Coexistence and function of glutamate receptor subtypes in the horizontal cells of the tiger salamander retina

1991 ◽  
Vol 7 (4) ◽  
pp. 377-382 ◽  
Author(s):  
Xiong-Li Yang ◽  
Samuel M. Wu
Keyword(s):  
Dicarboxylic Acid ◽  
Propionic Acid ◽  
Glutamate Receptor ◽  
Horizontal Cells ◽  
Receptor Subtypes ◽  
Tiger Salamander ◽  
Light Responses ◽  
Receptor Agonists ◽  
Glutamate Receptor Agonists ◽  
And Function

AbstractEffects of the major glutamate receptor agonists, kainate (KA), α-amino-3-hydroxy-5-methylisoxazole-4-propionic acid (AMPA), quisqualate (QA), N-methyl-D-aspartate (NMDA), L-α-amino-4-phosphonobutyrate (L-AP4), and trans-l-aminocyclopentane-1,3-dicarboxylic acid (ACPD) on horizontal cells (HCs) were studied in superfused larval tiger salamander retina. 20 μM of KA, AMPA, and QA mimicked the action of 3 mM glutamate in the absence and presence of 1 mM Co2+-20 μM 6-cyano-7-nitroquinoxaline-2,3-dione (CNQX) blocked the actions of KA and AMPA, but not those of QA and glutamate, indicative of the existence of CNQX-resistant QA receptors in the tiger salamander HCs. Prolonged application of ACPD hyperpolarized the HCs and enhanced the light responses, probably by shifting the resting HC voltage (Er) to a more hyperpolarized position. It is possible that the KA, AMPA, and CNQX-resistant QA receptors are involved in mediating the postsynaptic light responses in HCs, and ACPD receptors are involved in sensitivity adjustment of the HC responses.

Glutamate receptor agonists release [3H]GABA preferentially from horizontal cells

1986 ◽  
Vol 398 (2) ◽  
pp. 276-287 ◽  
Author(s):  
Julio Moran ◽  
Herminia Pasantes-Morales ◽  
Dianna A. Redburn
Keyword(s):  
Glutamate Receptor ◽  
Horizontal Cells ◽  
Receptor Agonists ◽  
Glutamate Receptor Agonists

scholarly journals Responses of developing pedunculopontine neurons to glutamate receptor agonists

2011 ◽  
Vol 105 (4) ◽  
pp. 1918-1931 ◽  
Author(s):  
Christen Simon ◽  
Abdallah Hayar ◽  
Edgar Garcia-Rill
Keyword(s):  
Glutamate Receptor ◽  
Rem Sleep ◽  
Cell Types ◽  
Pedunculopontine Nucleus ◽  
Receptor Subtypes ◽  
Receptor Agonists ◽  
Whole Cell Patch Clamp ◽  
Bath Application ◽  
Glutamate Receptor Agonists ◽  
Reticular Activating System

The pedunculopontine nucleus (PPN) is involved in the generation and maintenance of waking and rapid eye movement (REM) sleep, forming part of the reticular activating system. The PPN receives glutamatergic afferents from other mesopontine nuclei, and glutamatergic input is believed to be involved in the generation of arousal states. We tested the hypothesis that, from postnatal days 9 to 17 in the rat, there are developmental changes in the glutamate receptor subtypes that contribute to the responses of PPN neurons. Whole cell patch-clamp recordings were conducted using brainstem slices from 9- to 17-day-old rats. All cells (types I, II, and III; randomly selected or thalamic-projecting) responded to bath application of the glutamate receptor agonists N-methyl-d-aspartic acid (NMDA) and kainic acid (KA). A developmental decrease in the contribution of the NMDA receptor and developmental increase in the contribution of the KA receptor was observed following electrical stimulation-induced glutamate input. These changes were also observed following bath application in different cell types (randomly selected vs. thalamic-projecting). KA bath application produced an increase in the paired-pulse ratio (PPR) and a decrease in the frequency of miniature excitatory postsynaptic currents (mEPSCs), suggesting that presynaptic KA autoreceptors may decrease the probability of synaptic glutamate input. In contrast, NMDA application produced no changes in the PPR or mEPSCs. Changes in glutamatergic excitability of PPN cell types could underlie the developmental decrease in REM sleep.

Effects of CNQX, APB, PDA, and kynurenate on horizontal cells of the tiger salamander retina

1989 ◽  
Vol 3 (3) ◽  
pp. 207-212 ◽  
Author(s):  
Xiong-Li Yang ◽  
Samuel M. Wu
Keyword(s):  
Dicarboxylic Acid ◽  
Nmda Receptors ◽  
Receptor Antagonist ◽  
Horizontal Cells ◽  
Tiger Salamander ◽  
Light Responses ◽  
Aspartate Receptor ◽  
Synaptic Receptors

AbstractEffects of 6-cyano-7-nitroquinoxaline-2,3-dione (CNQX), 2-amino-4-phosphonobutyrate (APB), cis-2,3-piperidine dicarboxylic acid (PDA), and kynurenate (KYN) on the depolarizing actions of glutamate and kainate on horizontal cells (HCs) were studied in the larval tiger salamander retina. APB, PDA, and KYN hyperpolarized the HCs, but they failed to block either the actions of glutamate and kainate, or the HC light responses. APB and PDA did not cause membrane polarizations in either rods or cones, suggesting that the HC hyperpolarizations were not mediated by presynaptic actions of these compounds. CNQX, the newly synthesized non-NMDA (N-Methyl-D-Aspartate) receptor antagonist, blocked the HC light responses and the action of kainate, but not that of glutamate. These results suggest that the synaptic receptors in the tiger salamander HCs are probably non-NMDA although extra-synaptic NMDA receptors may exist in these cells.

Identification of glutamate receptor subtypes mediating inputs to bipolar cells and ganglion cells in the tiger salamander retina

1993 ◽  
Vol 69 (6) ◽  
pp. 2099-2107 ◽  
Author(s):  
S. H. Hensley ◽  
X. L. Yang ◽  
S. M. Wu
Keyword(s):  
Receptor Antagonist ◽  
Glutamate Receptor ◽  
Ganglion Cells ◽  
Extracellular Recording ◽  
Bipolar Cells ◽  
Receptor Subtypes ◽  
Tiger Salamander ◽  
Light Onset ◽  
Light Responses ◽  
Onset Responses

1. The effects of glutamate receptor agonists and antagonists on bipolar cells and ganglion cells were studied with the use of intracellular and extracellular recording in the superfused, isolated, flat-mounted tiger salamander retina. The goal of the experiments was to correlate glutamate receptor subtypes with their localization at specific synaptic sites in the tiger salamander retina. The drugs tested were the kainate/alpha-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid (AMPA) receptor antagonist 6-cyano-7-nitroquinoxaline-2,3-dione (CNQX), the N-methyl-D-aspartate (NMDA) receptor antagonist 3-(C+/-)-2-carboxy-piperazin-4-yl)-propyl-1-phosphonic acid (CPP) and L-2-amino-4-phosphonobutyrate (L-AP4). 2. The light responses of hyperpolarizing bipolar cells were suppressed by 20 microM CNQX, whereas L-AP4 had no effect on their light responses. In contrast, 20 microM CNQX had no effect on depolarizing bipolar cells, whereas L-AP4 abolished the light responses of these cells. 3. The light offset responses of OFF and ON-OFF ganglion cells were completely blocked by concentrations of CNQX as low as 5 microM. The light onset responses of ON-OFF ganglion cells were blocked when the concentration of CNQX was raised to 20 microM. In addition, 30 microM CPP partially blocked the light onset responses of ON-OFF ganglion cells but had a lesser effect on the light offset responses. 4. Twenty micromolars of CNQX blocked a transient component, and 20 microM CPP blocked a sustained component of the light response of sustained-ON ganglion cells.(ABSTRACT TRUNCATED AT 250 WORDS)

scholarly journals Glutamate, NMDA, and AMPA Induced Changes in Extracellular Space Volume and Tortuosity in the Rat Spinal Cord

2001 ◽  
Vol 21 (9) ◽  
pp. 1077-1089 ◽  
Author(s):  
Lýdia Vargová ◽  
Pavla Jendelová ◽  
Alexandr Chvátal ◽  
Eva Syková
Keyword(s):  
Spinal Cord ◽  
Glutamate Receptor ◽  
Extracellular Space ◽  
Volume Fraction ◽  
Glutamate Release ◽  
Extracellular Potassium ◽  
Receptor Agonists ◽  
Diffusion Parameters ◽  
Glutamate Receptor Agonists ◽  
Cellular Swelling

Glutamate release, particularly in pathologic conditions, may result in cellular swelling. The authors studied the effects of glutamate, N-methyl-d-aspartate (NMDA), and α-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid (AMPA) on extracellular pH (pHe), extracellular potassium concentration ([K+]e), and changes in extracellular space (ECS) diffusion parameters (volume fraction α, tortuosity λ) resulting from cellular swelling. In the isolated spinal cord of 4-to 12-day-old rats, the application of glutamate receptor agonists induced an increase in [K+]e, alkaline-acid shifts, a substantial decrease in α, and an increase in λ. After washout of the glutamate receptor agonists, α either returned to or overshot normal values, whereas λ remained elevated. Pretreatment with 20 mmol/L Mg++, MK801, or CNQX blocked the changes in diffusion parameters, [K+]e and pHe evoked by NMDA or AMPA. However, the changes in diffusion parameters also were blocked in Ca2+-free solution, which had no effect on the [K+]e increase or acid shift. The authors conclude that increased glutamate release may produce a large, sustained and [Ca2+]e-dependent decrease in α and increase in λ. Repetitive stimulation and pathologic states resulting in glutamate release therefore may lead to changes in ECS volume and tortuosity, affecting volume transmission and enhancing glutamate neurotoxicity and neuronal damage.

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