Journal
ENEURO
Volume 2, Issue 1, Pages -Publisher
SOC NEUROSCIENCE
DOI: 10.1523/ENEURO.0057-14.2015
Keywords
alpha9/alpha10 AChR current; analagesic mechanisms; baclofen; CaV2.2 current; rat sensory neurons
Categories
Funding
- NIH [GM48677, GM103801, AR59397]
- NATIONAL INSTITUTE OF ARTHRITIS AND MUSCULOSKELETAL AND SKIN DISEASES [R01AR059397] Funding Source: NIH RePORTER
- NATIONAL INSTITUTE OF GENERAL MEDICAL SCIENCES [R01GM103801, P01GM048677] Funding Source: NIH RePORTER
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Chronic pain is very difficult to treat. Thus, novel analgesics are a critical area of research. Strong preclinical evidence supports the analgesic effects of alpha-conopeptides, Vc1.1 and RgIA, which block alpha 9 alpha 10 nicotinic acetylcholine receptors (nAChRs). However, the analgesic mechanism is controversial. Some evidence supports the block of alpha 9 alpha 10 nAChRs as an analgesic mechanism, while other evidence supports the inhibition of N-type Ca-V (Ca(V)2.2) current via activation of GABA(B) receptors. Here, we reassess the effect of Vc1.1 and RgIA on Ca-V current in rat sensory neurons. Unlike the previous findings, we found highly variable effects among individual sensory neurons, but on average only minimal inhibition induced by Vc1.1, and no significant effect on the current by RgIA. We also investigated the potential involvement of GABAB receptors in the Vc1.1-induced inhibition, and found no correlation between the size of Ca-V current inhibition induced by baclofen (GABA(B) agonist) versus that induced by Vc1.1. Thus, GABA(B) receptors are unlikely to mediate the Vc1.1-induced Ca-V current inhibition. Based on the present findings, Ca-V current inhibition in dorsal root ganglia is unlikely to be the predominant mechanism by which either Vc1.1 or RgIA induce analgesia.
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