Ketamine differentially restores diverse alterations of neuroligins in brain regions in a rat model of neuropathic pain-induced depression.
Wei Pan, Guang-Fen Zhang, Hui-Hui Li, Mu-Huo Ji, Zhi-qiang Zhou, Kuan-Yu Li, Jian-Jun Yang
Neuroreport July 4, 2018 DOI: 10.1097/wnr.0000000000001045 (opens in new tab)
Study at a glance
AI-extracted from the abstract| Characteristics | Animal experimental study (rat model) Peer reviewed |
|---|---|
| Population | Rats with spared nerve injury-induced neuropathic pain and depressive-like behavior |
| Intervention | Ketamine |
| Dose | 10 mg/kg |
| Duration | Assessed at 24 h and 72 h after ketamine administration |
| Topics | Depression Esketamine Ketamine |
| Key findings | Spared nerve injury in rats produced mechanical allodynia and depressive-like symptoms with region-specific neuroligin changes (decreased NL1 and increased NL2 in medial prefrontal cortex, decreased NL1 in anterior cingulate cortex, decreased NL2 in hippocampus) and reduced BDNF. Ketamine at 10 mg/kg relieved depressive behaviors and restored BDNF and neuroligin alterations in medial prefrontal cortex and hippocampus at 24 and 72 hours, but only restored BDNF in anterior cingulate cortex. |
Abstract
Depression is present in a large proportion of patients suffering from chronic pain, and yet the underlying mechanisms remain to be elucidated. Neuroligins (NLs), as a family of cell-adhesion proteins, are involved in synaptic formation and have been linked to various neuropsychiatric disorders. Here, we studied the alterations in NL1 and NL2 in the medial prefrontal cortex (mPFC), the anterior cingulate cortex (ACC), and the hippocampus in a rat model of neuropathic pain-induced depression, and whether ketamine, a rapid and robust antidepressant, could restore these abnormalities. In the present study, we found that spared nerve injury induced significant mechanical allodynia and subsequent depressive-like symptoms, along with decreased NL1 and increased NL2 in the mPFC, decreased NL1 in the ACC, and decreased NL2 in the hippocampus. In addition, brain-derived neurotrophic factor (BDNF) was reduced in these brain regions. It is noteworthy that ketamine (10 mg/kg) relieved neuropathic pain-induced depressive behaviors and restored alterations of BDNF and NLs in the mPFC and the hippocampus at 24 h and 72 h after the administration of ketamine, but only restored BDNF in the ACC. In conclusion, NLs showed diverse changes in different brain regions in the rat model of neuropathic pain-induced depression, which could be reversed differentially by the administration of ketamine.
Comparable studies
Other preclinical and animal studies on ketamine for depression, most cited first.
Citations in the library
Cited by 3
- Chronic Neuropathic Pain and Comorbid Depression Syndrome: From Neural Circuit Mechanisms to Treatment. ACS Chemical Neuroscience July 3, 2024
- Exploring the Therapeutic Potential of N-Methyl-D-Aspartate Receptor Antagonists in Neuropathic Pain Management. International Journal of Molecular Sciences October 16, 2024
- Shared effects of electroconvulsive shocks and ketamine on neuroplasticity: A systematic review of animal models of depression. Neuroscience & Biobehavioral Reviews September 1, 2024
Cites 2
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- Increased anterior cingulate cortical activity in response to fearful faces: a neurophysiological biomarker that predicts rapid antidepressant response to ketamine. Biological Psychiatry February 15, 2009