The changes of mitochondrial cytochrome c and GABAergic neuron in neuropathic pain model.
10.4097/kjae.2012.62.4.365
- Author:
Won Sung KIM
1
;
Ju Yeon PARK
;
Tae Kyun KIM
;
Seong Wan BAIK
Author Information
1. Department of Anesthesia and Pain Medicine, School of Medicine, Pusan National University, Busan, Korea. wbaik@pusan.ac.kr
- Publication Type:Original Article
- Keywords:
Allodynia;
Cyclosporine A;
Cytochrome c;
Mitochondrial permeability transition pore;
Neuropathic pain
- MeSH:
1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine;
Animals;
Apoptosis;
Cell Death;
Cyclosporine;
Cytochromes;
Cytochromes c;
Cytosol;
GABAergic Neurons;
Homeostasis;
Hyperalgesia;
Mitochondrial Membrane Transport Proteins;
Mitochondrial Swelling;
Neuralgia;
Permeability;
Rats;
Salicylamides;
Sciatic Nerve;
Spinal Cord
- From:Korean Journal of Anesthesiology
2012;62(4):365-370
- CountryRepublic of Korea
- Language:English
-
Abstract:
BACKGROUND: Role of cytochrome c (Cyt c) is an apoptogenic agent under certain conditions. The mitochondrial permeability transition pore (MPTP) plays an important role in cell death since it opens, leading to mitochondrial swelling and release of Cyt c, which initiates apoptosis. By inhibiting the opening of MPTP, cyclosporine A (CSA) may contribute to maintaining mitochondrial homeostasis. We investigate the effects of the partial sciatic nerve injury (PSNI)-induced neuropathic pain model on mitochondrial Cyt c release and the effects of CSA on neuroprotection by mitochondrial stabilizing activity in PSNI rats. METHODS: Rats were assigned to two groups that received different operations (Group P; PSNI operation, Group S; sham operation). The changes of cyt c and GABAergic neuron were evaluated in the spinal cord tissue. After which, PSNI rats randomly received CSA (Group C) or saline (Group S), and the changes of mechanical thresholds with Cyt c and GABAergic neuron were checked. RESULTS: PSNI in rats increased the release of cytosolic Cyt c. However, GABAergic cells were not decreased in the spinal cord level on the ipsilateral side to the PSNI. The second experiment reveal a reduction in Cyt c release, using CSA in PSNI model. Rats receiving CSA were afforded the antiallodynia without decrease of GABAergic cell. CONCLUSIONS: The Cyt c probably contributes to nerve dysfunction after PSNI. PSNI induced neuropathic pain was profoundly linked to mitochondrial stabilization. Thus, the potent neuroprotector, CSA, might produce antiallodynia through its capability to inhibit the opening of MPTP.
