Hong X, Chan RC, Zhuang X, Jiang T, Wan X, Wang J et al. Neuroleptic effects on P50 sensory gating in patients with first-episode never-medicated schizophrenia. Schizophr Res 108: 151-157

Mental Health Center, Medical College of Shantou University, Shantou, China.
Schizophrenia Research (Impact Factor: 3.92). 12/2008; 108(1-3):151-7. DOI: 10.1016/j.schres.2008.11.016
Source: PubMed


Sensory gating deficit, as reflected by P50 suppression, has been demonstrated in schizophrenia. Despite extensive evidence of the irreversible effects of typical neuroleptics on this deficit, recent studies of atypical neuroleptics have produced inconsistent findings on the reversibility of P50 suppression in schizophrenia. As the majority of these studies were limited by either their cross-sectional design or the recruitment of patients on multiple medications, the current study was designed to examine the effects of different neuroleptic medications on the P50 sensory gating index in patients with first-episode, never-medicated schizophrenia. P50-evoked potential recordings were obtained from 62 normal controls when they entered the study and from 65 patients with first-episode, never-medicated schizophrenia at baseline and after six weeks of different neuroleptic treatments (sulpiride [n=24], risperidone [n=24] and clozapine [n=17]). The first-episode, never-medicated schizophrenia patients had impaired sensory gating relative to the normal controls (mean=94.19% [SD=61.31%] versus mean=41.22% [SD=33.82%]). The test amplitude S2 was significantly higher in the schizophrenia patients than in the normal controls. The conditioning amplitude S1 and the positive symptom scores were related to the P50 gating ratios in schizophrenia at baseline. There was no change in P50 sensory gating (P>0.10) and a significant improvement in the clinical ratings (P>0.10) after six-week neuroleptic treatment for schizophrenia. P50 sensory gating was not significant for the patients who received sulpiride, risperidone or clozapine at baseline (F=1.074, df=2, 62, P=0.348) or at endpoint (F=0.441, df=2, 62, p=0.646). Our findings indicate that there is P50 sensory gating impairment in first-episode, never-medicated schizophrenia and that treatment with typical and atypical antipsychotics has no significant impact on such gating in this illness.

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    • "Conditioning-testing paradigms have a long history of being used to assess the inhibitory properties of the central nervous system. This paradigm has been adapted in psychophysiological research as a test of 'sensory gating' (Hong et al., 2009), or the filtering of repetitive sensory stimuli in order to focus attention (Wildeboer and Stevens, 2008). Sensory gating refers to the pre-attentional habituation of responses following repeated exposure to the same sensory stimulus. "
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    ABSTRACT: Background The effects of smoking on cognitive performance have long been studied, with mixed results. P50 sensory gating has been used as endophenotype for studying nicotinic systems genetics, and P50 gating deficits have been reported to be a sensitive biomarker for cognitive impairment in schizophrenia. This study examined the inter-relationship between P50 suppression, cognitive function, and smoking in a healthy Han Chinese population, which has not been reported before. Methods We recruited 82 healthy male subjects, including 48 smokers and 34 non-smokers who were matched for age and education. The authors measured P50 sensory gating and administered the Chinese-language version of the MATRICS Consensus Cognitive battery (MCCB) and Stroop tests. Results The results showed that the smokers scored lower than nonsmokers on the MCCB Brief Visuospatial Memory Test (BVMT) index and the STROOP test. Furthermore, the MCCB total score was negatively associated with number of cigarettes smoked per day in the smoker group. However, P50 sensory gating was not associated with either smoking status or any cognitive performance. Conclusions Our results show that smoking is associated with cognitive impairment, but not with P50 sensory gating.
    Drug and Alcohol Dependence 10/2014; 143(1). DOI:10.1016/j.drugalcdep.2014.06.045 · 3.42 Impact Factor
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    • "With regard to P50 gating, neither conventional antipsychotic medications nor second generation antipsychotics, with the possible exception of clozapine (Nagamoto et al., 1999; Becker et al., 2004), seem to remedy sensory gating deficits in schizophrenia patients (Arango et al., 2003; Adler et al., 2004). In addition, no differential impact of antipsychotic medications has been found on P50 gating (Hong et al., 2009; Sánchez-Morla et al., 2009a, 2009b; Su et al., 2012). Therefore, the impact of antipsychotic treatment on P50 seems to be limited, at most. "
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    ABSTRACT: Impaired inhibition of P50 cerebral evoked response is one of the best validated endophenotypes in schizophrenia. There are controversial data on the relationship between P50 evoked potential deficit and measures of cognitive function in schizophrenia. A comprehensive clinical and neurocognitive assessment plus an evaluation of P50 sensory gating was performed in 160 schizophrenia patients and 64 controls. Neurocognitive scores from each cognitive domain were converted to demographically-adjusted T-scores (age, gender, and years of education) for all study participants. The relationship between P50 and neurocognitive variables was assessed via parametric and nonparametric correlations and categorical strategies: we compared neuropsychological test scores in patients and controls in the lowest P50 quartile vs. the highest. Controls had better performance than schizophrenia patients in all cognitive domains. Schizophrenia patients had significantly higher P50 ratios than controls, and no significant correlation was found between P50 gating measures and neuropsychological test scores in schizophrenia patients or healthy controls. Moreover, no differences in neurocognitive performance were found between subjects in the lowest P50 ratio quartile vs. the highest in healthy controls or patients with schizophrenia. We concluded that there is no evidence of an association between P50 ratio and cognitive measures in schizophrenia patients, and this seems to be also the case in healthy controls.
    Schizophrenia Research 11/2012; 143(1). DOI:10.1016/j.schres.2012.10.017 · 3.92 Impact Factor
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    • "The P50 wave amplitude is thought to reflect the brain's inhibitory gating effect, which mainly determined by reduced test (S2) wave amplitude in conditioning-test paradigms (Erwin et al., 1991). Consistent with previous findings, we found that treatment with antipsychotics has limited effect on P50 gating deficits (Erwin et al., 1994; Light et al., 2000; Adler et al., 2004; Hong et al., 2009). Of note, an elegant study by Hong et al. showed an advantage for theta-alpha-band gating as compared to traditional P50 gating (Hong et al., 2008), therefore, it is plausible that future studies employing theta-alpha gating measure would provide enhanced sensitivity to detect potential association with ADORA2A expression. "
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    ABSTRACT: Sensory gating deficits have been found in patients with schizophrenia and their unaffected relatives. However, the underlying neurobiological mechanism of this deficit remains unclear. Pre-clinical studies have implicated adenosine in sensory gating deficits in schizophrenia. Therefore, the current study investigated a possible relationship between peripheral adenosine A2A receptor (ADORA2A) and sensory gating indices (P50 measures) in medication-free schizophrenia (n=31) and healthy (n=21) groups. The effects of six-week antipsychotic treatment were examined. At baseline, schizophrenia patients showed impaired sensory gating compared to healthy controls. However, there was no significant difference in ADORA2A gene expression among groups. In addition, ADORA2A expression was not correlated with sensory gating at any time point. Following treatment, we found a significant upregulation of ADORA2A expression. Intriguingly, we observed a significant positive association between ADORA2A upregulation and baseline P50 amplitudes in the schizophrenia group. A main finding of the current pilot study is the upregulation of ADORA2A expression following treatment with antipsychotics. In addition, this upregulation was predicted by baseline P50 amplitude, an observation that awaits replication in an expanded sample.
    Psychiatry Research 06/2012; 200(2-3). DOI:10.1016/j.psychres.2012.04.021 · 2.47 Impact Factor
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