Journal ArticleDOI
Lysophosphatidylcholine causes neuropathic pain via the increase of neuronal nitric oxide synthase in the dorsal root ganglion and cuneate nucleus.
TLDR
Findings suggest that advanced NO made by the dramatically increased number of nNOS in the DRG and CN might be involved in the neuropathic sensation and boosted neuronal activity in the CN after LPC treatment.Abstract:
In this study, we investigated the role of nitric oxide (NO) in lysophosphatidylcholine (LPC) induced peripheral neuropathy by the use of nitric oxide synthase (NOS) inhibitors and NO donor. We found that LPC treatment of the median nerve induced neuropathic pain behaviors (allodynia and hyperalgesia) and nerve demyelination. Immunohistochemistry revealed that the amounts of neuronal NOS-like immunoreative (nNOS-LI) neurons in both the dorsal root ganglion (DRG) and cuneate nucleus (CN) increased and peaked at 1 week after LPC treatment. Following electrical stimulation of the LPC-treated nerve, the number of c-Fos-LI neurons in the ipsilateral CN also increased in a dose-dependent manner following LPC injection and peaked at 1 week. Administration of L-NAME (Nω-Nitro-L-arginine methyl ester) or 7-NI (7-nitroindazole) 1 week after 4% LPC injection attenuated tactile allodynia and thermal hyperalgesia. However, the application of the NO donor S-Nitroso-N-acetylpenicillamine (SNAP) only exacerbated thermal hyperalgesia. After electrical stimulation of the LPC-treated median nerve, the number of c-Fos-LI neurons in the CN diminished in the L-NAME and 7-NI groups, but increased in the SNAP group. Taken together, our findings suggest that advanced NO made by the dramatically increased number of nNOS in the DRG and CN might be involved in the neuropathic sensation and boosted neuronal activity in the CN after LPC treatment.read more
Citations
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Journal ArticleDOI
The mechanisms of lysophosphatidylcholine in the development of diseases
TL;DR: Targeting LPC and lipid metabolism might be a potential therapeutic method for inflammation-related diseases.
Journal ArticleDOI
Potential role of nitric oxide synthase isoforms in pathophysiology of neuropathic pain
TL;DR: Different nitric oxide synthases and their role in pathophysiology of neuropathic pain considering NOS as an important therapeutic target is focused on.
Journal ArticleDOI
Nitric oxide as a messenger between neurons and satellite glial cells in dorsal root ganglia.
Vitali Belzer,Menachem Hanani +1 more
TL;DR: It is proposed that NO synthesis in DRG neurons increases after peripheral inflammation and that NO induces SGC activation, which in turn contributes to neuronal hyperexcitability, and plays a major role in neuron–SGC communication.
Journal ArticleDOI
Nitric Oxide Signaling Contributes to Ectopic Orofacial Neuropathic Pain
T. Sugiyama,Masamichi Shinoda,Tetsuro Watase,Kuniya Honda,Reio Ito,Kaori Kaji,Kentaro Urata,Jun Lee,Kinuyo Ohara,O. Takahashi,S. Echizenya,Koichi Iwata +11 more
TL;DR: The present findings suggest that NO released from TG neurons regulates the excitability of TG neurons innervating the whisker pad skin, and the enhancement of TG neuronal excitability may underlie ectopic mechanical allodynia.
Journal ArticleDOI
Wen-Luo-Tong Decoction Attenuates Paclitaxel-Induced Peripheral Neuropathy by Regulating Linoleic Acid and Glycerophospholipid Metabolism Pathways.
TL;DR: A metabolomic method on the basis of UPLC- MS was developed and indicated that Wen-Luo-Tong attenuated mechanical allodynia and rebalanced the metabolic disturbances of PIPN by primarily regulating LA and glycerophospholipid metabolism pathway.
References
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