Olfactory bulb-medial prefrontal cortex theta synchronization is associated with anxiety.

Anxiety is among the most fundamental mammalian behaviors. Despite the physiological and pathological importance, its underlying neural mechanisms remain poorly understood. Here, we recorded the activity of olfactory bulb (OB) and medial prefrontal cortex (mPFC) of rats, which are critical structures to brain's emotional processing network, while exploring different anxiogenic environments. Our results show that presence in anxiogenic contexts increases the OB and mPFC regional theta activities. Also, these local activity changes are associated with enhanced OB-mPFC theta power- and phase-based functional connectivity as well as OB-to-mPFC information transfer. Interestingly, these effects are more prominent in the unsafe zones of the anxiogenic environments, compared to safer zones. This consistent trend of changes in diverse behavioral environments as well as local and long-range neural activity features suggest that the dynamics of OB-mPFC circuit theta oscillations might underlie different types of anxiety behaviors, with possible implications for anxiety disorders.

Corticosteroid treatment attenuates anxiety and mPFC-amygdala circuit dysfunction in allergic asthma.

AIMS: Allergic asthma is associated with anxiety-related behaviors, leading to poor quality of life. Previous studies mainly described the neuropathophysiology of asthma-induced anxiety. However, the effects of corticosteroids, the most common anti-inflammatory agents for asthma treatment, on the neurophysiological foundations of allergic asthma-induced anxiety are unexplored. MAIN METHODS: Here, we evaluated lung and brain inflammation as well as anxiety in an animal model of allergic asthma pretreated with inhaled fluticasone propionate. Furthermore, to define the neurophysiological bases of these conditions, we studied the medial prefrontal cortex (mPFC)-amygdala circuit, which is previously shown to accompany asthma-induced anxiety. KEY FINDINGS: Our data showed that allergen induces anxiety, mPFC and amygdala inflammation, as well as disruptions in the local and long-range oscillatory activities within the mPFC-amygdala circuit. Interestingly, we observed a roughly consistent trend of changes with inhaled fluticasone pretreatment. Namely, the asthma-induced behavioral, inflammatory, and neurophysiological changes were partly, but not totally, prevented by inhaled fluticasone pretreatment. SIGNIFICANCE: We suggest that early treatment of asthmatic patients with inhaled corticosteroids improves mPFC-amygdala circuit function by attenuating neuroinflammation leading to reduced anxiety. These findings could lead clinical guidelines of asthma to consider the neuropsychiatric disorders of patients in treatment recommendations.