ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2001
Group I metabotropic glutamate receptors elicit epileptiform discharges in the hippocampus through PLCbeta1 signaling.
Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2001. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 35 papers.
What it found
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Who cites it
35 citing papers in PubMed, 77 citations in OpenAlex.
- Phospholipase C beta 1 in the dentate gyrus gates fear memory formation through regulation of neuronal excitability.Science advances · 2024Article
- Metabotropic glutamate receptors (mGluRs) in epileptogenesis: an update on abnormal mGluRs signaling and its therapeutic implications.Neural regeneration research · 2024Review
- Group 1 Metabotropic Glutamate Receptors in Neurological and Psychiatric Diseases: Mechanisms and Prospective.The Neuroscientist : a review journal bringing neurobiology, neurology and psychiatry · 2022Review
- CaInternational journal of molecular sciences · 2022Review
- Enhanced hippocampal type II theta activity AND altered theta architecture in mice lacking the CaScientific reports · 2021Article
- TRPC1 Regulates the Activity of a Voltage-Dependent Nonselective Cation Current in Hippocampal CA1 Neurons.Cells · 2020Article
- Article
- Involvement of extrasynaptic glutamate in physiological and pathophysiological changes of neuronal excitability.Cellular and molecular life sciences : CMLS · 2018Review
- Metabotropic Glutamate Receptors and Interacting Proteins in Epileptogenesis.Current neuropharmacology · 2016Review
- Persistent receptor activity underlies group I mGluR-mediated cellular plasticity in CA3 neuron.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2013Article
- RGS4 overexpression in the rat dorsal striatum modulates mGluR5- and amphetamine-mediated behavior and signaling.Psychopharmacology · 2012Article
- Pathological plasticity in fragile X syndrome.Neural plasticity · 2012Review
- Metabotropic glutamate receptors regulate hippocampal CA1 pyramidal neuron excitability via Ca²⁺ wave-dependent activation of SK and TRPC channels.The Journal of physiology · 2011Article
- Cyclic ADP ribose-dependent Ca2+ release by group I metabotropic glutamate receptors in acutely dissociated rat hippocampal neurons.PloS one · 2011Article
- Molecular mechanisms of cognitive and behavioral comorbidities of epilepsy in children.Epilepsia · 2011Review
- Article
- Regulatory RNAs in brain function and disorders.Brain research · 2010Review
- BC1 regulation of metabotropic glutamate receptor-mediated neuronal excitability.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2009Article
- Regulated release of BDNF by cortical oligodendrocytes is mediated through metabotropic glutamate receptors and the PLC pathway.ASN neuro · 2009Article
- Cellular plasticity for group I mGluR-mediated epileptogenesis.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2009Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors at 2 institutions in 2 countries.
Funding
Abstract
Activation of metabotropic glutamate receptors (mGluRs) produces multiple effects in cortical neurons, resulting in the emergence of network activities including epileptiform discharges. The cellular mechanisms underlying such network responses are largely unknown. We examined the properties of group I mGluR-mediated cellular responses in CA3 neurons and attempted to determine their role in the generation of the network activities. Group I mGluR stimulation causes depolarization of hippocampal neurons. This depolarization is primarily mediated by two sets of conductance change: the opening of a voltage-dependent cationic conductance (mediating I(mGluR(V))) and the closing of a voltage-independent (background) K(+) conductance. I(mGluR(V)) was no longer elicited by group I mGluR agonists in the presence of U73122, a phospholipase C (PLC) blocker. Also, the current could not be activated in hippocampal CA3 neurons from PLCbeta1 knock-out mice. In contrast, suppression of PLC signaling did not affect the group I mGluR-mediated suppression of background K(+) conductance. Thus, the suppression of the background K(+) conductance occurred upstream to PLC activation, whereas the generation of I(mGluR(V)) occurred downstream to PLC activation. Group I mGluR agonists normally elicited rhythmic single cell and population burst responses in the CA3 neurons. In the absence of an I(mGluR(V)) response, CA3 neurons in slices prepared from PLCbeta1-/- mutant mice could no longer generate these responses. The results suggest that I(mGluR(V)) expression in CA3 hippocampal neuron is PLCbeta1-dependent and that I(mGluR(V)) plays a necessary role in the generation of rhythmic single cell bursts and synchronized epileptiform discharges in the CA3 region of the hippocampus.
Indexed as
Identifiers
11487662PMC6763182W2116507293What 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.