Presynaptic kainate receptors increase GABAergic neurotransmission in rat periaqueductal gray neurons

Nakamura, Michiko; Choi, Kyu-Hyung; Choi, Sung-Keun; Do, Chung-Sik; Jun, Ju-Hye; Kwon, Hyung-Kook; Lee, So-Min; Moon, Ryu-Jin; Yi, Ki-Joung; Jang, Il‐Sung

doi:10.1016/j.ejphar.2010.03.004

Cited by 6 publications

(3 citation statements)

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“…26). The majority of this work has been in the hippocampus, but presynaptic kainate receptor function is also apparent in the amygdala (Braga et al, 2003(Braga et al, , 2009Aroniadou-Anderjaska et al, 2012;Negrete-Diaz et al, 2012), cortex (Jouhanneau et al, 2011;Andrade-Talavera et al, 2013;Gelsomino et al, 2013;Rodriguez-Moreno and Sihra, 2013), cingulate cortex (Wu et al, 2007b), cerebellum (Delaney and Jahr, 2002;Cervetto et al, 2010;Falcon-Moya et al, 2018), periaqueductal gray (Nakamura et al, 2010), striatum (Marshall et al, 2018), and thalamus (Miyata and Imoto, 2009). Presynaptic DRG kainate receptors regulate release of glutamate from synapses in the superficial dorsal horn of the spinal cord (Kerchner et al, 2001).…”

Section: Roles Of Ampa and Kainate Receptors In Neuronal Functionsmentioning

confidence: 99%

Structure, Function, and Pharmacology of Glutamate Receptor Ion Channels

Hansen¹,

Wollmuth²,

Bowie³

et al. 2021

Pharmacol Rev

322

445

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Section: Roles Of Ampa and Kainate Receptors In Neuronal Functionsmentioning

confidence: 99%

Structure, Function, and Pharmacology of Glutamate Receptor Ion Channels

Hansen¹,

Wollmuth²,

Bowie³

et al. 2021

Pharmacol Rev

322

445

View full text Add to dashboard Cite

“…On the other hand, other authors (Nakamura et al, 2010) have shown that KA receptors containing the GLUK1 subunit can directly activate spontaneous GABA release from rat periaqueductal grey neurons, a phenomenon possibly explained by brain area-related differences in KA-receptor subtypes regulating GABA release. In addition, it should be emphasized that subunit composition influences the pharmacological and functional properties of the resulting KA receptor (Perrais et al, 2009).…”

Section: Discussionmentioning

confidence: 90%

Molecular and pharmacological evidence for a facilitatory functional role of pre‐synaptic GLUK2/3 kainate receptors on GABA release in rat trigeminal caudal nucleus

Samengo

Currò

Navarra

et al. 2012

European Journal of Pain

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BackgroundGamma-aminobutyric acid (GABA) and glutamate (GLU) are involved in nociceptive signals processing in the trigeminal system. In this study, we investigated the influence of excitatory transmission on GABA release in nerve terminals isolated from the rat trigeminal caudal nucleus (TCN).MethodsWe utilize biochemical (superfused synaptosomes loaded with [3H]GABA) and morphological (immunofluorescence experiments with specific antibody) techniques.ResultsOur results show that GLU potentiates the release of [3H]GABA evoked by 9, 15 and 30 mM [K+]e; 15 mM [K+]e-evoked [3H]GABA release was also reinforced by domoate and kainate (KA), two naturally occurring GLU-receptor agonists. The enhancement of 15 mM [K+]e-evoked [3H]GABA release produced by 100 μM KA was abolished by NBQX, a mixed AMPA/KA receptor antagonist, but was not affected by GYKI52466, a selective AMPA receptor antagonist. ATPA, a selective agonist for KA receptors containing the GLUK1 subunit, had no effect on depolarization-induced [3H]GABA release, and UBP310, which selectively antagonizes these same receptors, failed to reverse the KA-induced potentiation of 15 mM [K+]e-evoked [3H]GABA release. The KA-induced potentiation was also unaffected by concanavalin A (10 μM), a positive allosteric modulator of GLUK1- and GLUK2-containing KA receptors.Immunofluorescence experiments revealed that GABAergic nerve terminals in the TCN differentially expressed GLUK subunits, with GLUK2/3-positive terminals being twice more abundant than GLUK1-containing synaptosomes.ConclusionsThese findings indicate that pre-synaptic KA receptors facilitating GABA release from TCN nerve terminals mainly express GLUK2/GLUK3 subunits, supporting the notion that different types of KA receptors are involved in the various stages of pain transmission.

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“…Tonic inhibition regulates output of PAG neurons, and presynaptic GluK1-containing KARs modulate the release of GABA in cultures of dissociated PAG neurons (Nakamura et al, 2010).…”

Section: Peripheral and Central Pain Pathwaysmentioning

confidence: 99%

Kainate Receptor Signaling in Pain Pathways

Bhangoo

Swanson

2012

Mol Pharmacol

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Receptors and channels that underlie nociceptive signaling constitute potential sites of intervention for treatment of chronic pain states. The kainate receptor family of glutamate-gated ion channels represents one such candidate set of molecules. They have a prominent role in modulation of excitatory signaling between sensory and spinal cord neurons. Kainate receptors are also expressed throughout central pain neuraxis, where their functional contributions to neural integration are less clearly defined. Pharmacological inhibition or genetic ablation of kainate receptor activity reduces pain behaviors in a number of animal models of chronic pain, and small clinical trials have been conducted using several orthosteric antagonists. This review will cover kainate receptor function and participation in pain signaling as well as the pharmacological studies supporting further consideration as potential targets for therapeutic development.

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Presynaptic kainate receptors increase GABAergic neurotransmission in rat periaqueductal gray neurons

Cited by 6 publications

References 73 publications

Structure, Function, and Pharmacology of Glutamate Receptor Ion Channels

Structure, Function, and Pharmacology of Glutamate Receptor Ion Channels

Molecular and pharmacological evidence for a facilitatory functional role of pre‐synaptic GLUK2/3 kainate receptors on GABA release in rat trigeminal caudal nucleus

Kainate Receptor Signaling in Pain Pathways

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