Physiological and pharmacological basis of GABA and glycine action on neurons of mudpuppy retina. I. Receptors, horizontal cells, bipolars, and G-cells.

Miller, RF; Frumkes, Thomas E.; Slaughter, Malcolm M.; Dacheux, Ramon F.

doi:10.1152/jn.1981.45.4.743

Cited by 93 publications

(39 citation statements)

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“…The concentration of strychnine used in our experiments was very similar to that employed by electrophysiologists using comparable eye-cup preparations (e.g. Miller, Frumkes, Slaughter & Dacheux, 1981). The release of glycine from amacrine cells was increased by muscarine and this action was blocked by atropine, indicating an action at cholinergic muscarinic receptors.…”

Section: Resultssupporting

confidence: 56%

Baclofen enhancement of acetylcholine release from amacrine cells in the rabbit retina by reduction of glycinergic inhibition.

Neal

Cunningham

1995

The Journal of Physiology

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1. The mechanism by which the GABAB-receptor agonist, baclofen, enhances the lightevoked release of [3H]acetylcholine (ACh) from cholinergic amacrine cells was studied using an eye-cup preparation in anaesthetized rabbits and isolated retinas.2. WVhen applied locally to the rabbit retina, baclofen increased the release of ACh evoked by a ffickering light (3 Hz) by over 40 %. 3. In isolated retinas, baclofen strikingly inhibited the K+-evoked release of glycine but had no effect on GABA release. 4. In the rabbit eye cup, strychnine enhanced the light-evoked release of ACh to a similar degree to that produced by baclofen. The effects of baclofen and strychnine on the lightevoked release of ACh were not additive. In contrast, bicuculline did not affect the enhancing action of baclofen on the light-evoked release of ACh. 5. In order to see whether the glycinergic amacrine cells might be stimulated by ACh, isolated rat and rabbit retinas were exposed to muscarine. This cholinergic agonist potentiated the K+-evoked release of glycine by 54 %.6. We suggest that baclofen enhances the light-evoked release of ACh from amacrine cells by inhibiting glycine release from glycinergic amacrine cells which are stimulated by ACh and form an inhibitory feedback loop to the cholinergic neurones.

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Section: Resultssupporting

confidence: 56%

Baclofen enhancement of acetylcholine release from amacrine cells in the rabbit retina by reduction of glycinergic inhibition.

Neal

Cunningham

1995

The Journal of Physiology

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“…Other studies upon fish retinas (Murakami et al 1972;Murakami, Shimoda & Nakatani, 1978;Wu & Dowling 1980;Laufer, 260 EFFECTS OF DRUGS ON RETINAL HORIZONTAL CELLS 1982) are consistent with the findings just described. On the other hand, Miller, Frumkes, Slaughter & Dacheux (1981) reported that in mudpuppy retina, GABA markedly depolarized the horizontal cell; this action was blocked by cobalt. Other actions of GABA are not excluded, e.g.…”

Section: Discussionmentioning

confidence: 97%

“…The data on mudpuppy retina, moreover, may not apply to Xenopus since the effects of glycine on horizontal cells in these two species appear to be different. Miller et al (1981) reported that mudpuppy horizontal cells depolarized in response to millimolar concentrations of glycine, but that this action was blocked by cobalt, suggesting that the horizontal cell of the mudpuppy retina lacked a glycine receptor.…”

Section: S Stone and P Witko Vsk Y Cellular And Ionic Bases Of Glycmentioning

confidence: 99%

The actions of gamma‐aminobutyric acid, glycine and their antagonists upon horizontal cells of the Xenopus retina.

Stone¹,

Witkovsky²

1984

The Journal of Physiology

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We examined the effects of gamma‐aminobutyric acid (GABA) and glycine and their respective antagonists, picrotoxin and strychnine, upon the membrane potential and light‐evoked responses of the type H1 horizontal cell of the Xenopus retina. This horizontal cell receives mixed input from rod and cone receptors. Under control conditions the mean membrane potential was ‐37.8 +/‐ 9.7 mV. Addition of 5 mM‐GABA to the superfusate hyperpolarized the cell by 4.0 +/‐ 2.6 mV within 3‐5 min; addition of 0.5 mM‐picrotoxin depolarized the cell by 4.3 +/‐ 2.1 mV. Prolonged (greater than 15 min) exposures to the drugs elicited more pronounced changes in membrane potential. GABA and picrotoxin affected primarily the cone‐dependent input to the H1 horizontal cell. Under dark‐adapted conditions, response wave forms were essentially unaltered by the drugs, but when the horizontal cell was moderately or fully light adapted, GABA reduced and picrotoxin enhanced the cone‐dependent component of its response to light. Long‐term (greater than 15 min) exposures to GABA and picrotoxin elicited changes in response kinetics usually associated with dark and light adaptation, respectively. Glycine, at bath concentrations of 0.6 mM or greater, depolarized horizontal cells by 21 mV on average and reduced or abolished their light response. This action did not occur in the presence of 0.1 mM‐strychnine. When all light‐evoked activity was blocked by 20‐40 mM‐magnesium, the depolarizing action of glycine still occurred. Thus, glycine appears to act directly upon the horizontal cell membrane. Neither GABA nor glycine, nor their respective antagonists, affected the spatial extent of the horizontal cell receptive field.

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“…The mechanisms by which GABA may guide synaptic targeting has not been determined, but chemotactic mechanisms are likely; transmitter gradients can guide axonal outgrowth (Zheng et al, 19941, and focal application of GABA has been shown to affect neurite extension by hippocampal neurons (Mattson, 1988;Mattson and Kater, 1989). The near-random selectivity of regenerating photoreceptors for targets on the basis of GLU and GLY content would be predicted by the reported absence of excitatory amino acid (Eliasof and Werblin, 1993) and GLY receptors (Miller et al, 1981) on salamander photoreceptors, which would render photoreceptors "blind" to GLU and GLY. The apparent selectivity for the GLU-containing subset of multipolar cells might be explained by the high frequency of GLU and GABA colocalization in salamander amacrine cells (Yang and Yazulla, 1994a) or might be related to other nontransmitter factors.…”

Section: Neurochemical Selectivity and Potential Synaptic Targeting Mmentioning

confidence: 99%

Morphologic and neurochemical target selectivity of regenerating adult photoreceptors in vitro

1996

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Regenerating adult central nervous system (CNS) neurons must re-establish synaptic circuits in an environment very different from that present during development. However, the complexity of CNS circuitry has made it extremely difficult to assess the selectivity and mechanisms of synaptic regeneration at the cellular level in vivo. The synaptic preferences of adult photoreceptors were examined by using a defined cell culture system known to support regenerative process growth, presynaptic varicosity formation, and establishment of functional synapses. Immunolabeling for synaptic vesicle protein 2 and ultrastructural analysis demonstrated that cell-cell contacts made by photoreceptors were synaptic in nature. Target selectivity was determined by quantitative analysis of contacts onto normal and novel target cell types in cultures in which opportunities to contact all retinal cell types were present. Target cells were identified by morphology and immunolabeling for the amino acid neurotransmitters glutamate, aspartate, gamma-aminobutyric acid (GABA), and glycine. Regenerating photoreceptors showed a strong preference for novel multipolar cell targets (amacrine and ganglion cells) over normal photoreceptor, horizontal, and bipolar cell targets. Additionally, photoreceptors were selective for targets containing the transmitter GABA. These results indicate first, that the normal synaptic partners for photoreceptors are not intrinsically the optimal targets for regenerative synapse formation, and second, that GABA may modulate synaptic targeting by adult photoreceptors.

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Physiological and pharmacological basis of GABA and glycine action on neurons of mudpuppy retina. I. Receptors, horizontal cells, bipolars, and G-cells.

Cited by 93 publications

References 0 publications

Baclofen enhancement of acetylcholine release from amacrine cells in the rabbit retina by reduction of glycinergic inhibition.

Baclofen enhancement of acetylcholine release from amacrine cells in the rabbit retina by reduction of glycinergic inhibition.

The actions of gamma‐aminobutyric acid, glycine and their antagonists upon horizontal cells of the Xenopus retina.

Morphologic and neurochemical target selectivity of regenerating adult photoreceptors in vitro

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