ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2013
Persistent receptor activity underlies group I mGluR-mediated cellular plasticity in CA3 neuron.
Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.
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Who cites it
15 citing papers in PubMed, 20 citations in OpenAlex.
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- Intra- and Extracellular Pillars of a Unifying Framework for Homeostatic Plasticity: A Crosstalk Between Metabotropic Receptors and Extracellular Matrix.Frontiers in cellular neuroscience · 2019Review
- Non-Functional Trace Amine-Associated Receptor 1 Variants in Patients With Mental Disorders.Frontiers in pharmacology · 2019Article
- Group I metabotropic glutamate receptors generate two types of intrinsic membrane oscillations in hippocampal oriens/alveus interneurons.Neuropharmacology · 2018Article
- TNF-α increases the intrinsic excitability of cerebellar Purkinje cells through elevating glutamate release in Bergmann Glia.Scientific reports · 2018Article
- Lovastatin suppresses hyperexcitability and seizure in Angelman syndrome model.Neurobiology of disease · 2018Article
- Metabotropic glutamate receptor 2 inhibits thalamically-driven glutamate and dopamine release in the dorsal striatum.Neuropharmacology · 2017Article
- Article
- Sustained Activity of Metabotropic Glutamate Receptor: Homer, Arrestin, and Beyond.Neural plasticity · 2017Review
- Early-Onset Network Hyperexcitability in Presymptomatic Alzheimer's Disease Transgenic Mice Is Suppressed by Passive Immunization with Anti-Human APP/Aβ Antibody and by mGluR5 Blockade.Frontiers in aging neuroscience · 2017Article
- mGluR1 and mGluR5 Synergistically Control Cholinergic Synaptic Transmission in the Thalamic Reticular Nucleus.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2016Article
- Cannabinoid Type 2 Receptors Mediate a Cell Type-Specific Plasticity in the Hippocampus.Neuron · 2016Article
- Extracellular glutamate exposure facilitates group I mGluR-mediated epileptogenesis in the hippocampus.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2015Article
- Sex-dependence of synaptic depression induced by activation of metabotropic glutamate receptors in rat hippocampus.Brain and neuroscience advancesArticle
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5 authors at 1 institution in 1 country.
Funding
Abstract
Plastic changes in cortical activities induced by group I metabotropic glutamate receptor (mGluR) stimulation include epileptogenesis, expressed in vitro as the conversion of normal neuronal activity to persistent, prolonged synchronized (ictal) discharges. At present, the mechanism that maintains group I mGluR-induced plasticity is not known. We examined this issue using hippocampal slices from guinea pigs and mice. Agonist [(S)-3,5-dihydroxyphenylglycine (DHPG), 30-50 μm)] stimulation of group I mGluRs induces persistent prolonged synchronized (ictal-like) discharges in CA3 that are associated with three identified excitatory cellular responses-suppression of spike afterhyperpolarizations, activation of a voltage-dependent cationic current, and increase in neuronal input resistance. Persistent prolonged synchronized discharges and the underlying excitatory cellular responses maintained following induction were reversibly blocked by mGluR1 antagonists [(S)-+-α-amino-4-carboxy-2-methylbenzeneacetic acid (LY 367385), 50, 100 μm; CPCCOEt (hydroxyimino)cyclopropa[b]chromen-1a-carboxylate ethyl ester, 100 μm], and to a lesser extent by the mGluR5 antagonist MPEP [2-methyl-6-(phenylethynyl)pyridine hydrochloride, 50 μm]. Activation of persistent cellular responses to DHPG were unaffected by tetrodotoxin (0.5-1 μm) or perfusion with low Ca(2+)(0.2 mm)-Mn(2+)(0.5 mm) media-conditions that suppress endogenous glutamate release. The pharmacological profile of the blocking action of the group I mGluR antagonist MCPG [(RS)-α-methyl-4-carboxyphenylglycine, 50-500 μm] on persistent cellular responses was different from that on cellular responses directly activated by DHPG. These data indicate that transient stimulation of group I mGluRs alters receptor properties, rendering them persistently active in the absence of applied agonist or endogenous glutamate activation. Persistent receptor activities, primarily involving mGluR1, maintain excitatory cellular responses and emergent prolonged synchronized discharges.
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