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Pain Medicine 2017

October 19-20, 2017

Volume 6, Issue 6 (Suppl)

J Pain Relief, an open access journal

ISSN: 2167-0846

October 19-20, 2017 San Francisco, USA

4

th

International Conference on

Pain Medicine

The role of the endocannabinoid system in a mouse model of ddC-Induced neuropathic pain

Neha Munawar

Kuwait University, Kuwait

Statement of the Problem:

Nucleoside reverse transcriptase inhibitors (NRTIs) are the cornerstone in the treatment of HIV/AIDS.

Sometimes, their use is limited by the development of a painful neuropathy, which does not respond well to drugs. However, some HIV

patients with painful neuropathy report relief after using cannabis. The aim of this study is to evaluate whether the endocannabinoid

system plays a role in NRTI-induced painful neuropathy.

Methodology & Theoretical Orientation:

Female BALB/c mice were treated with 25 mg/kg of 2′, 3′-dideoxycytidine (ddC). The

expression of the endocannabinoid system molecules was evaluated by real-time RT-PCR in the brain, spinal cord and paw skin

at days two, six and nine post ddC administration. The effects of the endocannabinoids, N-arachidonoyl ethanolamine (AEA),

2-arachidonoyl glycerol (2-AG), cannabinoid receptor antagonists, AM 251 and AM 630 on ddC-induced thermal hyperalgesia were

evaluated using the hot plate test.

Findings:

Mice treated with ddC developed mechanical and cold allodynia, thermal hyperalgesia and chemical hyposensitivity. Mice

are sacrificed at a time point when they had developed allodynia, hyperalgesia or hyposensitivity which had increased transcripts of

phospholipase C-1beta and acylglycerol kinase in the paw skins and spinal cords but not in the brain. On the other hand, transcripts

of fatty acid amide hydrolase and monoacyl glycerol were down regulated in the paw skins and brains but not in the spinal cord. AEA

and 2-AG had antihyperalgesic effects against ddC-induced thermal hyperalgesia, but had no effect in naïve mice. The antihyperalgesic

activity of AEA was antagonized by AM251 and AM630, whereas the activity of 2-AG was antagonized by AM251 but not by AM630.

Conclusion & Significance:

Our results show that ddC induces painful neuropathy, which is associated with dysregulation of the

endocannabinoid system. Agonists of cannabinoid receptors could be useful therapeutic agents for the management of NRTI-induced

painful sensory neuropathy.

neha_med@hotmail.com

J Pain Relief 2017, 6:6 (Suppl)

DOI: 10.4172/2167-0846-C1-018