Effect of ZBD-2 on chronic pain, depressive-like behaviors, and recovery of motor function following spinal cord injury in mice
| Autor: | Lin tao Li, Yong Chen, Xu-bo Li, Xiaoming Li, Qi Yang, Jian-ning Zhao, Jia Meng, Qi-xin Shi, Ting Guo, Liu-kun Yang |
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| Rok vydání: | 2017 |
| Předmět: |
Male
0301 basic medicine medicine.medical_specialty Purinones Pain Spinal cord injury Motor Activity CREB Article Random Allocation 03 medical and health sciences Behavioral Neuroscience 0302 clinical medicine Receptors GABA Neurotrophic factors Internal medicine Acetamides medicine Translocator protein Animals Spinal Cord Injuries Depression (differential diagnoses) Dose-Response Relationship Drug Microglia biology Depression Chronic pain Brain Recovery of Function medicine.disease Spinal cord Mice Inbred C57BL Disease Models Animal 030104 developmental biology medicine.anatomical_structure Endocrinology Spinal Cord biology.protein Chronic Pain Psychology Neuroscience 030217 neurology & neurosurgery Central Nervous System Agents |
| Zdroj: | Behavioural Brain Research |
| ISSN: | 0166-4328 |
| DOI: | 10.1016/j.bbr.2017.01.025 |
| Popis: | Highlights • ZBD-2 significantly attenuated the symptoms of chronic SCI-pain and pain-induced depressive-like behaviors. • ZBD-2 inhibited the decreases in the expression of synaptic plasticity-related signaling proteins. • ZBD-2 reversed chronic, SCI-induced gliocyte activation at the lesion site. In addition to debilitating sensory and motor deficits, patients with spinal cord injury (SCI) may experience chronic hyperpathic pain (SCI-pain). Recent studies have revealed that translocator protein (TSPO) is involved in repairing neural cells as well as reducing anxiety and depression. However, the role of TSPO in SCI-pain and pain-induced depression remains unknown. The present study aimed to determine the effects of a new TSPO ligand, ZBD-2, on SCI-pain and consequent pain-induced depressive-like behaviors in mice. Treatment with ZBD-2 at either dose significantly attenuated the symptoms of chronic SCI-pain and pain-induced depressive-like behaviors. ZBD-2 reversed SCI-induced elevation of serum corticosterone levels, an index of hyper-activation of the hypothalamic–pituitary–adrenal (HPA) axis. Additionally, administration of ZBD-2 inhibited decreases in the expression of synaptic plasticity-related signaling proteins, including brain-derived neurotrophic factor (BDNF) and cyclic AMP-responsive element binding protein (CREB). Moreover, ZBD-2 administration reversed chronic, SCI-induced gliocyte activation at the lesion site. Therefore, ZBD-2 may improve chronic SCI-pain and pain-induced depressive-like behaviors via suppression of gliocyte activation and restoration of the synaptic plasticity-related signaling systems. |
| Databáze: | OpenAIRE |
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