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• Simulated microgravity disturbed neural oscillations in the hippocampus of mice. • rTMS treatment significantly modulated theta oscillatory patterns in Hu mice. • rTMS treatment could ameliorate the disturbance of oscillatory patterns in Hu mice. • A potential underlying mechanism was associated with improving the E/I balance. Microgravity, as a part of the stress of space flight, has several negative effects on cognitive functions. Repetitive transcranial magnetic stimulation (rTMS), as a novel non-invasive technique, could be an effective approach to alleviated cognitive decline, applied in both preclinical and clinical studies. Neural oscillations and their interactions are involved in cognitive functions and support the communication of neural information. The neural oscillation could be a window from which we may understand what happens in the brain. The current study aimed to explore if 15 Hz rTMS plays a neural modulation role in a mouse model of hindlimb unloading. We hypothezed that rTMS can improve the cognitive and neural oscillatory deficits induced by hindlimb unloading via maintaining the balance between glutamatergic and GABAergic systems. Our data show that rTMS can significantly alleviate behavior deficits, modulate theta oscillation, improve the disturbed power distribution of theta oscillation and the decreased strength of Cross-Frequency Coupling in the dentate gyrus region, and effectively mitigated the blocked communication of neural information in the perforant pathway (PP)―dentate gyrus (DG) neural pathway in Hu mice. Furthermore, biochemical analysis using high-performance liquid chromatography and Western blot assay confirmed that rTMS increases the low expression of glutamate (Glu) and N-Methyl d -Aspartate receptor subtype 2B (NR2B) and decreases the high expression of γ-aminobutyric acid (GABA), 67 KDa isoform of glutamate decarboxylase (GAD67), and GABA type A receptor subunit alpha1 (GABAAR α1) in the hippocampus of Hu mice. Taken together, the results suggest that rTMS plays a significant neural modulation role in the hippocampal neural activity disorders induced by Hu, which possibly depends on rTMS maintaining the balance of glutamatergic and gamma-aminobutyric acidergic (GABAergic) systems. [ABSTRACT FROM AUTHOR]

We injected mice with an adenovirus coated with an interference sequence, and the results showed that GABAergic synapses signaling pathway, Glutamatergic synapses signaling pathway and Cholinergic synapses pathway were damaged.At the mesoscopic level, the phase synchronization and phase amplitude coupling of the oscillating signals and synaptic plasticity in the hippocampus of mice were all impaired. At the macro level, the cognitive memory ability and the maintenance of working memory of mice were abnormal. Neural oscillation pattern provides a potential diagnosis approach for mental disorders. [Display omitted] • Knocking down Disc1 gene is a proper animal model of mental disorders. • Disc1 gene knockdown mice show memory deficits and synaptic plasticity impairments. • Disc1 gene knockdown mice exhibit abnormal neural oscillations in the hippocampus. • Neural oscillation analysis offers a potential diagnosis method for mental disorders. The gene of Disrupted-in-schizophrenia 1 (Disc1) is closely related to mental diseases with cognitive deficits, but there are few studies on the changes in neural oscillations and recognition memory. Neural oscillations plays a key role in the nervous system in a dynamic form, which is closely related to advanced cognitive activities such as information processing and memory consolidation. Hence, we aimed to investigate if Disc1 knockdown disrupted the normal pattern of neural activities in the mouse hippocampus network, and determined if quantitative neural oscillation approach could be a potential diagnostic tool for mental disorders. In the study, we reported that Disc1 gene, downregulated by short-hairpin RNA (shRNA), not only induced anxiety-like behavior and sociability impairment but also damaged both synaptic plasticity and recognition memory in mice. Moreover, Disc1 knockdown mice exhibited evidently abnormal power spectral distributions, reduced phase synchronizations, and decreased phase-amplitude coupling strength compared to that of normal animals. In addition, transcriptome analyses showed that there were clearly transcriptional changes in Disc1 knockdown mice. Altogether, our findings suggest that the abnormal pattern of neural activities in the hippocampus network disrupts information processing and finally leads to the impairments of synaptic plasticity and recognition in Disc1 knockdown mice, which are possibly associated with the obstruction of neurotransmitter transmission. Importantly, the data imply that the analysis of neural oscillation pattern provides a potential diagnosis approach for mental disorders. [ABSTRACT FROM AUTHOR]