Impaired Neuropathic Pain and Preserved Acute Pain in Rats Overexpressing Voltage-Gated Potassium Channel Subunit Kv1.2 in Primary Afferent Neurons

• Published in: Molecular pain 2014-01, Vol.10 (1), p.8-8
• Main Authors: Fan, Longchang, Guan, Xiaowei, Wang, Wei, Zhao, Jian-Yuan, Zhang, Hongkang, Tiwari, Vinod, Hoffman, Paul N, Li, Min, Tao, Yuan-Xiang
• Format: Article
• Language: English
• Subjects: Acute pain; Acute Pain - metabolism; Acute Pain - pathology; Acute Pain - physiopathology; Anesthesiology; Animals; Antisense RNA; Axotomy; Behavior; Capsaicin; Channel gating; Colleges & universities; Dorsal root ganglia; Excitability; Experiments; Ganglia, Spinal - metabolism; HEK293 Cells; Humans; Kv1.2 Potassium Channel - genetics; Kv1.2 Potassium Channel - metabolism; Ligation; Male; Medicine; Motor Activity; Neuralgia - metabolism; Neuralgia - pathology; Neuralgia - physiopathology; Neurons; Neurons, Afferent - metabolism; Neurons, Afferent - pathology; Nociception; Pain; Pain management; Peripheral Nerve Injuries - metabolism; Peripheral Nerve Injuries - pathology; Peripheral Nerve Injuries - physiopathology; Peripheral nerves; Peripheral neuropathy; Physiological aspects; Potassium; Potassium channels; Potassium channels (voltage-gated); Protein Transport; Proteins; Rats; Rats, Sprague-Dawley; RNA, Antisense - genetics; RNA, Antisense - metabolism; RNA, Messenger - genetics; RNA, Messenger - metabolism; Rodents; Sciatic nerve; Sensory neurons; Spinal nerves; Spinal Nerves - metabolism; Spinal Nerves - pathology; Spinal Nerves - physiopathology; Time Factors; Transfection; Up-Regulation
• ISSN: 1744-8069; 1744-8069
• DOI: 10.1186/1744-8069-10-8

Voltage-gated potassium (Kv) channels are critical in controlling neuronal excitability and are involved in the induction of neuropathic pain. Therefore, Kv channels might be potential targets for prevention and/or treatment of this disorder. We reported here that a majority of dorsal root ganglion (DRG) neurons were positive for Kv channel alpha subunit Kv1.2. Most of them were large and medium, although there was a variety of sizes. Peripheral nerve injury caused by lumbar (L)5 spinal nerve ligation (SNL) produced a time-dependent reduction in the number of Kv1.2-positive neurons in the ipsilateral L5 DRG, but not in the contralateral L5 DRG. Such reduction was also observed in the ipsilateral L5 DRG on day 7 after sciatic nerve axotomy. Rescuing nerve injury-induced reduction of Kv1.2 in the injured L5 DRG attenuated the development and maintenance of SNL-induced pain hypersensitivity without affecting acute pain and locomotor function. This effect might be attributed to the prevention of SNL-induced upregulation of endogenous Kv1.2 antisense RNA, in addition to the increase in Kv1.2 protein expression, in the injured DRG. Our findings suggest that Kv1.2 may be a novel potential target for preventing and/or treating neuropathic pain.