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Neural synchrony in brain circuits is the mainstay of cognition, including memory processes. Alzheimer's disease (AD) is a progressive neurodegenerative disorder that disrupts neural synchrony in specific circuits, associated with memory dysfunction before a substantial neural loss. Recognition memory impairment is a prominent cognitive symptom in the early stages of AD. The entorhinal-hippocampal circuit is critically engaged in recognition memory and is known as one of the earliest circuits involved due to AD pathology. Notably, the olfactory bulb is closely connected with the entorhinal-hippocampal circuit and is suggested as one of the earliest regions affected by AD. Therefore, we recorded simultaneous local field potential from the olfactory bulb (OB), entorhinal cortex (EC), and dorsal hippocampus (dHPC) to explore the functional connectivity in the OB-EC-dHPC circuit during novel object recognition (NOR) task performance in a rat model of AD. Animals that received amyloid-beta (Aβ) showed a significant impairment in task performance and a marked reduction in OB survived cells. We revealed that Aβ reduced coherence and synchrony in the OB-EC-dHPC circuit at theta and gamma bands during NOR performance. Importantly, our results exhibit that disrupted functional connectivity in the OB-EC-dHPC circuit was correlated with impaired recognition memory induced by Aβ. These findings can elucidate dynamic changes in neural activities underlying AD, helping to find novel diagnostic and therapeutic targets., (© 2022. The Author(s).)

Allergic asthma is a chronic inflammatory respiratory disease. Psychiatric disorders, including anxiety are associated with poorer treatment response and disease control in asthmatic patients. To date, there is no experimental evidence describing the role of peripheral inflammation on the oscillatory activities in the anterior cingulate cortex (ACC) and basolateral amygdala (BLA), two major brain structures modulating anxiety. In the present work we evaluated lung and brain inflammatory responses, anxiety-like behavior, in association with oscillatory features of the ACC-BLA circuit in an animal model of allergic inflammation. Our data showed that allergic inflammation induced anxiety-like behavior and reactivation of microglia and astrocytes in ACC and BLA. Allergic inflammation also enhanced neuronal activities and functional connectivity of the ACC-BLA circuit which were correlated with the level of anxiety. Together, we suggest that disruption in the dynamic oscillatory activities of the ACC-BLA circuit, maybe due to regional inflammation, is an underlying mechanism of allergic asthma-induced anxiety-like behavior. Our findings could pave the way for better understanding the neuro-pathophysiology of the psychiatric disorders observed in asthmatic patients, possibly leading to develop novel treatment strategies., (© 2022. The Author(s).)

Anxiety is prevalent in asthma, and is associated with disease severity and poor quality of life. However, no study to date provides direct experimental evidence for the effect of allergic inflammation on the structure and function of medial prefrontal cortex (mPFC) and amygdala, which are essential regions for modulating anxiety and its behavioral expression. We assessed the impact of ovalbumin (OVA)-induced allergic inflammation on the appearance of anxiety-like behavior, mPFC and amygdala volumes using MRI, and the mPFC-amygdala circuit activity in sensitized rats. Our findings exhibited that the OVA challenge in sensitized rats induced anxiety-like behavior, and led to more activated microglia and astrocytes in the mPFC and amygdala. We also found a negative correlation between anxiety-like behavior and amygdala volume. Moreover, OVA challenge in sensitized rats was associated with increases in mPFC and amygdala activity, elevation of amygdala delta-gamma coupling, and the enhancement of functional connectivity within mPFC-amygdala circuit - accompanied by an inverted direction of information transferred from the amygdala to the mPFC. We indicated that disrupting the dynamic interactions of the mPFC-amygdala circuit may contribute to the induction of anxiety-related behaviors with asthma. These findings could provide new insight to clarify the underlying mechanisms of allergic inflammation-induced psychiatric disorders related to asthma.