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Enhanced T-type calcium channel 3.2 activity in sensory neurons contributes to neuropathic-like pain of monosodium iodoacetate-induced knee osteoarthritis. | LitMetric

AI Article Synopsis

  • The study focuses on the monosodium iodoacetate model for knee osteoarthritis, which is used to understand chronic pain mechanisms, particularly examining the role of T-type calcium channel 3.2 (Ca3.2) in primary sensory neurons.
  • Researchers induced osteoarthritis in rats through an injection of monosodium iodoacetate and observed various pain and inflammatory responses, including increased hypersensitivity and structural changes in the knee joint and nervous system.
  • Results indicated significant upregulation of Ca3.2 expression and activity in sensory neurons, suggesting that Ca3.2 could be a potential target for pain relief therapies in osteoarthritis.

Article Abstract

The monosodium iodoacetate knee osteoarthritis model has been widely used for the evaluation of osteoarthritis pain, but the pathogenesis of associated chronic pain is not fully understood. The T-type calcium channel 3.2 (Ca3.2) is abundantly expressed in the primary sensory neurons, in which it regulates neuronal excitability at both the somata and peripheral terminals and facilitates spontaneous neurotransmitter release at the spinal terminals. In this study, we investigated the involvement of primary sensory neuron-Ca3.2 activation in monosodium iodoacetate osteoarthritis pain. Knee joint osteoarthritis pain was induced by intra-articular injection of monosodium iodoacetate (2 mg) in rats, and sensory behavior was evaluated for 35 days. At that time, knee joint structural histology, primary sensory neuron injury, and inflammatory gliosis in lumbar dorsal root ganglia, and spinal dorsal horn were examined. Primary sensory neuron-T-type calcium channel current by patch-clamp recording and Ca3.2 expression by immunohistochemistry and immunoblots were determined. In a subset of animals, pain relief by Ca3.2 inhibition after delivery of Ca3.2 inhibitor TTA-P2 into sciatic nerve was investigated. Knee injection of monosodium iodoacetate resulted in osteoarthritis histopathology, weight-bearing asymmetry, sensory hypersensitivity of the ipsilateral hindpaw, and inflammatory gliosis in the ipsilateral dorsal root ganglia, sciatic nerve, and spinal dorsal horn. Neuronal injury marker ATF-3 was extensively upregulated in primary sensory neurons, suggesting that neuronal damage was beyond merely knee-innervating primary sensory neurons. T-type current in dissociated primary sensory neurons from lumbar dorsal root ganglia of monosodium iodoacetate rats was significantly increased, and Ca3.2 protein levels in the dorsal root ganglia and spinal dorsal horn ipsilateral to monosodium iodoacetate by immunoblots were significantly increased, compared to controls. Perineural application of TTA-P2 into the ipsilateral sciatic nerve alleviated mechanical hypersensitivity and weight-bearing asymmetry in monosodium iodoacetate osteoarthritis rats. Overall, our findings demonstrate an elevated Ca3.2 expression and enhanced function of primary sensory neuron-T channels in the monosodium iodoacetate osteoarthritis pain. Further study is needed to delineate the importance of dysfunctional primary sensory neuron-Ca3.2 in osteoarthritis pain.

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Source
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC7570798PMC
http://dx.doi.org/10.1177/1744806920963807DOI Listing

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