ArticleNeuroscience2007
Activation of presynaptic kainate receptors suppresses GABAergic synaptic transmission in the rat globus pallidus.
Article in Neuroscience, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
12 citing papers in PubMed, 24 citations in OpenAlex.
- Neuronal Plasticity: Neuronal Organization is Associated with Neurological Disorders.Journal of molecular neuroscience : MN · 2020Review
- Roles of Glutamate Receptors in Parkinson's Disease.International journal of molecular sciences · 2019Review
- Kainate Receptors Play a Role in Modulating Synaptic Transmission in the Olfactory Bulb.Neuroscience · 2018Article
- Neurotoxic Agent-Induced Injury in Neurodegenerative Disease Model: Focus on Involvement of Glutamate Receptors.Frontiers in molecular neuroscience · 2018Review
- Neuroprotective effects of the MAO-B inhibitor, PF9601N, in an in vivo model of excitotoxicity.CNS neuroscience & therapeutics · 2014Article
- Modulation of in vivo GABA-evoked responses by nitric oxide-active compounds in the globus pallidus of rat.Journal of neural transmission (Vienna, Austria : 1996) · 2012Article
- GABA transporter subtype 1 and GABA transporter subtype 3 modulate glutamatergic transmission via activation of presynaptic GABA(B) receptors in the rat globus pallidus.The European journal of neuroscience · 2012Article
- Differential localization and function of GABA transporters, GAT-1 and GAT-3, in the rat globus pallidus.The European journal of neuroscience · 2011Article
- Localization and functions of kainate receptors in the basal ganglia.Advances in experimental medicine and biology · 2011Review
- Glia-dependent switch of kainate receptor presynaptic action.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2010Article
- Robust short-latency perisomatic inhibition onto neocortical pyramidal cells detected by laser-scanning photostimulation.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2009Article
- Activation of presynaptic kainate receptors suppresses GABAergic synaptic transmission in the rat globus pallidus.Neuroscience · 2007Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors at 2 institutions in 1 country.
Funding
Abstract
The globus pallidus (GP) plays a central integrative role in the basal ganglia circuitry. It receives strong GABAergic inputs from the striatum (Str) and significant glutamatergic afferents from the subthalamic nucleus (STN). The change in firing rate and pattern of GP neurons is a cardinal feature of Parkinson's disease pathophysiology. Kainate receptor (KAR) GluR6/7 subunit immunoreactivity is expressed presynaptically in GABAergic striatopallidal terminals which provides a substrate for regulation of GABAergic transmission in GP. To test this hypothesis, we recorded GABA(A)-mediated inhibitory postsynaptic currents (IPSCs) in the GP following electrical stimulation of the Str. Following blockade of AMPA and N-methyl-d-aspartate receptors with selective antagonists, bath application of kainate (KA) (0.3-3 microM) reduced significantly the amplitude of evoked IPSCs. This inhibition was associated with a significant increase in paired-pulse facilitation ratio and a reduction of the frequency, but not amplitude, of miniature inhibitory postsynaptic currents (mIPSCs), suggesting a presynaptic site of KA action. The KA effects on striatopallidal GABAergic transmission were blocked by the G-protein inhibitor, N-ethylmaleimide (NEM), or protein kinase C (PKC) inhibitor calphostin C. Our results demonstrate that KAR activation inhibits GABAergic transmission through a presynaptic G protein-coupled, PKC-dependent metabotropic mechanism in the rat GP. These findings open up the possibility for the development of KA-mediated pharmacotherapies aimed at decreasing the excessive and abnormally regulated inhibition of GP neurons in Parkinson's disease.
Indexed as
Identifiers
What 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.