|1.||Lewis, R J: 3 articles (02/2010 - 11/2000)|
|2.||Adams, D J: 2 articles (02/2010 - 11/2000)|
|3.||Drinkwater, R: 2 articles (02/2010 - 11/2000)|
|4.||Alewood, P F: 2 articles (02/2010 - 11/2000)|
|5.||Wright, Christine E: 2 articles (01/2005 - 09/2002)|
|6.||Angus, James A: 2 articles (01/2005 - 09/2002)|
|7.||Scott, David A: 2 articles (01/2005 - 09/2002)|
|8.||Lewis, Richard J: 2 articles (08/2004 - 01/2004)|
|9.||Schroeder, Christina I: 2 articles (08/2004 - 01/2004)|
|10.||Nielsen, K J: 2 articles (11/2000 - 03/2000)|
02/01/2010 - "These N-type Ca(2+) channel-selective omega-conotoxins are therefore useful as neurophysiological tools and as potential therapeutic agents to inhibit nociceptive pain pathways."
02/01/2010 - "Neuronal (N)-type Ca(2+) channel-selective omega-conotoxins have emerged as potential new drugs for the treatment of chronic pain. "
08/13/2004 - "These results may have implications for the antinociceptive properties of omega-conotoxins, given that the alpha(2)delta subunit is up-regulated in certain pain states."
03/01/2013 - "Omega-conotoxins as experimental tools and therapeutics in pain management."
11/10/2000 - "omega-Conotoxins selective for N-type calcium channels are useful in the management of severe pain. "
09/20/2002 - "These observations show that intrathecal omega-conotoxins are effective in attenuating tactile allodynia in the rat without significantly affecting acute nociceptive responses. "
01/04/2005 - "Both dexmedetomidine and omega-conotoxin CVID completely inhibited allodynia (ED50 0.78+/-0.02 and 0.35+/-0.08 microg/kg, respectively; n=63, 41). "
09/20/2002 - "The ED(50) (and 95% CI) for attenuation of tactile allodynia by intrathecal administration for omega-conotoxin CVID, GVIA, MVIIA and morphine was 0.36 (0.27-0.48), 0.12 (0.06-0.24), 0.32 (0.23-0.45) and 4.4 (2.9-6.5) microg/kg, respectively. "
05/01/2009 - "Treatment with omega-conotoxin MV IIA before ischemia (0.1pmol/eye, intravitreous injection) significantly reduced the retinal damage. "
01/01/1992 - "Inhibition of ischemia-induced dopamine release by omega-conotoxin, a calcium channel blocker, in the striatum of spontaneously hypertensive rats: in vivo brain dialysis study."
05/01/1995 - "In both species neither omega-conotoxin (100 nmol/l) nor cadmium chloride (100 mumol/l) affected ischemia-induced noradrenaline overflow in both rat heart and atrium as well as in human atrium. "
05/01/2009 - "We histologically examined the effects of cilnidipine on neuronal injury induced by ischemia-reperfusion, intravitreous N-methyl-D-aspartate (NMDA) (200nmol/eye) and intravitreous NOC12 (400nmol/eye), an nitric oxide donor, in the rat retina, and compared its effects with those of omega-conotoxin MV IIA, an N-type Ca(2+) channel blocker and amlodipine, an L-type Ca(2+) channel blocker. "
08/15/1993 - "The synthetic omega-conotoxin peptide SNX-111, which selectively blocks depolarization-induced calcium fluxes through neuronal N-type voltage-sensitive calcium channels, protected the pyramidal neurons in the CA1 subfield of the hippocampus from damage caused by transient forebrain ischemia in the rat model of four-vessel occlusion. "
04/01/2009 - "Recent studies have demonstrated that brief CED infusions of nondiffusible peptides that inhibit the release of excitatory neurotransmitters, including omega-conotoxins and botulinum neurotoxins, can produce long-lasting (weeks to months) seizure protection in the rat amygdala-kindling model. "
|5.||Paraneoplastic Syndromes (Paraneoplastic Syndrome)
|1.||Calcium Channels (Calcium Channel)
|2.||N-Type Calcium Channels (N-Type Calcium Channel)
|3.||Neurotransmitter Agents (Neurotransmitter)
|4.||Immunoglobulin G (IgG)
|4.||Transcutaneous Electric Nerve Stimulation (TENS)