We are analyzing https://link.springer.com/article/10.1007/s11064-005-9036-0.

Title:
NGP1-01 is a Brain-permeable Dual Blocker of Neuronal Voltage- and Ligand-operated Calcium Channels | Neurochemical Research
Description:
Calcium overload of neurons leads to cell death and is a key feature in neurodegenerative diseases. The polycyclic amine NGP1-01 blocks L-type voltage operated calcium channels in cardiomyocytes. Here, we tested whether NGP1-01 blocks neuronal calcium channels. NGP1-01 (1 μM) inhibited depolarization-induced calcium influx by 78% in cortical neurons preloaded with fura-2 AM, with a potency similar to nimodipine. NGP1-01 (1 μM) also inhibited N-methyl-d-aspartate (NMDA)-induced (1 mM) calcium influx by 52%, only slightly less potent than memantine. Using in vivo-microdialysis, we monitored choline release during NMDA infusion as a measure of excitotoxic membrane breakdown. Intraperitoneal injection of NGP1-01 (40 mg/kg) reduced NMDA-induced membrane breakdown by 31% (P<0.01) while memantine (10 mg/kg) reduced choline release by 40%. Our results demonstrate that NGP1-01 simultaneously blocks both major neuronal calcium channels and is sufficiently brain-permeable. We conclude that NGP1-01 is a promising lead structure for a new class of dual-mechanism neuroprotective agents.
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article, google, scholar, pubmed, cas, calcium, ngp, van, channels, schyf, cell, neuronal, memantine, brain, stroke, privacy, cookies, content, research, klein, neurons, polycyclic, nmda, access, rat, ischemic, rev, ischemia, protection, publish, search, amine, nimodipine, nmdainduced, choline, release, neuroprotective, channel, neurosci, drug, therapy, med, geldenhuys, malan, pharmacol, data, information, log, journal, brainpermeable,

Topics {✒️}

l-type voltage-gated ca inhibited n-methyl-d-aspartate n-methyl-d-aspartate receptor ligand-operated calcium channels aromatic polycyclic amine brain-permeable dual blocker dual-mechanism neuroprotective agents month download article/chapter van der schyf ngp1-01 simultaneously blocks reduced choline release full article pdf homeostatic mechanism counteracting nmda channels cortical neurons preloaded monitored choline release +-evoked choline release nmda receptor pathways privacy choices/manage cookies neural cell cultures nmda-induced neurodegeneration vivo-microdialysis van rooyen jm sufficiently brain-permeable geldenhuys wj excitotoxic membrane breakdown traumatic brain injury brain neurons ischemic brain damage multi-functional drugs neuronal cell culture global brain ischemia channel antagonists suppress european economic area promising lead structure designed multiple ligands texas tech school article kiewert ischemic cell death conditions privacy policy check access instant access fura-2 structure-activity relationships potential therapeutic agents serum-free media glutamate-dependent neurodegeneration acute ischemic stroke drug targets transient forebrain ischemia

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      description:Calcium overload of neurons leads to cell death and is a key feature in neurodegenerative diseases. The polycyclic amine NGP1-01 blocks L-type voltage operated calcium channels in cardiomyocytes. Here, we tested whether NGP1-01 blocks neuronal calcium channels. NGP1-01 (1 μM) inhibited depolarization-induced calcium influx by 78% in cortical neurons preloaded with fura-2 AM, with a potency similar to nimodipine. NGP1-01 (1 μM) also inhibited N-methyl-d-aspartate (NMDA)-induced (1 mM) calcium influx by 52%, only slightly less potent than memantine. Using in vivo-microdialysis, we monitored choline release during NMDA infusion as a measure of excitotoxic membrane breakdown. Intraperitoneal injection of NGP1-01 (40 mg/kg) reduced NMDA-induced membrane breakdown by 31% (P<0.01) while memantine (10 mg/kg) reduced choline release by 40%. Our results demonstrate that NGP1-01 simultaneously blocks both major neuronal calcium channels and is sufficiently brain-permeable. We conclude that NGP1-01 is a promising lead structure for a new class of dual-mechanism neuroprotective agents.
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         Neurology
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