Direct paraventricular thalamus-basolateral amygdala circuit modulates neuropathic pain and emotional anxiety

The comorbidity of chronic pain and mental dysfunctions such as anxiety disorders has long been recognized, but the underlying mechanisms remained poorly understood. Here, using a mouse model of neuropathic pain, we demonstrated that the thalamic paraventricular nucleus (PVT) played a critical role...

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Published in:Neuropsychopharmacology (New York, N.Y.) N.Y.), 2024-01, Vol.49 (2), p.455-466
Main Authors: Tang, Qian-Qian, Wu, Yuanyuan, Tao, Qiang, Shen, Yanan, An, Xiaohu, Liu, Di, Xu, Zifeng
Format: Article
Language:English
Subjects:
Amygdala
Anxiety
Anxiety Disorders
Basolateral Nuclear Complex
Behavior
Chronic Disease
Chronic Pain
Comorbidity
Electrophysiology
Excitability
Glutamatergic transmission
Humans
Neuralgia
Neurons
Pain perception
Paraventricular nucleus
Phenotypes
Photometry
Thalamus
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Summary:The comorbidity of chronic pain and mental dysfunctions such as anxiety disorders has long been recognized, but the underlying mechanisms remained poorly understood. Here, using a mouse model of neuropathic pain, we demonstrated that the thalamic paraventricular nucleus (PVT) played a critical role in chronic pain-induced anxiety-like behavioral abnormalities. Fiber photometry and electrophysiology demonstrated that chronic pain increased the activities in PVT glutamatergic neurons. Chemogenetic manipulation revealed that suppression of PVT glutamatergic neurons relieved pain-like behavior and anxiety-like behaviors. Conversely, selective activation of PVT glutamatergic neurons showed algesic and anxiogenic effects. Furthermore, the elevated excitability of PVT glutamatergic neurons resulted in increased excitatory inputs to the basolateral complex (BLA) neurons. Optogenetic manipulation of the PVT-BLA pathway bilaterally modulates both the pain-like behavior and anxiety-like phenotypes. These findings shed light on how the PVT-BLA pathway contributed to the processing of pain-like behavior and maladaptive anxiety, and targeting this pathway might be a straightforward therapeutic strategy to both alleviate nociceptive hypersensitivity and rescue anxiety behaviors in chronic pain conditions.
ISSN:0893-133X
1740-634X
1740-634X
DOI:10.1038/s41386-023-01748-4