ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience1998
Differences in Ca2+ channels governing generation of miniature and evoked excitatory synaptic currents in spinal laminae I and II.
Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 1998. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 62 papers.
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Who cites it
62 citing papers in PubMed, 118 citations in OpenAlex.
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- Neurobiology of ARID1B haploinsufficiency related to neurodevelopmental and psychiatric disorders.Molecular psychiatry · 2022Review
- Painful diabetic neuropathy leads to functional CaExperimental neurology · 2021Article
- The physiological function of different voltage-gated sodium channels in pain.Nature reviews. Neuroscience · 2021Review
- The development of pain circuits and unique effects of neonatal injury.Journal of neural transmission (Vienna, Austria : 1996) · 2020Review
- Article
- Cav3.2 T-type calcium channels shape electrical firing in mouse Lamina II neurons.Scientific reports · 2019Article
- Effects of intravesical administration of sensory neuron-specific receptor agonist on voiding function in rats with cyclophosphamide-induced cystitis.Central European journal of urology · 2019Article
- Ablation of αProceedings of the National Academy of Sciences of the United States of America · 2018Article
- Presynaptic Inhibition of Primary Nociceptive Signals to Dorsal Horn Lamina I Neurons by Dopamine.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2018Article
- Presynaptic inhibition of transient receptor potential vanilloid type 1 (TRPV1) receptors by noradrenaline in nociceptive neurons.The Journal of physiology · 2017Article
- Targeting human Mas-related G protein-coupled receptor X1 to inhibit persistent pain.Proceedings of the National Academy of Sciences of the United States of America · 2017Article
- Molecular Basis of Regulating High Voltage-Activated Calcium Channels by S-Nitrosylation.The Journal of biological chemistry · 2015Article
- Activation of transient receptor potential ankyrin 1 induces CGRP release from spinal cord synaptosomes.Pharmacology research & perspectives · 2015Article
- Dopaminergic modulation of GABAergic transmission in the entorhinal cortex: concerted roles of α1 adrenoreceptors, inward rectifier K⁺, and T-type Ca²⁺ channels.Cerebral cortex (New York, N.Y. : 1991) · 2014Article
- T-type calcium channels in chronic pain: mouse models and specific blockers.Pflugers Archiv : European journal of physiology · 2014Review
- T-type channel-mediated neurotransmitter release.Pflugers Archiv : European journal of physiology · 2014Review
- The many faces of T-type calcium channels.Pflugers Archiv : European journal of physiology · 2014Review
- Calcium current homeostasis and synaptic deficits in hippocampal neurons from Kelch-like 1 knockout mice.Frontiers in cellular neuroscience · 2014Article
2 more citing papers are in PubMed but not listed here.
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
Many neurons of spinal laminae I and II, a region concerned with pain and other somatosensory mechanisms, display frequent miniature "spontaneous" EPSCs (mEPSCs). In a number of instances, mEPSCs occur often enough to influence neuronal excitability. To compare generation of mEPSCs to EPSCs evoked by dorsal root stimulation (DR-EPSCs), various agents affecting neuronal activity and Ca2+ channels were applied to in vitro slice preparations of rodent spinal cord during tight-seal, whole-cell, voltage-clamp recordings from laminae I and II neurons. The AMPA/kainate glutamate receptor antagonist CNQX (10-20 microM) regularly abolished DR-EPSCs. In many neurons CNQX also eliminated mEPSCs; however, in a number of cases a proportion of the mEPSCs were resistant to CNQX suggesting that in these instances different mediators or receptors were also involved. Cd2+ (10-50 microM) blocked evoked EPSCs without suppressing mEPSC occurrence. In contrast, Ni2+ (</=100 microM), a low-threshold Ca2+ channel antagonist, markedly decreased mEPSC frequency while leaving evoked monosynaptic EPSCs little changed. Selective organic antagonists of high-threshold (HVA) Ca2+ channels, nimodipine, omega-Conotoxin GVIA, and Agatoxin IVA partially suppressed DR-EPSCs, however, they had little or no effect on mEPSC frequency. La3+ and mibefradil, agents interfering with low-threshold Ca2+ channels, regularly decreased mEPSC frequency with little effect on fast-evoked EPSCs. Increased [K+]o (5-10 mM) in the superfusion, producing modest depolarizations, consistently increased mEPSC frequency; an increase suppressed by mibefradil but not by HVA Ca2+ channel antagonists. Together these observations indicate that different Ca2+ channels are important for evoked EPSCs and mEPSCs in spinal laminae I and II and implicate a low-threshold type of Ca2+ channel in generation of mEPSCs.
Indexed as
Identifiers
9786981PMC6793560W1799107001What OpenQuestion holds
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.