CNQX increases GABA-mediated synaptic transmission in the cerebellum by an AMPA/kainate receptor-independent mechanism

@article{Brickley2001CNQXIG,
  title={CNQX increases GABA-mediated synaptic transmission in the cerebellum by an AMPA/kainate receptor-independent mechanism},
  author={Stephen G Brickley and Mark Farrant and G T Swanson and S. G. Cull-Candy},
  journal={Neuropharmacology},
  year={2001},
  volume={41},
  pages={730-736}
}
Presynaptic AMPA receptor-mediated modulation of GABA release from cerebellar molecular layer interneurons
TLDR
The absence of AMPAR-mediated effects in recordings from stargazer dissociated Purkinje cells, suggests that presynaptic AMPARs do not function without γ-2-association, which is identified as a crucial subunit for presyn synaptic modulation of GABA release that occurs via regulation of VGCCs remote from active zones.
Complex effects of CNQX on CA1 interneurons of the developing rat hippocampus
AMPA/Kainate Receptor-Mediated Downregulation of GABAergic Synaptic Transmission by Calcineurin after Seizures in the Developing Rat Brain
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AMPA/kainate and group-I metabotropic receptor antagonists infused into different brain areas impair memory formation of inhibitory avoidance in rats
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The data suggest that the consolidation of the avoidance memory requires intact non-NMDA receptor function in the hippocampus and the basolateral nucleus of the amygdala, but not necessarily in the entorhinal and parietal cortex, for long periods after training.
Ethanol Sensitivity of GABAergic Currents in Cerebellar Granule Neurons Is Not Increased by a Single Amino Acid Change (R100Q) in the α6 GABAA Receptor Subunit
TLDR
The α6-R100Q GABAA receptor subunit polymorphism does not in-crease the acute ethanol sensitivity of extrasynaptic receptors, lending further support to the hypothesis that ethanol modulates these currents indirectly via a presynaptic mechanism.
Development of GABA(A) receptor-mediated inhibitory postsynaptic currents in hippocampus.
TLDR
The rate, amplitude, and kinetics of GABA(A,fast) mIPSCs showed significant changes between P10 and P30, suggesting counterbalancing changes in action potential-dependent inhibitory postsynaptic currents in IPSCs, consistent with the hypothesis that developmental changes in GABA (A,slow) IPSCs are due to changes in presynaptic excitability.
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The effects of a potent and selective agonist and a selective antagonist are used to show that kainate receptors, comprised of or containing GluR5 subunits, regulate synaptic inhibition in the hippocampus, an action that could contribute to the epileptogenic effects of kainates.
Kainate receptors are involved in synaptic plasticity
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It is found that LY382884 is a selective antagonist at neuronal kainate receptors containing the GluR5 subunit, which has no effect on long-term potentiation (LTP) that is dependent onNMDA receptors but prevents the induction of mossy fibre LTP, which is independent of NMDA receptors.
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It is suggested that KA receptors located on presynaptic FS cell terminals decrease the release of GABA and can be activated by glutamate released from the somatodendritic compartment of the postsynaptic pyramidal cells.
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TLDR
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