A pharynx-to-brain axis controls pharyngeal inflammation-induced anxiety.
Wan ZhaoKe ZhangWan-Ying DongHao-Di TangJia-Qiang SunJi-Ye HuangGuang-Lun WanRui-Rui GuanXiao-Tao GuoPing-Kai ChengRan TaoJing-Wu SunZhi ZhangXia ZhuPublished in: Proceedings of the National Academy of Sciences of the United States of America (2024)
Anxiety is a remarkably common condition among patients with pharyngitis, but the relationship between these disorders has received little research attention, and the underlying neural mechanisms remain unknown. Here, we show that the densely innervated pharynx transmits signals induced by pharyngeal inflammation to glossopharyngeal and vagal sensory neurons of the nodose/jugular/petrosal (NJP) superganglia in mice. Specifically, the NJP superganglia project to norepinephrinergic neurons in the nucleus of the solitary tract (NTS NE ). These NTS NE neurons project to the ventral bed nucleus of the stria terminalis (vBNST) that induces anxiety-like behaviors in a murine model of pharyngeal inflammation. Inhibiting this pharynx→NJP→NTS NE →vBNST circuit can alleviate anxiety-like behaviors associated with pharyngeal inflammation. This study thus defines a pharynx-to-brain axis that mechanistically links pharyngeal inflammation and emotional response.
Keyphrases
- oxidative stress
- spinal cord
- diabetic rats
- quality improvement
- working memory
- type diabetes
- multiple sclerosis
- metabolic syndrome
- adipose tissue
- spinal cord injury
- signaling pathway
- skeletal muscle
- resting state
- depressive symptoms
- endothelial cells
- ultrasound guided
- high glucose
- insulin resistance
- subarachnoid hemorrhage
- blood brain barrier