| Apoptosis of the GABAergic interneuron in the dorsal horn of the chronic post-ischemic pain model. |
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Joo Hyeuk Park, Tae Kyun Kim, Hae Kyu Kim, Seong Wan Baik |
1Department of Anesthesia and Pain Medicine, School of Medicine, Pusan National University, Busan, Korea. swbaik@pusan.ac.kr
2Department of Anesthesia and Pain Medicine, Kwang Hye Hospital, Busan, Korea. |
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| Abstract |
BACKGROUND
It is well known that the GABAergic inhibitory interneuronal system plays an important role in modulation of the noxious stimulation transmitted from the primary afferent input. Some studies have revealed the role that the GABA inhibitory interneuronal system plays in the modulation of pain transmission and the changes in the GABAergic interneurons that occur during the neuropathic pain. This study was conducted to evaluate the apoptosis of the GABAergic interneuron, which is assumed to contribute to neuropathic pain. METHODS: Male Sprague-Dawley rats weighing 290-310 g were used to create a CPIP (chronic post-ischemic pain) model, which was made by placing a tourniquet on the left hindpaw of the rats. The tourniquet was maintained for 3 hours, after which it was released to allow reperfusion.
Thirty minutes prior to reperfusion, N-acetyl-L-cysteine (NAC group) or normal saline (control group) was injected.
After reperfusion, mechanical allodynia and cold allodynia were measured. In addition, the release of cytochrome c into the cytosol was evaluated through western blot or immunohistochemistry of the spinal cord. RESULTS: Mechanical and cold allodynia developed and the number of GABA interneurons was reduced in the control group. Additionally, The cytochrome c from the GABA interneuron was released into the cytosol in the control group, but the amount released was reduced in response to treatment with NAC. CONCLUSIONS: The results of this study showed that the GABA interneuron in the Rexed laminae I, II released cytochrome c into the cytosol in CPIP neuropathic pain model, which is known to lead to apoptosis. However, treatment with N-acetyl-L-cysteine prevented this process. |
| Key Words:
Acetylcysteine; Complex regional pain syndromes; Cytochrome c; Interneurons; Ischemia; Reperfusion |
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