ArticleThe Journal of general physiology2002
Interactions among toxins that inhibit N-type and P-type calcium channels.
Article in The Journal of general physiology, 2002. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 papers.
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Who cites it
31 citing papers in PubMed, 90 citations in OpenAlex.
- Pharmacological Inhibition of Cav2.2 Channels by Recombinant Phα1β Toxin (CTK01512-2).Basic & clinical pharmacology & toxicology · 2026Article
- Research progress in glioma-related epilepsy (Review).Biomedical reports · 2025Article
- Selective blockade of CaNature communications · 2024Article
- Prospecting for candidate molecules fromThe journal of venomous animals and toxins including tropical diseases · 2022Article
- Mass spectrometric identification andSaudi journal of biological sciences · 2021Article
- Pain-related toxins in scorpion and spider venoms: a face to face with ion channels.The journal of venomous animals and toxins including tropical diseases · 2021Review
- Voltage-gated ion channels mediate the electrotaxis of glioblastoma cells in a hybrid PMMA/PDMS microdevice.APL bioengineering · 2020Article
- Abnormal intrinsic dynamics of dendritic spines in a fragile X syndrome mouse model in vivo.Scientific reports · 2016Article
- From foe to friend: using animal toxins to investigate ion channel function.Journal of molecular biology · 2015Review
- Native store-operated calcium channels are functionally expressed in mouse spinal cord dorsal horn neurons and regulate resting calcium homeostasis.The Journal of physiology · 2014Article
- Bioactive marine drugs and marine biomaterials for brain diseases.Marine drugs · 2014Article
- Omega-conotoxin MVIIC attenuates neuronal apoptosis in vitro and improves significant recovery after spinal cord injury in vivo in rats.International journal of clinical and experimental pathology · 2014Article
- Systemic effects induced by intralesional injection of ω-conotoxin MVIIC after spinal cord injury in rats.The journal of venomous animals and toxins including tropical diseases · 2014Article
- Zebrafish calls for reinterpretation for the roles of P/Q calcium channels in neuromuscular transmission.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2013Article
- Review
- P/Q-type calcium channel modulators.British journal of pharmacology · 2012Review
- Regulation by L-type calcium channels of endocytosis: an overview.Journal of molecular neuroscience : MN · 2012Review
- Analgesic conotoxins: block and G protein-coupled receptor modulation of N-type (Ca(V) 2.2) calcium channels.British journal of pharmacology · 2012Review
- Article
- Activity-dependent increases in local oxygen consumption correlate with postsynaptic currents in the mouse cerebellum in vivo.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2011Article
Corrections and comments
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Authors and funding
4 authors at 4 institutions in 1 country.
Funding
Abstract
A number of peptide toxins from venoms of spiders and cone snails are high affinity ligands for voltage-gated calcium channels and are useful tools for studying calcium channel function and structure. Using whole-cell recordings from rat sympathetic ganglion and cerebellar Purkinje neurons, we studied toxins that target neuronal N-type (Ca(V)2.2) and P-type (Ca(V)2.1) calcium channels. We asked whether different toxins targeting the same channels bind to the same or different sites on the channel. Five toxins (omega-conotoxin-GVIA, omega-conotoxin MVIIC, omega-agatoxin-IIIA, omega-grammotoxin-SIA, and omega-agatoxin-IVA) were applied in pairwise combinations to either N- or P-type channels. Differences in the characteristics of inhibition, including voltage dependence, reversal kinetics, and fractional inhibition of current, were used to detect additive or mutually occlusive effects of toxins. Results suggest at least two distinct toxin binding sites on the N-type channel and three on the P-type channel. On N-type channels, results are consistent with blockade of the channel pore by omega-CgTx-GVIA, omega-Aga-IIIA, and omega-CTx-MVIIC, whereas grammotoxin likely binds to a separate region coupled to channel gating. omega-Aga-IIIA produces partial channel block by decreasing single-channel conductance. On P-type channels, omega-CTx-MVIIC and omega-Aga-IIIA both likely bind near the mouth of the pore. omega-Aga-IVA and grammotoxin each bind to distinct regions associated with channel gating that do not overlap with the binding region of pore blockers. For both N- and P-type channels, omega-CTx-MVIIC binding produces complete channel block, but is prevented by previous partial channel block by omega-Aga-IIIA, suggesting that omega-CTx-MVIIC binds closer to the external mouth of the pore than does omega-Aga-IIIA.
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