Neuroscience
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There has been a long history that chronic circadian disruption such as jet lag or shift work negatively affects brain and body physiology. Studies have shown that circadian misalignment act as a risk factor for developing anxiety and mood-related depression-like behavior. Till date, most studies focused on simulating jet lag in model animals under laboratory conditions by repeated phase advances or phase delay only, while the real-life conditions may differ. ⋯ In addition, CJL-exposed mice showed an increased level of serum corticosterone and proinflammatory cytokine, TNF-α in both serum and hippocampus. Moreover, CJL-exposed mice exhibited a reduction in structural complexity of hippocampal CA1 neurons along with decreased expression of neurotrophic growth factors, BDNF and NGF in the hippocampus compared to LD control. Taken together, our findings suggest that simulated chronic jet lag adversely affects structural and functional complexity in hippocampal neurons along with interrelated endocrine and inflammatory responses, ultimately leading to stress, anxiety, and depression-like behavior in mice.
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Meta Analysis
Functional and Structural Abnormalities in the Pain Network of Generalized Anxiety Disorder Patients with Pain Symptoms.
Pain symptoms significantly impact the well-being and work capacity of individuals with generalized anxiety disorder (GAD), and hinder treatment and recovery. Despite existing literature focusing on the neural substrate of pain and anxiety separately, further exploration is needed to understand the possible neuroimaging mechanisms of the pain symptoms in GAD patients. We recruited 73 GAD patients and 75 matched healthy controls (HC) for clinical assessments, as well as resting-state functional and structural magnetic resonance imaging scans. ⋯ Further correlation analysis revealed a positive correlation between ReHo of the left anterior insula and pain scores in GAD patients, while a respective negative correlation between GMV of the bilateral thalamus and PHQ-15 scores. In summary, GAD patients exhibit structural and functional abnormalities in pain-related networks. The enhanced ReHo in the left anterior insula is correlated with pain symptoms, which might be a crucial brain region of pain symptoms in GAD.
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In males but not in females, brain derived neurotrophic factor (BDNF) plays an obligatory role in the onset and maintenance of neuropathic pain. Afferent terminals of injured peripheral nerves release colony stimulating factor (CSF-1) and other mediators into the dorsal horn. These transform the phenotype of dorsal horn microglia such that they express P2X4 purinoceptors. ⋯ Possible mechanisms promoting the preferential release of BDNF in pain signaling structures are discussed. In females, invading T-lymphocytes increase dorsal horn excitability but it remains to be determined whether similar processes operate in supra-spinal structures. Despite its ubiquitous role in pain aetiology neither BDNF nor TrkB receptors represent potential therapeutic targets.
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Sex-specific differences in resting oscillatory dynamics in children with prenatal alcohol exposure.
At rest children with prenatal alcohol exposure (PAE) exhibit impaired static and dynamic functional connectivity, along with decreased alpha oscillations. Sex-specific information regarding the impact of PAE on whole-brain resting-state gamma spectral power remains unknown. Eyes-closed and eyes-open MEG resting-state data were examined in 83 children, ages 6-13 years of age. ⋯ The reduced delta oscillations in female participants with PAE/FASD were detected in several source regions during eyes-closed rest and were evident at younger ages. These results indicate PAE alters neural oscillations during rest in a sex-specific manner, with females with PAE/FASD showing the largest perturbations. These results further demonstrate PAE has global effects on resting-state spectral power and connectivity, creating long-term consequences by potentially disrupting the excitation/inhibition balance in the brain, interrupting normative neurodevelopment.