ArticleHippocampus2004
P/Q Ca2+ channel blockade stops spreading depression and related pyramidal neuronal Ca2+ rise in hippocampal organ culture.
Article in Hippocampus, 2004. 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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The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
22 citing papers in PubMed, 45 citations in OpenAlex.
- Activation of central and peripheral transient receptor potential melastatin 8 increases susceptibility to spreading depolarization and facilitates trigeminal neuroinflammation.The journal of headache and pain · 2025Article
- Plasticity of perisynaptic astroglia during ischemia-induced spreading depolarization.Cerebral cortex (New York, N.Y. : 1991) · 2023Article
- Intranasally administered IGF-1 inhibits spreading depression in vivo.Brain research · 2017Article
- Abnormal synaptic Ca(2+) homeostasis and morphology in cortical neurons of familial hemiplegic migraine type 1 mutant mice.Annals of neurology · 2015Article
- Article
- Characterization of inhibitory GABA-A receptor activation during spreading depolarization in brain slice.PloS one · 2014Article
- The changing landscape of voltage-gated calcium channels in neurovascular disorders and in neurodegenerative diseases.Current neuropharmacology · 2013Article
- Sustained NMDA receptor activation by spreading depolarizations can initiate excitotoxic injury in metabolically compromised neurons.The Journal of physiology · 2012Article
- Article
- P/Q-type calcium channel modulators.British journal of pharmacology · 2012Review
- Synaptic release and extracellular actions of Zn2+ limit propagation of spreading depression and related events in vitro and in vivo.Journal of neurophysiology · 2012Article
- Migraine is a neuronal disease.Journal of neural transmission (Vienna, Austria : 1996) · 2011Review
- Strategies for study of neuroprotection from cold-preconditioning.Journal of visualized experiments : JoVE · 2010Article
- Gabapentin suppresses cortical spreading depression susceptibility.Journal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism · 2010Article
- The neurobiology of migraine.Handbook of clinical neurology · 2010Article
- Cortical spreading depression-new insights and persistent questions.Cephalalgia : an international journal of headache · 2009Article
- Contributions of Ca2+ and Zn2+ to spreading depression-like events and neuronal injury.Journal of neurochemistry · 2009Review
- Genetic and hormonal factors modulate spreading depression and transient hemiparesis in mouse models of familial hemiplegic migraine type 1.The Journal of clinical investigation · 2009Article
- Zn2+ influx is critical for some forms of spreading depression in brain slices.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2008Article
- Optical current source density analysis in hippocampal organotypic culture shows that spreading depression occurs with uniquely reversing currents.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2005Article
Corrections and comments
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
Ca2+ channels and pyramidal cell Ca2+ are involved in hippocampal spreading depression (SD), but their roles remain elusive. Accordingly, we characterized Ca2+ changes during SD in CA3 pyramidal neurons and determined whether Ca2+ channel antagonists could prevent SD. SD was induced in hippocampal organotypic cultures (HOTCs), in which experimental conditions can be rigorously controlled. SD was triggered by transient exposure to sodium acetate (NaAc)-based Ringer's coupled to an electrical pulse in the dentate gyrus and its occurrence confirmed with interstitial DC recordings. Pyramidal cell Ca2+ was measured with fura-2 filled cells and was quantified at the soma, proximal and more distal apical dendrites. Regional Ca2+ changes began simultaneously with the triggering pulse of SD and reached three distinct peaks before returning to baseline concomitant with the interstitial DC potential of SD. The first peak occurred within 5 s of the triggering pulse, was smallest, and heralded the onset of SD. The second Ca2+ change was the greatest and reached a peak 6 s later, during the early phase of SD. The third was intermediate in size and occurred 18 s later, as SD reached its maximum interstitial DC change. SD was prevented by nonselective Ca2+ blockade (Ni2+ and Cd2+) but not by either L-Ca2+ channel (nifedipine) or N-Ca2+ channel inhibition (omega-conotoxin GVIA). Importantly, SD was blocked by P/Q Ca2+ channel antagonism (omega-agatoxin-IVA), which also prompted a significant reduction in pyramidal cell Ca2+ change and hyperexcitability. These results show that the spatiotemporal pattern of pyramidal cell Ca2+ change with SD is multiphasic; they provide further evidence that these changes begin before electrophysiologic evidence of SD. Furthermore, they show that P/Q Ca2+ channel antagonism can prevent SD in HOTCs and it appears to do so by preventing the NaAc-induced increased pyramidal cell excitability from NaAc exposure, which may involve altered GABAergic transmission.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.