ArticleThe Journal of physiology2012
A new signalling pathway for parallel fibre presynaptic type 4 metabotropic glutamate receptors (mGluR4) in the rat cerebellar cortex.
Article in The Journal of physiology, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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Who cites it
8 citing papers in PubMed, 14 citations in OpenAlex.
- Interplay between metabotropic glutamate type 4 and adenosine type 1 receptors modulate synaptic transmission in the cerebellar cortex.Frontiers in pharmacology · 2024Article
- Super-resolution imaging reveals the nanoscale organization of metabotropic glutamate receptors at presynaptic active zones.Science advances · 2020Article
- Prefrontal cortex miR-29b-3p plays a key role in the antidepressant-like effect of ketamine in rats.Experimental & molecular medicine · 2018Article
- A Light-Controlled Allosteric Modulator Unveils a Role for mGluFrontiers in cellular neuroscience · 2018Article
- Dendritic excitation-inhibition balance shapes cerebellar output during motor behaviour.Nature communications · 2016Article
- Activation of Group II Metabotropic Glutamate Receptors Promotes LTP Induction at Schaffer Collateral-CA1 Pyramidal Cell Synapses by Priming NMDA Receptors.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2016Article
- Functional contributions of glutamate transporters at the parallel fibre to Purkinje neuron synapse-relevance for the progression of cerebellar ataxia.Cerebellum & ataxias · 2014Article
- Persistent posttetanic depression at cerebellar parallel fiber to Purkinje cell synapses.PloS one · 2013Article
Corrections and comments
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Authors and funding
4 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
In the rodent cerebellum, pharmacological activation of mGluR4 acutely depresses excitatory synaptic transmission at parallel fibre–Purkinje cell synapses. This depression involves the inhibition of presynaptic calcium (Ca2+) influx that ultimately controls glutamate release. In this study, we investigate the molecular basis of mGluR4-mediated inhibition of presynaptic Ca2+ transients. Our results demonstrate that the mGluR4 effect does not depend on selective inhibition of a specific type of presynaptic voltage-gated Ca2+ channel, but rather involves modulation of all classes of Ca2+ channels present in the presynaptic terminals. In addition, this inhibitory effect does not involve the activation of G protein-activated inwardly rectifying potassium channels, TEA-sensitive potassium channels or two-pore-domain potassium channels. Furthermore, this inhibition does not require pertussis toxin-sensitive G proteins, and is independent of any effect on adenylyl cyclases, protein kinase A, mitogen-activated protein kinases or phosphoinositol-3 kinase activity. Interestingly we found that mGluR4 inhibition of presynaptic Ca2+ influx employs a newly defined signalling pathway, notably that involving the activation of phospholipase C and ultimately protein kinase C.
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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.