|1.||Richardson, Michael: 2 articles (11/2009 - 10/2006)|
|2.||Romano-Silva, Marco A: 2 articles (11/2009 - 10/2006)|
|3.||Prado, Marco Antonio M: 2 articles (11/2009 - 10/2006)|
|4.||Batista, Monalise Costa: 1 article (11/2009)|
|5.||da Silva, Adriano Jesus: 1 article (11/2009)|
|6.||Gomez, Marcus Vinicius: 1 article (11/2009)|
|7.||Massensini, André Ricardo: 1 article (11/2009)|
|8.||Kushmerick, Christopher: 1 article (11/2009)|
|9.||Guatimosim, Cristina: 1 article (11/2009)|
|10.||Pinheiro, Ana Cristina do Nascimento: 1 article (11/2009)|
08/01/1997 - "During hypoxia, omega-CgTX diminished K+-induced changes by 50-75% in both parts of the cell, but only immediately after depolarization. "
02/23/2001 - "About 85% of SP release by hypoxia was inhibited by omega-conotoxin GVIA (1 microM), an N-type Ca2+ channel blocker, whereas nitrendipine (1.5 microM), an inhibitor of L-type Ca2+ channel partially attenuated ( approximately 65%) hypoxia-induced SP release. "
11/01/1997 - "The response to hypoxia was inhibited by the removal of extracellular Ca2+ and by nifedipine and omega-conotoxin GVIA. "
08/01/1997 - "The combination of nifedipine and omega-CgTX diminished the [Ca2+]i response to K+ with or without hypoxia by >90% in the cell body and 70% in the growth cones. "
01/01/1994 - "The N-type calcium antagonists, omega-conotoxin GVIA (0.5 microM) and neomycin (300 microM) significantly (P < 0.01) increased the probability of the recovery of the CA1 population spike after hypoxia but not after NMDA (50 microM). "
02/01/1994 - "Omega-conotoxin GVIA protects against ischemia-induced neuronal death in the Mongolian gerbil but not against quinolinic acid-induced neurotoxicity in the rat."
11/01/2009 - "Tx3-3, Tx3-4, omega-conotoxin GVIA or omega-conotoxin MVIIC inhibited the ischemia-induced increase on glutamate release by 54, 72, 60, and 70%, respectively. "
10/01/2006 - "The SN56 cells subjected to ischemia were almost completely protected from damage by PhTx3 while with omega-conotoxin GVIA or omega-conotoxin MVIIC the cell protection was only partial. "
10/01/2006 - "Confocal images of CA1 region of the rat hippocampal slices subjected to ischemia insult and treated with omega-conotoxin GVIA, omega-conotoxin MVIIC and PhTx3 showed a percentage of dead cells of 68%, 54% and 18%, respectively. "
02/01/1994 - "Since evidence is accumulating that N-type voltage-sensitive calcium channels (N-channels) regulate the release of neurotransmitters, we investigated the effects of omega-conotoxin GVIA (omega-CTX), an antagonist of N-channels, on delayed neuronal death following transient ischemia in gerbils. "
|3.||Hypotension (Low Blood Pressure)
01/01/1999 - "This study assesses the effect of neuronal voltage-sensitive Ca2+ channel blockers, omega-conotoxin GVIA (CTX), and omega-agatoxin IVA (AgTX) on the vasodilation and release of calcitonin gene-related peptide (CGRP), both of which were induced by either application of capsaicin or acute stepwise hypotension. "
08/13/2007 - "In protocol 2, AVP-induced hypotension was abolished by EGTA (extracellular Ca(++) chelator) and Ca(++) blockers such as nifedipine, nimodipine (L-types), and omega-conotoxin MVIIC (P/Q-type), but not by omega-conotoxin GVIA (N-type). "
|4.||Ganglion Cysts (Ganglion)
07/01/1995 - "5. The N-type Ca2+ channel blocker omega-conotoxin GVIA (1.4-6.3 microM) did not abolish directional selectivity in the ganglion cells. "
02/01/2001 - "Patch-clamp recordings showed that K(+) channels on ganglion cell layer neurons are not modulated by GABA(B) receptors, whereas Ca(2+) channels are; however, Ca(2+) channel blockade with omega-conotoxin-GVIA or nimodipine did not prevent Ca(2+) waves. "
08/15/1997 - "These data are consistent with earlier findings that the pharmacology of acetylcholine release from ciliary ganglion nerve terminals changes during development from sensitivity to both dihydropyridines and omega-CgTX GVIA to selective sensitivity to omega-CgTX GVIA (Gray et al., 1992). "
12/01/1994 - "We have used atomic force microscopy on the calyx-type nerve terminal of the chick ciliary ganglion to localize single calcium channels tagged via biotinylated omega-conotoxin GVIA to avidin-coated 30 nm gold particles. "
11/01/2002 - "Intracisternal administration of omega-conotoxin GVIA (N-type Ca(2+) antagonist) only tended to inhibit the NMDA-induced tonic convulsions. "
07/01/1996 - "Omega-Conotoxin GVIA was anticonvulsant in DBA/2 mice, but only at high doses (3 micrograms ICV prevented tonic seizures in 60% of the animals; 10 micrograms ICV prevented clonic seizures in 60% and tonic seizures in 90% of the animals), whereas omega-conotoxin MVIIA did not inhibit sound-induced seizures in doses up to 10 micrograms ICV. "
07/01/1989 - "[3H]Nimodipine and high-affinity [125I]omega-conotoxin GVIA (CgTX) binding were investigated in membranes from rat cerebral cortex, cerebellum, and hippocampus after electrically and chemically induced seizures. "
07/01/1989 - "Differential effects of acute and repeated electrically and chemically induced seizures on [3H]Nimodipine and [125I]omega-conotoxin GVIA binding in rat brain."
11/01/2007 - "Prolonged attenuation of amygdala-kindled seizure measures in rats by convection-enhanced delivery of the N-type calcium channel antagonists omega-conotoxin GVIA and omega-conotoxin MVIIA."
|1.||Calcium Channels (Calcium Channel)
|9.||Calcitonin Gene-Related Peptide