ArticleCNS neuroscience & therapeutics2024
HCN channels in the lateral habenula regulate pain and comorbid depressive-like behaviors in mice.
Article in CNS neuroscience & therapeutics, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
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Who cites it
6 citing papers in PubMed.
- Synaptic Plasticity-Intrinsic Excitability and Antidepressant Discovery.Biomedicines · 2026Review
- Article
- A common Iba1 antibody labels vasopressin neurons in mice.bioRxiv : the preprint server for biology · 2025Article
- Electroacupuncture Ameliorates Chronic Inflammatory Pain and Depression Comorbidity by Inhibiting Nrf2-Mediated Ferroptosis in Hippocampal Neurons.Neurochemical research · 2025Article
- Altered synaptic homeostasis: a key factor in the pathophysiology of depression.Cell & bioscience · 2025Review
- HCN channels in the lateral habenula regulate pain and comorbid depressive-like behaviors in mice.CNS neuroscience & therapeutics · 2024Article
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12 authors.
Funding
Abstract
aimsComorbid anxiodepressive-like symptoms (CADS) in chronic pain are closely related to the overactivation of the lateral habenula (LHb). Hyperpolarization-activated cyclic nucleotide-gated (HCN) channels have been implicated to play a key role in regulating neuronal excitability. However, the role of HCN channels in the LHb during CADS has not yet been characterized. This study aimed to investigate the effect of HCN channels in the LHb on CADS during chronic pain.
methodsAfter chronic neuropathic pain induction by spared nerve injury (SNI), mice underwent a sucrose preference test, forced swimming test, tail suspension test, open-field test, and elevated plus maze test to evaluate their anxiodepressive-like behaviors. Electrophysiological recordings, immunohistochemistry, Western blotting, pharmacological experiments, and virus knockdown strategies were used to investigate the underlying mechanisms.
resultsEvident anxiodepressive-like behaviors were observed 6w after the SNI surgery, accompanied by increased neuronal excitability, enhanced HCN channel function, and increased expression of HCN2 isoforms in the LHb. Either pharmacological inhibition or virus knockdown of HCN2 channels significantly reduced LHb neuronal excitability and ameliorated both pain and depressive-like behaviors.
conclusionOur results indicated that the LHb neurons were hyperactive under CADS in chronic pain, and this hyperactivation possibly resulted from the enhanced function of HCN channels and up-regulation of HCN2 isoforms.
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