INVESTIGATING THE CONTRIBUTION OF ION CHANNEL DYSREGULATION AND NEURONAL HYPEREXCITABILITY TO THE PATHOGENESIS OF NEUROPATHIC PAIN AND ASSOCIATED NEURONAL DAMAGE
MOHD RAHMAN BIN ABDULLAH
Department of Neurology, Sultan Qaboos University, Al Khoudh Road, Muscat, 123, Oman.
HASSAN NOORANI
Department of Neurology, University of Jordan, Al-Jamia Street, Amman, 11941, Jordan.
Abstract
Neuropathic pain arises from direct damage or dysfunction within the somatosensory nervous system, leading to persistent and debilitating pain. A key aspect of its pathogenesis involves the dysregulation of ion channels and the subsequent neuronal hyperexcitability. Ion channels, such as voltage-gated sodium, potassium, and calcium channels, along with transient receptor potential (TRP) channels, play pivotal roles in regulating neuronal excitability and synaptic transmission. In neuropathic pain, injury-induced alterations in these channels contribute to abnormal signaling within sensory neurons, resulting in spontaneous activity, increased sensitivity to stimuli, and exaggerated pain perception. Furthermore, changes in ion channel expression and function, often driven by inflammatory mediators and injury-induced cellular changes, exacerbate neuronal hyperexcitability and contribute to neuronal damage. This review explores the role of ion channel dysregulation in the pathogenesis of neuropathic pain, focusing on specific channels such as Nav1.7, Nav1.8, TRPV1, and Kv channels. We also examine the molecular mechanisms underlying these changes, including the influence of neuroinflammation and the involvement of key signaling pathways like MAPK and NF-$\kappa$B. Understanding these mechanisms provides insight into potential therapeutic targets for managing neuropathic pain. By modulating ion channel activity and reducing hyperexcitability, it may be possible to alleviate pain and prevent further neuronal damage. This review aims to highlight the importance of ion channel dysregulation in neuropathic pain and suggest potential avenues for targeted therapeutic intervention.
Author Biography
HASSAN NOORANI, Department of Neurology, University of Jordan, Al-Jamia Street, Amman, 11941, Jordan.
