Differences in waveforms of cerebral evoked potentials among healthy subjects, schizophrenics, manic-depres-sives and epileptics

Ikuta, Takumi; Furuta, Noriko; Kihara, Shouichi; Okura, Masao; Nagamine, Isao; Nakayama, Hiroshi; Ishimoto, Yasuhito; Kaneda, Yasufumi; Tomotake, Masahito; Izaki, Yumiko; Xu, Minpeng

doi:10.2152/jmi.54.303

Cited by 7 publications

(4 citation statements)

References 26 publications

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“…Previous EEG and MEG studies revealed that in response to somatosensory stimulation, schizophrenic subjects display enhanced ERP amplitudes (Ikuta et al 2007; Shagass 1977), decreased phase locking (Teale et al 2013), reduced phase coherence and decreased power in the 20–40 Hz band (Arnfred 2012; Arnfred et al 2006; Arnfred et al 2011). Our findings in NRG1 (+/−) mutants parallel these reports, suggesting that NRG1 (+/−) mice display an electrophysiological endophenotype of schizophrenia linked to deficient somatosensory information processing.…”

Section: Elevated Baseline Firing In Nrg1 (+/−) Micementioning

confidence: 99%

“…Using electroencephalography (EEG) or magnetoencephalography (MEG), several studies have measured neuronal activity in response to sustained visual, auditory and somatosensory stimuli in patients. Schizophrenic subjects displayed reduced amplitudes of steady-state oscillations during sustained 20–40 Hz sensory stimulation, and a decreased temporal precision of responses (Edgar et al 2013; Ikuta et al 2007; Krishnan et al 2005; Kwon et al 1999; Light et al 2006; Mulert et al 2011; Spencer et al 2008; Teale et al 2013; Tsuchimoto et al 2011). In addition to these stimulus-related deficits, an aberrant increase in oscillatory power (20–50 Hz) during baseline conditions has been observed in schizophrenic subjects (Brockhaus-Dumke et al 2008; Itil et al 1972; Kikuchi et al 2011; Spencer 2012; Venables et al 2009).…”

Section: Introductionmentioning

confidence: 99%

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Sensory encoding in Neuregulin 1 mutants

et al. 2014

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Schizophrenic patients show altered sensory perception as well as changes in electrical and magnetic brain responses to sustained, frequency-modulated sensory stimulation. Both the amplitude and temporal precision of the neural responses differ in patients as compared to control subjects, and these changes are most pronounced for stimulation at gamma frequencies (20–40 Hz). In addition, patients display enhanced spontaneous gamma oscillations, which has been interpreted as ‘neural noise’ that may interfere with normal stimulus processing. To investigate electrophysiological markers of aberrant sensory processing in a model of schizophrenia, we recorded neuronal activity in primary somatosensory cortex of mice heterozygous for the schizophrenia susceptibility gene Neuregulin 1. Sensory responses to sustained 20–70 Hz whisker stimulation were analyzed with respect to firing rates, spike precision (phase locking) and gamma oscillations, and compared to baseline conditions. The mutants displayed elevated spontaneous firing rates, a reduced gain in sensory-evoked spiking and gamma activity, and reduced spike precision of 20–40 Hz responses. These findings present the first in vivo evidence of the linkage between a genetic marker and altered stimulus encoding, thus suggesting a novel electrophysiological endophenotype of schizophrenia.

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Section: Elevated Baseline Firing In Nrg1 (+/−) Micementioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Sensory encoding in Neuregulin 1 mutants

et al. 2014

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“…İşitsel, görsel ve bedensel uyarılmış potansiyeller epilepsi, şizofreni, bipolar bozukluk ve sağlıklı kontrol grupları için özgün ve cinsiyete özgü bulgular vermektedir. [16] Onaltı epilepsi ya da organik beyin disfonksiyonu eştanılı major depresyon ve 16 saf major depresyon olgusunu karşılaştıran bir çalışmada, ilk grupta çok sayıda olağandışı özellik saptansa da epileptiform aktivite anlamlı olarak daha çok bulunmamıştır. [17] Yüksek temporal delta amplitüdleri ve interhemisferik temporal delta asimetrisi epilepsi ve organik beyin disfonksiyonu olan olgularda daha sık bulunmuştur.…”

Section: Risk Etkenleriunclassified

Epilepsy and Mood Disorders

Kesebir¹,

Güven²,

Koç³

2012

Psikiyatride Guncel Yaklasimlar - Current Approaches in Psychia

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Duygudurum bozuklukları epilepside yaşam kalitesini ve prognozu etkileyen önemli bir psikiyatrik eştanıdır. Depresyon ile epilepsi arasındaki ilişki çift yönlüdür. Epileptik olgular arasındaki depresyon geliştirme riski sağlıklı kontrollerden yüksek olduğu kadar, depresif olgular arasında da epilepsi geliştirme riski sağlıklı kontrollerden yüksektir. Özkıyım epilepside beş kat, temporal lob epilepsisinde 25 kat artar. Epilepside depresyondan bağımsız var olan özkıyım riski, depresyonun varlığında daha da artar. Epilepsi, depresyon ve özkıyım arasındaki ortak yol hipofrontalite ve serotonin metabolizmasındaki düzensizliktir. Dizin daha çok depresyonla ilgili bilgi sağlarken bipolar bozuklukla ilgili veriler daha sınırlıdır. Oysa duygudurum düzensizliği, irritabilite ile karakterli karma dönemler ve mani sanıldığından daha sıktır. Her iki bozukluk da döngüsel olup süregenleşebilir. Ateşleme fenomeni, nörotransmiter, voltaj kapılı iyon kanallarında ve ikincil mesajcı sistemlerdeki düzensizlikler her iki bozukluğun etiyolojisinde öne sürülen değişikliklerdir. Duygudurum düzenleyici etkileri olan antikonvülzan ilaçlar ortak tedavi noktasını oluşturmaktadır. Bu ilaçların etki mekanizmalarının anlaşılması patofizyolojik süreçlere ışık tutacaktır. Bu yazıda epilepsi ile duygudurum bozuklukları arasındaki ilişki, eştanı, ikincil durumlar ve her iki durumda tedavi seçenekleri ele alınmıştır.

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“…Studies using RNA interference demonstrate that Grb modulates microtubules assembly and facilitates axon elongation via a DISC1-dependent process (Shinoda et al, 2007). Fasciculation and Elongation Factor Zeta (FEZ1) also has been shown to interacts with DISC1 in rat brain (Honda et al, 2004;Ikuta et al, 2007). Reduced expression of FEZ1 compromises axon growth, while over-expression of FEZ1 increases DISC1 binding and neurite length (Miyoshi et al, 2003).…”

Section: Disc1 Protein Interactionmentioning

confidence: 99%

Phosphodiesterase-4 in the Brain: Effects of Pharmacological Inhibition and Mutation of DISC1

Xiao¹

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Phosphodiesterase-4 in the Brain: Effects of Pharmacological Inhibition and Mutation of DISC1 Lan Xiao The effects of treatment with PDE4 inhibitors on cAMP/pCREB signaling, hippocampal neurogenesis and immobility in forced-swim test and the effects of DISC1 mutation on cAMP/pCREB signaling, PDE4 subtypes and PDE4 activity and highaffinity rolipram binding state were determined. Acute treatment with PDE4 inhibitors increased cAMP and pCREB transiently, as determined by ELISA and Western blotting, respectively. Repeated treatment with PDE4 inhibitors for 16 days produced antidepressant-like effect as evidence by decreased immobility in forced-swim test, increased cAMP/pCREB signaling and enhanced hippocampal neurogenesis. PDE4 inhibitors which preferentially interact with the high-affinity rolipram binding state, such as rolipram and piclamilast, produced greater effects than CDP840, which preferentially interacts with the low-affinity rolipram binding state. PDE4 exerts its normal functions by interacting with a variety of binding proteins. The effects of mutation of one of the most important binding proteins DISC1, a risk factor gene for mental disorders, were determined. In this study, DISC1 mutant mice that carried truncated DISC1 proteins were used. DISC1 mutation increased cAMP and pCREB levels, and decreased PDE4 activity in prefrontal cortex, hippocampus and striatum. The PDE4B1, B3 and B4 splice variants were decreased in these three brain regions, while the D3 and D5 variants were decreased only in the hippocampus; PDE4A1 and A5 splice variants were not affected by the DISC1 mutation. Previous work has shown greater DISC1 association with the PDE4B subtype than the other subtypes. Radioligand binding assays showed that the high affinity rolipram binding state was decreased in brain regions of DISC1 mutant mice, suggesting high affinity rolipram binding state is functionally associated with DISC1. Overall, PDE4 inhibitors which preferentially interact with the high-affinity rolipram binding states produced greater effects on cAMP/pCREB and behavior, as well as for increasing hippocampal neurogenesis. In addition, DISC1 mutation decreased PDE4 activity and upregulated cAMP/pCREB levels. These suggest DISC1 is important for the normal function of PDE4 and downstream cAMP signaling. Mutation of DISC1 also induced a decrease in PDE4B and PDE4D, but not PDE4A splice variants. The studies shed light on the understanding of the function of high-affinity rolipram binding state in the central nervous system and may provide a new target for antidepressant drug discovery and development.

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Differences in waveforms of cerebral evoked potentials among healthy subjects, schizophrenics, manic-depres-sives and epileptics

Cited by 7 publications

References 26 publications

Sensory encoding in Neuregulin 1 mutants

Sensory encoding in Neuregulin 1 mutants

Epilepsy and Mood Disorders

Phosphodiesterase-4 in the Brain: Effects of Pharmacological Inhibition and Mutation of DISC1

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