Chronic pain enhances excitability of corticotropin-releasing factor-expressing neurons in the oval part of the bed nucleus of the stria terminalis.
Ryoko UchidaYasutaka MukaiTaiju AmanoKenji SakimuraKeiichi ItoiAkihiro YamanakaMasabumi MinamiPublished in: Molecular brain (2024)
We previously reported that enhanced corticotropin-releasing factor (CRF) signaling in the bed nucleus of the stria terminalis (BNST) caused the aversive responses during acute pain and suppressed the brain reward system during chronic pain. However, it remains to be examined whether chronic pain alters the excitability of CRF neurons in the BNST. In this study we investigated the chronic pain-induced changes in excitability of CRF-expressing neurons in the oval part of the BNST (ovBNST CRF neurons) by whole-cell patch-clamp electrophysiology. CRF-Cre; Ai14 mice were used to visualize CRF neurons by tdTomato. Electrophysiological recordings from brain slices prepared from a mouse model of neuropathic pain revealed that rheobase and firing threshold were significantly decreased in the chronic pain group compared with the sham-operated control group. Firing rate of the chronic pain group was higher than that of the control group. These data indicate that chronic pain elevated neuronal excitability of ovBNST CRF neurons.
Keyphrases
- chronic pain
- spinal cord
- neuropathic pain
- pain management
- transcranial direct current stimulation
- mouse model
- white matter
- type diabetes
- single cell
- stem cells
- bone marrow
- cerebral ischemia
- machine learning
- clinical trial
- mesenchymal stem cells
- skeletal muscle
- electronic health record
- subarachnoid hemorrhage
- mass spectrometry
- high resolution
- working memory
- multiple sclerosis
- acute respiratory distress syndrome
- intensive care unit
- single molecule