Gamma oscillation is the synchronization with a frequency of 30–90 Hz of neural oscillations, which are rhythmic electric processes of neuron groups in the brain. The inhibitory interneuron network is necessary for the production of gamma oscillations, but certain disruptions such as brain inflammation, oxidative stress, and metabolic imbalances can cause this network to malfunction. Gamma oscillations specifically control the connectivity between different brain regions, which is crucial for perception, movement, memory, and emotion. Studies have linked abnormal gamma oscillations to conditions of the central nervous system, including Alzheimer’s disease, Parkinson’s disease, and schizophrenia. Evidence suggests that gamma entrainment using sensory stimuli (GENUS) provides significant neuroprotection. This review discusses the function of gamma oscillations in advanced brain activities from both a physiological and pathological standpoint, and it emphasizes gamma entrainment as a potential therapeutic approach for a range of neuropsychiatric diseases.

BackgroundPhobic anxiety present after stroke (called poststroke anxiety, PSA) can hamper the rehabilitation of patients and disrupt their usual activities. Besides, the symptoms and mechanisms of PSA are different from those in nonstroke populations that have generalized anxiety disorder. What’s more, the treatment approaches for phobic anxiety are confined to unitary or general methods with poor efficiency.MethodsBehavioural test screen combined bioinformatics analysis explored molecular changes between generalized anxiety disorder in nonstroke mice (restraint stress, RS) and photothrombotic stroke mice exposed to environmental stress (PTS + RS, mimicking PSA). Multiple molecular biological and neurobiological methods were employed to explain mechanisms in vitro and in vivo. And exploiting gamma flicker stimulation device for therapy.ResultsMicroglial (MG) overactivation is a prominent characteristic of PTS + RS. HDAC3 was mainly upregulated in activated-microglia from damaged cortex and that local prostaglandin E2 (PGE2) production increased in MG via HDAC3-mediated activation of NF-κB signalling by p65 deacetylation. A high content of PGE2 in damaged ischaemic cortex could diffuse freely to amygdala, eliciting anxiety susceptibility of PSA via EP2. Importantly, gamma flicker stimulation relieved anxious behaviour of PTS + RS by modulating the HDAC3/Cox1/EP2 network at some extent.ConclusionsHDAC3-regulated PGE2 production by microglia constitutes phobic anxiety susceptibility after stroke and a protective approach of gamma visual stimulation can be a candidate new therapy.

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Following systemic inflammatory response syndrome (SIRS), the brain is one of the most sensitive organs vulnerable to an external stressor. According to our previous study, ketamine had a protective effect on alleviating SIRS-associated neuronal necroptosis and cecal epithelial cell necroptosis by inhibiting the RIP1-RIP3-MLKL pathway. In this study, we further provided valid evidence that ketamine could safeguard the integrity of the blood-brain barrier (BBB), modulate microglia over-activation, and prevent neural network damage, resulting in relieving cerebral edema and improving system symptoms significantly. Simultaneously, cecum damage was partly reversed by ketamine intervention, which was attributed to a decrease in circulating high mobility group protein 1 (HMGB1). Interestingly, the result showed less cecum injury and relieved BBB disturbance in Rip3-/- mice. Furthermore, circulating HMGB1 content between Rip3-/- mice and mice with ketamine intervention significantly decreased. Moreover, anti-HMGB1 neutralizing antibody identically reversed BBB damage, indicating that cecum-promoted HMGB1 releases extravagated SIRS and BBB leakage. In addition, we clarified that cecectomy reduced serum HMGB1 release level and alleviated BBB damage and microglial activation. Altogether, our work shed light on the new view about the pathogenesis of SIRS, establishing the connection between cecum damage and BBB damage. Besides, we identified ketamine as a candidate to protect the brain from damage like BBB leakage and microglia over-activation, which attributed to the effect on alleviating cecum damage and decreasing circulation HMGB1 release. Our results provided a new theoretical view and therapeutic target for the application of ketamine in SIRS.