Effects of Temporal Variability on P50 and the Gating Ratio in Schizophrenia

Patterson, Julie V.; Jin, Yi; Gierczak, Matt; Hetrick, William P.; Potkin, Steven G.; Bunney, William E.; Sandman, Curt A.

doi:10.1001/archpsyc.57.1.57

Cited by 77 publications

(59 citation statements)

References 60 publications

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“…Such increase was found in all groups of patients with epilepsy, regardless of seizure control. In agreement with the results reported here, several authors have found that the decrease in P50 suppression in patients with schizophrenia is due to a smaller amplitude of S1, although some increase in the amplitude of S2 has also been reported 11,[17][18][19][20] . One possible explanation is that there may be a direct effect on the inhibition of the response to the second stimulus in epilepsy, thus leading to greater amplitude of S2.…”

Section: Age Range and Mean Age±standard Deviation (Yearssupporting

confidence: 93%

“…The sensory filter depends on complex brain circuits. In schizophrenia, the decrease in the S2/S1 ratio is usually due to a decrease in S1 amplitude 11,[17][18][19][20] , whereas in other disorders, such as Machado-Joseph disease 18 and traumatic brain injury 4 , S2 amplitude is increased, which may indicate the existence of different mechanisms affecting the sensory filter.…”

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confidence: 99%

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Pattern of P50 suppression deficit in patients with epilepsy and individuals with schizophrenia

Becker

Filho

et al. 2011

Arq. Neuro-Psiquiatr.

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Objective: To identify P50 suppression in patients with epilepsy, to investigate the effect of seizure control on P50 suppression, and to compare epilepsy patients with individuals with schizophrenia and healthy volunteers. Method: P50 evoked potential parameters and P50 suppression were studied crossectionally in patients with uncontrolled or controlled epilepsy, in individuals with schizophrenia and in healthy volunteers. Results: Individuals with schizophrenia had significantly smaller conditioning stimulus (S1) amplitude, and patients with epilepsy had larger test stimulus (S2) amplitude. Mean S2/S1 ratio was 0.71±0.33 for patients with uncontrolled epilepsy; 0.68±0.36 for patients with controlled epilepsy; 0.96±0.47 for individuals with schizophrenia, and 0.42±0.24 for healthy volunteers. Conclusion: The sensory filter of patients with epilepsy is altered, and this alteration is not associated with seizure control. Also, it works differently from the sensory filter of individuals with schizophrenia. Key words: epilepsy, P50 auditory evoked potential, schizophrenia, sensory filter.Padrão do déficit de supressão do P50 em pacientes com epilepsia e em indivíduos com esquizofrenia RESUMO Objetivo: Identificar se existe déficit de supressão do P50 em pacientes com epilepsia, verificar a influência do controle das crises nesse déficit, comparando com pacientes com esquizofrenia e com voluntários saudáveis. Método: Os parâmetros do potencial evocado P50 e sua supressão foram estudados, com um corte transversal, em pacientes com epilepsia controlada ou não, esquizofrenia e em voluntários saudáveis. Resultados: Indivíduos com esquizofrenia apresentam uma amplitude de S1 significativamente menor que os demais, sendo que os pacientes com epilepsia apresentavam uma resposta S2 de maior amplitude. A média da razão S2/S1 foi de 0,71±0,33 nos pacientes com epilepsia não controlada; 0,68±0,36 naqueles com epilepsia controlada; 0,96±0,47 nos com esquizofrenia e 0,42±0,24 nos controles normais. Conclusão: O filtro sensitivo de pacientes com epilepsia é alterado, e essa alteração não está associada com o controle das crises. Além disso, ele funciona de forma diferente do filtro sensitivo dos indivíduos com esquizofrenia. Palavras-chave: epilepsia, potencial evocado auditivo P50, esquizofrenia, filtro sensitivo.

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Section: Age Range and Mean Age±standard Deviation (Yearssupporting

confidence: 93%

mentioning

confidence: 99%

Pattern of P50 suppression deficit in patients with epilepsy and individuals with schizophrenia

Becker

Filho

et al. 2011

Arq. Neuro-Psiquiatr.

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“…Our hypothesis was based on evidence implicating glutamatergic and cholinergic receptors in sensory gating (Adler et al, 1986;Luntz-Leybman et al, 1992;Miller et al, 1992a;Bickford and Wear, 1995) and on data showing that cortical and CSF KYNA levels are elevated in schizophrenia (Erhardt et al, 2001;Schwarcz et al, 2001), a disorder characterized by marked auditory gating deficits (Adler et al, 1982;Boutros et al, 1991;Jin et al, 1997;Clementz et al, 1998a, b;Patterson et al, 2000). Since KYNA penetrates the bloodbrain barrier very poorly (Fukui et al, 1991), an indirect approach was implemented, involving blockade of the PBCD-sensitive transporter alone and in conjunction with the administration of KYNA's immediate bioprecursor KYN.…”

Section: Discussionmentioning

confidence: 99%

“…Altered responsiveness to auditory stimuli has also been observed in humans. Thus, several laboratories have reported that the amplitude of the conditioning response is significantly reduced in schizophrenic patients (Jin et al, 1997;Patterson et al, 2000;Blumenfeld and Clementz, 2001). Moreover, in normal controls, the amplitude of the conditioning response is more tightly correlated with other indices of sensory gating (e.g.…”

Section: Discussionmentioning

confidence: 99%

“…The diminished response to the second tone is thought to reflect the neural processes involved in gating sensory input and is typically quantified as the ratio of test to conditioning (T/C) response amplitude (Adler et al, 1999;Light and Braff, 1999). Numerous studies have demonstrated that persons with schizophrenia exhibit a blunted response to conditioning stimuli and a failure to show the characteristic reduction in ERP amplitude to the test stimulus (Adler et al, 1982;Boutros et al, 1991;Jin et al, 1997;Clementz et al, 1998a, b;Patterson et al, 2000). Notably, these deficits are strongly correlated with neuropsychological measures of attention (Erwin et al, 1998) and vigilance (Cullum et al, 1993).…”

Section: Introductionmentioning

confidence: 99%

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Micromolar Brain Levels of Kynurenic Acid are Associated with a Disruption of Auditory Sensory Gating in the Rat

Shepard

Joy

Clerkin

et al. 2003

Neuropsychopharmacol

127

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Brain levels of kynurenic acid (KYNA), an endogenous antagonist of glycine B /NMDA and a-7 nicotinic acetylcholine receptors, are elevated in individuals with schizophrenia. Both receptors are broadly implicated in the pathophysiology of this disease, particularly in the deficits many patients show in filtering the sensorium. In the present study, we sought to determine whether elevated brain levels of KYNA disrupt auditory gating in anesthetized rats. A mid-latency evoked potential was recorded from the hippocampus in response to a pair of auditory tones. Gating was assessed by determining the ratio of the amplitude of test and conditioning responses (T/C ratio) in rats that had received KYNA's precursor L-kynurenine (KYN; 150 mg/kg, i.p.) together with probenecid (PBCD; 200 mg/kg, i.p.) 2 h prior to the start of the recording session. KYNA levels in the hippocampus of KYN+PBCD-treated rats were increased 500-fold, and accompanied by a significant increase in T/C ratio consistent with a disruption in sensory gating. PBCD alone increased hippocampal KYNA 12-fold, but did not significantly elevate T/C ratio. L-701,324 (3-30 mg/kg, i.v.), a centrally acting glycine B site antagonist, also failed to disrupt gating; however, large quantities of the competitive NMDA receptor antagonist DL-2-amino-5-phosphopentanoate (200 nmol, i.c.v.) markedly increased T/C ratio. Thus, while total blockade of NMDA receptors disrupts auditory gating, partial blockade achieved by antagonism of its glycine coagonist binding site does not. These observations indicate that the disruption in auditory processing in rats with greatly elevated KYNA levels is not attributable to the compound's antagonist actions at the glycine B receptor.

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Association of Promoter Variants in the α7 Nicotinic Acetylcholine Receptor Subunit Gene With an Inhibitory Deficit Found in Schizophrenia

Leonard

Gault²,

Hopkins³

et al. 2002

Arch Gen Psychiatry

427

330

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Effects of Temporal Variability on P50 and the Gating Ratio in Schizophrenia

Abstract: These findings suggest that temporal variability contributes significantly to the P50 response as measured using the gating procedure. The measure of temporal variability may provide a new index of inhibitory and attentional function in schizophrenia.

Cited by 77 publications

References 60 publications

Pattern of P50 suppression deficit in patients with epilepsy and individuals with schizophrenia

Pattern of P50 suppression deficit in patients with epilepsy and individuals with schizophrenia

Micromolar Brain Levels of Kynurenic Acid are Associated with a Disruption of Auditory Sensory Gating in the Rat

Association of Promoter Variants in the α7 Nicotinic Acetylcholine Receptor Subunit Gene With an Inhibitory Deficit Found in Schizophrenia

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