 in schizophrenia

Gönül, Ali Saffet; Süer, Cem; Coburn, Kerry L.; Özesmi, Çiğdem; Oğuz, Aslan; Yilmaz, Alpaslan

doi:10.1016/s0278-5846(02)00349-4

Cited by 37 publications

(25 citation statements)

References 27 publications

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“…medication (Coburn et al, 1998;Demiralp et al, 2002;Gonul et al, 2003;Wang et al, 2005). Differences in treatment could thus account for the larger P300 amplitudes observed in the aforementioned studies compared to the present study.…”

Section: Discussioncontrasting

confidence: 50%

P300 asymmetry and positive symptom severity: A study in the early stage of a first episode of psychosis

Renoult

Prévost

Brodeur

et al. 2007

Schizophrenia Research

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The amplitude of the P300 event-related potential (ERP) has been reported to be reduced over left compared to right temporal sites in schizophrenia patients. This left temporal P300 reduction has been associated with positive symptom severity and gray matter reduction in the left superior temporal gyrus. We investigated a group of patients with a first episode of schizophrenia spectrum psychosis and a group of normal controls to verify if P300 amplitude asymmetry already exists around the time of presentation for treatment. Relative to normal control subjects, no P300 asymmetry was found in patients. Nevertheless, P300 asymmetry was correlated with the severity of positive symptoms and worse global functioning (GAF), a good predictor of poor outcome.

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Section: Discussioncontrasting

confidence: 50%

P300 asymmetry and positive symptom severity: A study in the early stage of a first episode of psychosis

Renoult

Prévost

Brodeur

et al. 2007

Schizophrenia Research

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“…Schizophrenia patients also experience loss of effective responsiveness, verbal expression, personal motivation, enjoyment, social drive, or attention to the environment, which are conceptualized as negative symptoms. Although studies indicate that antipsychotics provide minimal improvement in some cognitive and physiologic abnormalities (Gonul et al, 2003;Keefe et al, 2004), it is unclear whether these improvements are due to medication or practice effects (Goldberg et al, 2007). Negative and cognitive symptoms remain largely untouched and emerge among the most debilitating domain for affected patients over time (Elvevåg and Goldberg, 2000).…”

mentioning

confidence: 99%

Antipsychotic-Like Properties of Phosphodiesterase 4 Inhibitors: Evaluation of 4-(3-Butoxy-4-methoxybenzyl)-2-imidazolidinone (RO-20-1724) with Auditory Event-Related Potentials and Prepulse Inhibition of Startle

Halene¹,

Siegel²

2008

J Pharmacol Exp Ther

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Antipsychotic medications function through antagonism of D2 dopamine receptors. Blockade of D2 receptors causes an increase in intracellular cAMP, a ubiquitous second messenger. Inhibition of phosphodiesterase (PDE) activity, a family of enzymes that degrade cyclic nucleotides, causes the same effect. The conceptual linkage between dopamine D2 receptors and PDE activity via cAMP suggests a possible therapeutic potential for PDE inhibitors in schizophrenia. The limited number of studies in support of this hypothesis used rolipram, a specific inhibitor of the PDE4 family. In this study, we investigated the impact of 4-(3-butoxy-4-methoxybenzyl)-2-imidazolidinone (RO-20-1724), another PDE4-specific inhibitor, on auditory event-related potentials (ERPs), prepulse inhibition (PPI) of the startle reflex, and locomotor activity in mice. The ability to reverse amphetamine-induced alterations in ERPs and PPI was used as a model for psychosis. ERPs after RO-20-1724 revealed increased amplitude for the P20 and N40 ERP components. RO-20-1724 reversed the disruptive effect of amphetamines on ERPs and restored gating at a dose that did not impair locomotor activity. However, RO-20-1724 failed to reverse a amphetamine-induced decrease of PPI. Inconsistent results between these two psychosis models suggest that pure sensory processing, as measured with auditory ERPs, may be more sensitive to the effects of intracellular cAMP than sensorimotor effects as assessed with PPI. It remains unclear whether antipsychotic-like properties are a common feature of PDE4 inhibition, or if they are restricted to the pharmacological profile of rolipram. Future studies should examine how PDE4 subtype specificity might contribute to differences between rolipram and RO-20-1724 in sensorimotor gating.Antipsychotic medications were introduced more than 50 years ago for the treatment of hallucinations, delusions, thought disorganization, and behavioral disorders. Although initially targeted for the treatment of schizophrenia, these medications act on psychotic symptoms irrespective of cause. Currently approved antipsychotic medications produce their beneficial effects through antagonism of the dopamine D2 receptor. Their potency is proportional to their affinity for this target (Kapur and Mamo, 2003). Blockade of D2 receptors causes an increase in intracellular cAMP, a ubiquitous second messenger. Inhibition of phosphodiesterase (PDE) activity, a family of enzymes with the ability to degrade cyclic nucleotides, causes the same effect. The conceptual linkage between the dopamine D2 receptor and PDE activity via cAMP suggests a possible therapeutic potential for PDE inhibitors in schizophrenia (Fig. 1).No single antipsychotic substance has emerged as the gold standard for a first-line treatment in clinical trials or expert consensus guidelines, and with the notable exception of clozapine, all approved antipsychotics are of comparable efficacy. Antipsychotics vary in side effects including risk of extrapyramidal symptoms, weight gain, metabolic ...

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“…It may be presumed that olanzapine might be more effective in this respect in that kind of patients, as suggested by the results of Gonul et al [5] in unmedicated patients. However, against that possibility is the fact that both at baseline and after treatment our patients showed a significantly decreased amplitude in comparison to normals.…”

Section: Discussionmentioning

confidence: 83%

“…On the one hand, available data support no significant changes in P300 parameters with risperidone, despite some latency decrease [2]. Similarly no changes in either P300 amplitude or latency were observed after 4-week olanzapine therapy in schizophrenia by Gallinat et al [3], or in healthy controls after a single dose by Hubl et al [4], whereas Gonul et al [5] have recently reported in unmedicated patients a P300 normalization at frontal leads but not at parietal leads after 6 weeks of olanzapine treatment. On the other hand, olanzapine enhances neuropsychological performance in schizophrenia [6], P300 being related to neuropsychological performance in that illness [7,8].…”

Section: Introductionmentioning

confidence: 93%

Long-Term Olanzapine Treatment and P300 Parameters in Schizophrenia

et al. 2004

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The well-known amplitude reduction of the P300 appears to be unaffected by the treatment with classical antipsychotics in schizophrenia, whereas the effects of atypical neuroleptics on this event-related potential are less understood. The study of these changes could help in deciding whether the P300 amplitude reduction in schizophrenia is a trait or state marker of that illness and in better describing the effect of atypical antipsychotics on altered cognitive functions. We present a prospective longitudinal study of P300 amplitude and latency before and after 6 months’ treatment with olanzapine in 11 patients with schizophrenia. A healthy control group (n = 30) was also studied. Overall, no significant changes, either in amplitude or in latency as measured at Pz and Fz electrodes, were found when comparing the pre- and postolanzapine conditions, despite the overall improvement in positive and negative symptoms. Nevertheless a direct specific association was observed between a P300 amplitude increase with olanzapine and the improvement in negative symptoms. These data would suggest that P300 amplitude reduction in schizophrenia may be relatively independent from clinical state and treatment, thus constituting a trait marker of schizophrenia. Our data also suggest that, in addition to this, some further changes in P300 amplitude might depend on the clinical state of the patients.

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Effects of olanzapine on auditory P300 in schizophrenia

Cited by 37 publications

References 27 publications

P300 asymmetry and positive symptom severity: A study in the early stage of a first episode of psychosis

P300 asymmetry and positive symptom severity: A study in the early stage of a first episode of psychosis

Antipsychotic-Like Properties of Phosphodiesterase 4 Inhibitors: Evaluation of 4-(3-Butoxy-4-methoxybenzyl)-2-imidazolidinone (RO-20-1724) with Auditory Event-Related Potentials and Prepulse Inhibition of Startle

Long-Term Olanzapine Treatment and P300 Parameters in Schizophrenia

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