Kynurenic acid distinguishes kainate and quisqualate receptors in the vertebrate retina

Coleman, Paul A.; Massey, Steve; Miller, Robert F.

doi:10.1016/0006-8993(86)90708-0

Cited by 55 publications

(48 citation statements)

References 16 publications

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“…An important turning point came with a series of observations revealing that KA was a key pharmacological tool for distinguishing between NMDA and non-NMDA ionotropic glutamate receptor families [32]. From this work, the consensus view emerged that KA was selective for nonNMDARs [308,309] where its effects were insensitive to NMDAR antagonists such as external Mg 2+ ions [36,37], D--aminoadipate [310] and 2-amino-5-phosphovaleric acid (APV) [311,312] but sensitive to block by L-glutamic acid diethyl ester (GDEE) [313], -D-glutamylglycine ( -GG) [314] and kynurenic acid [315].…”

Section: Historical Emergence Of Kainate Receptors In Epilepsymentioning

confidence: 99%

Ionotropic Glutamate Receptors & CNS Disorders

Bowie

2008

CNSNDDT

195

130

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Disorders of the central nervous system (CNS) are complex disease states that represent a major challenge for modern medicine. Although aetilogy is often unknown, it is established that multiple factors such as defects in genetics and/or epigenetics, the environment as well as imbalance in neurotransmitter receptor systems are all at play in determining an individual's susceptibility to disease. Gene therapy is currently not available and therefore, most conditions are treated with pharmacological agents that modify neurotransmitter receptor signaling. Here, I provide a review of ionotropic glutamate receptors (iGluRs) and the roles they fulfill in numerous CNS disorders. Specifically, I argue that our understanding of iGluRs has reached a critical turning point to permit, for the first time, a comprehensive re-evaluation of their role in the cause of disease. I illustrate this by highlighting how defects in AMPA receptor (AMPAR) trafficking are important to fragile X mental retardation and ectopic expression of kainate receptor (KAR) synapses contributes to the pathology of temporal lobe epilepsy. Finally, I discuss how parallel advances in studies of other neurotransmitter systems may allow pharmacologists to work towards a cure for many CNS disorders rather than developing drugs to treat their symptoms.

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Section: Historical Emergence Of Kainate Receptors In Epilepsymentioning

confidence: 99%

Ionotropic Glutamate Receptors & CNS Disorders

Bowie

2008

CNSNDDT

195

130

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“…Kynurenic acid, a glutamate antagonist, blocks the excitatory input from the cones to the horizontal cells by binding to the postsynaptic receptor sites (Coleman et al, 1986). Cobalt ions act on presynaptic terminals to inhibit the release of neurotransmitters.…”

Section: Blocked Synaptic Transmissionmentioning

confidence: 99%

The effects of GABA and related drugs on horizontal cells in the isolated turtle retina

Perlman

Normann

1990

Vis Neurosci

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The role of GABA in the outer plexiform layer of the turtle retina has been examined by intracellular recordings from L-and C-type horizontal cells in the isolated retina preparation.GABA (1-5 mM) slightly depolarized the L-type horizontal cells, reduced the amplitude of their photoresponses, and slowed down the rate of hyperpolarization during the ON component of the photoresponse. These effects could not be replicated by either muscimol or baclofen. When synaptic transmission from the photoreceptors had been blocked by either kynurenic acid or cobalt ions, GABA depolarized L-type horizontal cells and augmented the remaining photoresponses. Neither muscimol nor baclofen exerted any effect on L-type horizontal cells under these conditions. Nipecotic acid, a competitive inhibitor of the GABA-uptake system, induced effects on turtle L-type horizontal cells which were similar to those exerted by GABA. Thus, the complex GABA effect on turtle L-type horizontal cells seems to represent the summation of at least two actions; an indirect one mediated by the red cones via GABA a -type receptors and a direct one which probably reflects the activation of an electrogenic GABA-uptake system. GABA (1-5 mM) induced a transient depolarization in C-type horizontal cells but eliminated color opponency in only three cells out of seven studied. This observation is inconsistent with the notion that the only neural mechanism responsible for the chromatic properties of C-type horizontal cells in the turtle retina is a GABAergic negative feedback from the L-type horizontal cells onto the green ones.

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“…On the other hand, GABA nearly eliminates the center responses of Xenopus OFF-center bipolar cells but only slightly reduces the center response of ON-center bipolar cells (Stone & Schutte, 1991). The glutamate analog APB (2amino-4-phosphonobutyric acid) for instance blocks the light response of ON-center bipolar cells and the b-wave of the ERG (Stockton & Slaughter, 1989), while kynurenic acid blocks the light response of OFF-center bipolar cells and horizontal cells (Coleman et al, 1986) and the OFF response (rf-wave) of the ERG (Stockton & Slaughter, 1989). In addition, we have attempted to establish the sites of action of GABA on the Xenopus ERG by modifying the light responses and synaptic transmission between retinal neurons with glutamate analogs that act specifically on neuronal subtypes, and simultaneously examining the effects of GABAergic agonists and antagonists on the ERG under these modified conditions.…”

Section: Introductionmentioning

confidence: 99%

The role of GABA in modulating the Xenopus electroretinogram

Arnarsson

Eysteinsson

1997

Vis Neurosci

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We have recorded the electroretinogram (ERG) from the superfused eyecup of the Xenopus retina in order to assess the effects of the inhibitory neurotransmitter gamma-aminobutyric acid (GABA), and its agonists and antagonists, on individual ERG components. We found that GABA (0.5-10 mM) reduced the amplitudes of both the b-and d-waves of the Xenopus ERG. The GABA uptake blocker nipecotic acid (1 mM) had similar effects on b-and d-waves. GABA at 5 mM and 10 mM also caused an increase in the a-wave. The GABA antagonist picrotoxin (0.1-2 mM) and the GABA/a antagonist bicuculline (0.2 mM) both increased the amplitude of the b-and rf-waves of the ERG. The GABA/b agonist baclofen (0.3 mM) reduced the amplitude of the ERG i-wave, enhanced the amplitude of the a-wave, and slightly reduced the amplitude and increased the peak time of the

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Kynurenic acid distinguishes kainate and quisqualate receptors in the vertebrate retina

Cited by 55 publications

References 16 publications

Ionotropic Glutamate Receptors & CNS Disorders

Ionotropic Glutamate Receptors & CNS Disorders

The effects of GABA and related drugs on horizontal cells in the isolated turtle retina

The role of GABA in modulating the Xenopus electroretinogram

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