Prolonged cortical silent period among drug-naive subjects at ultra-high risk of psychosis

Tang, Yingying; Zhang, Tianhong; Edelman, Bradley J.; Zeng, Botao; Zhao, Shanshan; Li, Chunyan; Zhuo, Kaiming; Qian, Zhenying; Li, Hui; Guo, Qian; Cui, Huiru; Zhu, Yikang; Jiang, Lijuan; Li, Chunbo; Yu, Dehua; Wang, Jijun

doi:10.1016/j.schres.2014.10.004

Cited by 13 publications

(30 citation statements)

References 52 publications

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“…A recent MRS study indicated an elevated GABA/water ratio in the mPFC in UHR subjects [17]. In our previous study, we found that GABA B -mediated cortical inhibition was impaired in UHR, whereas GABA A -mediated cortical inhibition was not altered yet [69]. Whether GABA dysfunction has occurred before the onset of psychosis remains unclear.…”

Section: Discussionmentioning

confidence: 98%

“…There was interplay between two GABA-mediated neurotransmitter systems (GABA A -mediated and GABA B -mediated ones) [70, 71]. Thus, there might be a compensatory effect between two GABA subsystems, leading to GABA deficits in FES patients rather than UHR subjects [64, 69]. Previous studies indicated that FES patients showed a reduced SICI and a prolonged duration of CSP, implying both GABA A and GABA B dysfunction, whereas UHR subjects only had a reduced SICI or prolonged duration of CSP, suggesting partially impaired GABA functions [64, 69].…”

Section: Discussionmentioning

confidence: 99%

“…Thus, there might be a compensatory effect between two GABA subsystems, leading to GABA deficits in FES patients rather than UHR subjects [64, 69]. Previous studies indicated that FES patients showed a reduced SICI and a prolonged duration of CSP, implying both GABA A and GABA B dysfunction, whereas UHR subjects only had a reduced SICI or prolonged duration of CSP, suggesting partially impaired GABA functions [64, 69]. Thus, medial prefrontal GABA reductions could be a candidate biomarker for the early stages of psychosis.…”

Section: Discussionmentioning

confidence: 99%

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Reducedγ-Aminobutyric Acid and Glutamate+Glutamine Levels in Drug-Naïve Patients with First-Episode Schizophrenia but Not in Those at Ultrahigh Risk

et al. 2016

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Altered γ-aminobutyric acid (GABA), glutamate (Glu) levels, and an imbalance between GABAergic and glutamatergic neurotransmissions have been involved in the pathophysiology of schizophrenia. However, it remains unclear how these abnormalities impact the onset and course of psychosis. In the present study, 21 drug-naïve subjects at ultrahigh risk for psychosis (UHR), 16 drug-naïve patients with first-episode schizophrenia (FES), and 23 healthy controls (HC) were enrolled. In vivo GABA and glutamate+glutamine (Glx) levels in the medial prefrontal cortex were measured using proton magnetic resonance spectroscopy. Medial prefrontal GABA and Glx levels in FES patients were significantly lower than those in HC and UHR, respectively. GABA and Glx levels in UHR were comparable with those in HC. In each group, there was a positive correlation between GABA and Glx levels. Reduced medial prefrontal GABA and Glx levels thus may play an important role in the early stages of schizophrenia.

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Section: Discussionmentioning

confidence: 98%

Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

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Reducedγ-Aminobutyric Acid and Glutamate+Glutamine Levels in Drug-Naïve Patients with First-Episode Schizophrenia but Not in Those at Ultrahigh Risk

et al. 2016

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“…4C). Schizophrenia is associated with altered brain plasticity [3,4,10,11]. The common mechanisms are N-methyl-Daspartate receptor deficiency [12], aberrant synaptic connections [13], disrupted inhibitory circuits [10,14], and dysregulated dopaminergic signaling [15].…”

Section: Impact Of History and Antipsychotic Dosage On Cortical Plastmentioning

confidence: 99%

Altered Motor-Striatal Plasticity and Cortical Functioning in Patients with Schizophrenia

et al. 2016

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Patients with schizophrenia undergo changes in brain plasticity. In the present study, we characterized motor cortical-striatal plasticity in such patients. Compared with the potentiation following high-frequency repetitive transcranial magnetic stimulation in the control group, the patients demonstrated impaired plasticity of corticostriatal motor-evoked potentials recorded from hand muscles. Notably, the loss of cortical plasticity was correlated with impaired motor learning in a rotary pursuit task. Moreover, the loss of plasticity was correlated with the symptoms of schizophrenia. The results suggest that the progression of schizophrenia is accompanied by altered cortical plasticity and functioning.

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“…In comparison, most studies did not show a significant deficit in ICF in schizophrenia patients [14,21-25]. These studies often referenced to abnormal GABAergic mechanisms as the explanation to the SICI deficit although direct evidence of a GABAergic abnormality in the motor cortex of schizophrenia patients is scarce.…”

Section: Introductionmentioning

confidence: 99%

The role of white matter microstructure in inhibitory deficits in patients with schizophrenia

Kochunov

Summerfelt

et al. 2017

Brain Stimulation

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Background Inhibitory-excitatory (I-E) imbalance has increasingly been proposed as a fundamental mechanism giving rise to many schizophrenia-related pathophysiology. The integrity of I-E functions should require precise and rapid electrical signal transmission. Objective/Hypothesis We hypothesized that part of the I-E abnormality in schizophrenia may originate from their known abnormal white matter connectivity that may interfere the I-E functions. Methods We test this using short-interval intracortical inhibition (SICI) vs. intracortical facilitation (ICF) which is a non-invasive measurement of I-E signaling. SICI-ICF from left motor cortex and white matter microstructure were assessed in schizophrenia patients and healthy controls. Results Schizophrenia patients showed significantly reduced SICI but not ICF. White matter microstructure as measured by fraction anisotropy (FA) in diffusion tensor imaging had a significant effect on SICI in patients, such that weaker SICI was associated with lower FA in several white matter tracts, most strongly with left corona radiata (r=−0.68, p=0.0002) that contains the fibers connecting with left motor cortex. Left corticospinal tract, which carries the motor fibers to peripheral muscular output, also showed significant correlation with SICI (r=−0.54, p=0.005). Mediation analysis revealed that much of the schizophrenia disease effect on SICI can be accounted for by mediation through left corona radiata. SICI was also significantly associated with the performance of processing speed in patients. Conclusion This study demonstrated the importance of structural circuitry integrity in inhibitory signaling in schizophrenia, and encouraged modeling the I-E dysfunction in schizophrenia from a circuitry perspective.

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Prolonged cortical silent period among drug-naive subjects at ultra-high risk of psychosis

Cited by 13 publications

References 52 publications

Reducedγ-Aminobutyric Acid and Glutamate+Glutamine Levels in Drug-Naïve Patients with First-Episode Schizophrenia but Not in Those at Ultrahigh Risk

Reducedγ-Aminobutyric Acid and Glutamate+Glutamine Levels in Drug-Naïve Patients with First-Episode Schizophrenia but Not in Those at Ultrahigh Risk

Altered Motor-Striatal Plasticity and Cortical Functioning in Patients with Schizophrenia

The role of white matter microstructure in inhibitory deficits in patients with schizophrenia

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