ArticleProceedings of the National Academy of Sciences of the United States of America2003
Nifedipine facilitates neurotransmitter release independently of calcium channels.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2003. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.
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Who cites it
22 citing papers in PubMed, 54 citations in OpenAlex.
- Voltage-gated sodium channel, Nav 1.8, regulates calcium dynamics in the dorsal root ganglion induced by cold nociceptive stimulus.PloS one · 2026Article
- Modulation of CaScientific reports · 2024Article
- The Alzheimer's disease risk gene BIN1 regulates activity-dependent gene expression in human-induced glutamatergic neurons.Molecular psychiatry · 2024Article
- A de novo missense mutation in synaptotagmin-1 associated with neurodevelopmental disorder desynchronizes neurotransmitter release.Molecular psychiatry · 2024Article
- Calcium Homeostasis, Transporters, and Blockers in Health and Diseases of the Cardiovascular System.International journal of molecular sciences · 2023Review
- Nifedipine Ameliorates Cellular Differentiation Defects of Smn-Deficient Motor Neurons and Enhances Neuromuscular Transmission in SMA Mice.International journal of molecular sciences · 2023Article
- Electrographic seizures and brain hyperoxia may be key etiological factors for postconcussive deficits.Journal of neurophysiology · 2022Article
- Role of L-Type Voltage-Gated Calcium Channels in Epileptiform Activity of Neurons.International journal of molecular sciences · 2021Article
- Multiple sources of internal calcium stores mediate ethanol-induced presynaptic inhibitory GABA release in the central nucleus of the amygdala in mice.Psychopharmacology · 2020Article
- Validation of impaired Transient Receptor Potential Melastatin 3 ion channel activity in natural killer cells from Chronic Fatigue Syndrome/ Myalgic Encephalomyelitis patients.Molecular medicine (Cambridge, Mass.) · 2019Article
- Bioactivity Profile of the Diterpene Isosteviol and its Derivatives.Molecules (Basel, Switzerland) · 2019Review
- Further characterization of the effect of ethanol on voltage-gated Ca(2+) channel function in developing CA3 hippocampal pyramidal neurons.Brain research · 2016Article
- Concentration-dependent activation of dopamine receptors differentially modulates GABA release onto orexin neurons.The European journal of neuroscience · 2015Article
- Article
- Multivesicular release underlies short term synaptic potentiation independent of release probability change in the supraoptic nucleus.PloS one · 2013Article
- Activation of steroid-sensitive TRPM3 channels potentiates glutamatergic transmission at cerebellar Purkinje neurons from developing rats.Journal of neurochemistry · 2011Article
- Analog modulation of mossy fiber transmission is uncoupled from changes in presynaptic Ca2+.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2008Article
- Short-term potentiation of mEPSCs requires N-, P/Q- and L-type Ca2+ channels and mitochondria in the supraoptic nucleus.The Journal of physiology · 2008Article
- Bidirectional dopaminergic modulation of excitatory synaptic transmission in orexin neurons.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2006Article
- Dendritically released transmitters cooperate via autocrine and retrograde actions to inhibit afferent excitation in rat brain.The Journal of physiology · 2004Article
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Authors and funding
2 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Nifedipine, a drug used for treatment of hypertension and angina, exerts its effect by calcium channel blockade and nitric oxide production. We report here a previously uncharacterized action of nifedipine on central synaptic transmission that may partially explain its side effects. Nifedipine causes a long-lasting facilitation of tetrodotoxin-insensitive spontaneous glutamate release. This effect is independent of its L-type calcium channel blocking effect, and is not mimicked by other dihydropyridines such as nimodipine, nicardipine, or Bay K 8644. The effect was dose dependent, with EC(50) of 7.8 microM, with the lowest effective dose being 100 nM, a clinically relevant dose. At 10 microM, the increase is 14.7-fold. This effect is largely calcium-independent, because Cd(2+), thapsigargin, or BAPTA-AM [1,2-bis(2-aminophenoxy)ethane-N,N,N',N'-tetraacetic acid-acetoxymethyl ester] did not inhibit the nifedipine effect. Thus, nifedipine seems to act on the release process downstream of calcium entry or release. Protein kinases A or C do not mediate its effect, because it is not blocked by inhibitors of these kinases. Our finding indicates that nifedipine may be a useful tool as a secretagogue to directly target the release process, but raises caution for its use as an L-type calcium channel blocker.
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