ArticleCell calcium2009
2-Aminoethoxydiphenyl-borate (2-APB) increases excitability in pyramidal neurons.
Article in Cell calcium, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.
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Who cites it
16 citing papers in PubMed, 36 citations in OpenAlex.
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- Calcium channel-coupled transcription factors facilitate direct nuclear signaling.Research square · 2025Article
- Neuroprotective Effect of 2-Aminoethoxydiphenyl Borate (2-APB) in Amyloid β-Induced Memory Dysfunction: A Mechanistic Study.Cellular and molecular neurobiology · 2022Article
- Mitochondria-endoplasmic reticulum contacts in sepsis-induced myocardial dysfunction.Frontiers in cell and developmental biology · 2022Review
- Mind the Gap: Mitochondria and the Endoplasmic Reticulum in Neurodegenerative Diseases.Biomedicines · 2021Review
- How TRPC Channels Modulate Hippocampal Function.International journal of molecular sciences · 2020Review
- Transcriptomic correlates of neuron electrophysiological diversity.PLoS computational biology · 2017Article
- Molecular Pathogenesis of Alzheimer's Disease: An Update.Annals of neurosciences · 2017Review
- The Ca(2+) channel inhibitor 2-APB reverses β-amyloid-induced LTP deficit in hippocampus by blocking BAX and caspase-3 hyperactivation.British journal of pharmacology · 2015Article
- Article
- Disrupted in schizophrenia 1 modulates medial prefrontal cortex pyramidal neuron activity through cAMP regulation of transient receptor potential C and small-conductance K+ channels.Biological psychiatry · 2014Article
- Metabotropic glutamate receptors regulate hippocampal CA1 pyramidal neuron excitability via Ca²⁺ wave-dependent activation of SK and TRPC channels.The Journal of physiology · 2011Article
- 2-Aminoethoxydiphenyl borate blocks electrical coupling and inhibits voltage-gated K+ channels in guinea pig arteriole cells.American journal of physiology. Heart and circulatory physiology · 2011Article
- 2-aminoethyl diphenyl borinate (2-APB) inhibits TRPM7 channels through an intracellular acidification mechanism.Channels (Austin, Tex.)Article
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
Abstract
Calcium ions (Ca(2+)) released from inositol trisphosphate (IP(3))-sensitive intracellular stores may participate in both the transient and extended regulation of neuronal excitability in neocortical and hippocampal pyramidal neurons. IP(3) receptor (IP(3)R) antagonists represent an important tool for dissociating these consequences of IP(3) generation and IP(3)R-dependent internal Ca(2+) release from the effects of other, concurrently stimulated second messenger signaling cascades and Ca(2+) sources. In this study, we have described the actions of the IP(3)R and store-operated Ca(2+) channel antagonist, 2-aminoethoxydiphenyl-borate (2-APB), on internal Ca(2+) release and plasma membrane excitability in neocortical and hippocampal pyramidal neurons. Specifically, we found that a dose of 2-APB (100 microM) sufficient for attenuating or blocking IP(3)-mediated internal Ca(2+) release also raised pyramidal neuron excitability. The 2-APB-dependent increase in excitability reversed upon washout and was characterized by an increase in input resistance, a decrease in the delay to action potential onset, an increase in the width of action potentials, a decrease in the magnitude of afterhyperpolarizations (AHPs), and an increase in the magnitude of post-spike afterdepolarizations (ADPs). From these observations, we conclude that 2-APB potently and reversibly increases neuronal excitability, likely via the inhibition of voltage- and Ca(2+)-dependent potassium (K(+)) conductances.
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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.