Dysfunctional long-term potentiation-like plasticity in schizophrenia revealed by transcranial direct current stimulation

Hasan, Alkomiet; Nitsche, Michael A.; Rein, Bettina; Schneider‐Axmann, Thomas; Guse, Birgit; Gruber, Oliver; Falkai, Peter; Wobrock, Thomas

doi:10.1016/j.bbr.2011.05.017

Cited by 138 publications

(128 citation statements)

References 58 publications

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“…A study of cortical thickness in patients with schizophrenia found decreases in the structural connectivity of the left and right DLPFC to be correlated with poor WM performance (36). Additionally, real-time transcranial magnetic stimulation techniques, which allow researchers to indirectly study synaptic plasticity in vivo (37,38), have shown that inducing synaptic plasticity in the right DLPFC leads to altered prefrontal-hippocampal functional interactions during WM (3). These findings are in keeping with the "two hit" hypothesis of schizophrenia, whereby early environmental and genetic factors confer vulnerability of neural circuitry to adverse events during adolescence, such as excessive synaptic pruning or impaired plasticity (14,39).…”

Section: Resultsmentioning

confidence: 99%

RETRACTED: Identification of gene ontologies linked to prefrontal–hippocampal functional coupling in the human brain

Dixson¹,

Walter

Schneider³

et al. 2014

Proc. Natl. Acad. Sci. U.S.A.

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Significance This study combines neuroimaging and whole-genome genotyping techniques with a gene set enrichment analysis to unravel the genetic basis of a well-validated intermediate phenotype for schizophrenia, dorsolateral prefrontal cortex–hippocampal connectivity. We found significant enrichment of genes with roles in synaptic plasticity and neurodevelopment that are consistent with the neurobiological basis of prefrontal–hippocampal interactions in schizophrenia. We further provide additional independent evidence for the intermediate phenotype concept and present a readily generalizable approach for a biologically driven analysis of imaging and genetic data.

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Section: Resultsmentioning

confidence: 99%

RETRACTED: Identification of gene ontologies linked to prefrontal–hippocampal functional coupling in the human brain

Dixson¹,

Walter

Schneider³

et al. 2014

Proc. Natl. Acad. Sci. U.S.A.

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“…The complete protocol has been described previously (Hasan et al, 2012b;Hasan et al, 2011). Electromyographic activity (EMG) was recorded by surface electrodes on the right dorsal interosseus muscle in a belly-tendon montage.…”

Section: Tmsmentioning

confidence: 99%

“…Reviewing the available literature for cortical excitability and plasticity in schizophrenia using noninvasive brain stimulation, a clear picture emerges. Reduced cortical inhibition (eg, reduced short-interval intracortical inhibition, for review see (Bunse et al, 2014)) might cause enhanced cortical noise, leading to reduced spike-timing-dependent plasticity (as measured by paired-associative stimulation) (Frantseva et al, 2008) and reduced nonfocal plasticity (as measured by anodal and cathodal tDCS) via enhanced asynchronous baseline cortical activity (Hasan et al, 2012b;Hasan et al, 2011) Our observed effect of enhanced LTD-like plasticity associated with nicotine intake through chronic smoking might reduce cortical noise and thus increase the signal-tonoise ratio in schizophrenia patients. This would be in line with the observation that LTD has an important role in hippocampal-based learning and memory functions (Collingridge et al, 2010), suggesting a direct contribution of LTD to information storage (Kemp and ManahanVaughan, 2007).…”

Section: Functional Implicationsmentioning

confidence: 99%

Smoking Restores Impaired LTD-Like Plasticity in Schizophrenia: a Transcranial Direct Current Stimulation Study

Strube

Bunse

Nitsche

et al. 2014

Neuropsychopharmacol

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Impaired neuroplastic responses following noninvasive brain stimulation have been reported repeatedly in schizophrenia patients. These findings have been associated with deficits in GABAergic, glutamatergic, and cholinergic neurotransmission. Although various neurophysiological studies have indicated a relationship between nicotine and neuroplasticity in healthy individuals, the present study is the first investigation into the impact of nicotine on LTD-like plasticity in patients with schizophrenia. Cortical excitability and cortical plasticity were explored in 30 schizophrenia patients (17 smoker, 13 nonsmoker) and 45 healthy controls (13 smoker, 32 nonsmoker) by using single-pulse transcranial magnetic stimulation (TMS) before and following cathodal transcranial direct current stimulation (tDCS) applied to the left primary motor cortex. Our analysis revealed abolished LTD-like plasticity in nonsmoking schizophrenia patients. However, these plasticity deficits were not present in smoking schizophrenia patients. In healthy controls, significant MEP reductions following cathodal tDCS were observed in nonsmoking individuals, but only trend-level reductions in smokers. In smoking schizophrenia patients, the severity of negative symptoms correlated positively with reduced neuroplasticity, whereas nonsmoking patients displayed the opposite effect. Taken together, the data of our study support the notion of an association between chronic smoking and the restitution of impaired LTD-like plasticity in schizophrenia patients. Although replication and further research are needed to better understand this relationship, our findings indicate that nicotine intake might stabilize the impaired inhibition-facilitation balance in the schizophrenic brain through a complex interaction between cortical plasticity, and GABAergic and cholinergic neurotransmission, and might explain the reduced prevalence of negative symptoms in this population.

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“…In the present study, we found an increase in synaptic transmission in the hippocampal CA1 area, which indicated that the balance of excitation/inhibition might be impaired in Fut8 Ϫ/Ϫ mice. On the other hand, several studies have provided direct neurophysiological evidence for disrupted LTP-like plasticity in schizophrenia (4,5,42). The evaluation of experimental LTP could be used to analyze the schizophrenialike phenotype in Fut8 Ϫ/Ϫ mice.…”

Section: Discussionmentioning

confidence: 99%

Loss of α1,6-Fucosyltransferase Decreases Hippocampal Long Term Potentiation

Fukuda

Isaji

et al. 2015

Journal of Biological Chemistry

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Background: High expression levels of core fucosylated N-glycans in brain tissues remain unexplained. Results: Loss of core fucosylation enhanced AMPA receptor heteromerization and decreased long term potentiation. Conclusion: Core fucosylation is required for hippocampal long term potentiation. Significance: Core fucosylation may be very important for the neuronal synaptic plasticity that is required for learning and memory.

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Dysfunctional long-term potentiation-like plasticity in schizophrenia revealed by transcranial direct current stimulation

Cited by 138 publications

References 58 publications

RETRACTED: Identification of gene ontologies linked to prefrontal–hippocampal functional coupling in the human brain

RETRACTED: Identification of gene ontologies linked to prefrontal–hippocampal functional coupling in the human brain

Smoking Restores Impaired LTD-Like Plasticity in Schizophrenia: a Transcranial Direct Current Stimulation Study

Loss of α1,6-Fucosyltransferase Decreases Hippocampal Long Term Potentiation

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