GABA<sub>C</sub>Receptors Control Adaptive Changes in a Glycinergic Inhibitory Pathway in Salamander Retina

Cook, P.B.; Lukasiewicz, Peter D.; McReynolds, John S.

doi:10.1523/jneurosci.20-02-00806.2000

Cited by 19 publications

(15 citation statements)

References 22 publications

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“…The spatial antagonism of glycinergic cells by GABAergic cells is also consistent with previous reports of serial inhibitory influences on ganglion-cell light responses in amphibian retina (Zhang et al, 1997;Cook et al, 2000). Of course, the interpretation of neurotransmitter antagonist effects in serial inhibition is very complex.…”

Section: Gabaergic Modulation Of the Glycinergic Mechanismsupporting

confidence: 89%

Inhibitory network properties shaping the light evoked responses of cat alpha retinal ganglion cells

2003

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Cat retinal ganglion cells of the Y (or alpha) type respond to luminance changes opposite those preferred by their receptive-field centers with a transient hyperpolarization. Here, we examine the spatial organization and synaptic basis of this light response by means of whole-cell current-clamp recordings made in vitro. The hyperpolarization was largest when stimulus spots approximated the size of the receptive-field center, and diminished substantially for larger spots. The hyperpolarization was largely abolished by bath application of strychnine, a blocker of glycinergic inhibition. Picrotoxin, an antagonist of ionotropic GABA receptors, greatly reduced the attenuation of the hyperpolarizing response for large spots. The data are consistent with a model in which (1) the hyperpolarization reflects inhibition by glycinergic amacrine cells of bipolar terminals presynaptic to the alpha cells, and perhaps direct inhibition of the alpha cell as well; and (2) the attenuation of the hyperpolarization by large spots reflects surround inhibition of the glycinergic amacrine by GABAergic amacrine cells. This circuitry may moderate nonlinearities in the alpha-cell light response and could account for some excitatory and inhibitory influences on alpha cells known to arise from outside the classical receptive field.

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Section: Gabaergic Modulation Of the Glycinergic Mechanismsupporting

confidence: 89%

Inhibitory network properties shaping the light evoked responses of cat alpha retinal ganglion cells

2003

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“…Blocking GABAergic inhibition with picrotoxin can cause an increase in glycinergic inhibition in dark-adapted tiger salamander retina (Cook et al, 2000). We tested to see whether the ineffectiveness of picrotoxin and TTX in blocking the primate parasol cell surround was attributable to an increase in glycinergic inhibition by applying a mixture that contained both picrotoxin and the glycine antagonist strychnine (100 M picrotoxin plus 0.5 M TTX plus 5 M strychnine, n ϭ 1 ONcenter cell, n ϭ 1 OFF-center cell; 100 M picrotoxin plus 0.5 M TTX plus 2 M strychnine plus 10 M I4AA, n ϭ 2 ONcenter cells).…”

Section: Application Of Drug Mixturesmentioning

confidence: 99%

The Classical Receptive Field Surround of Primate Parasol Ganglion Cells Is Mediated Primarily by a Non-GABAergic Pathway

McMahon¹,

Packer²,

Dacey³

2004

J. Neurosci.

107

103

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Although the center-surround receptive field is a fundamental property of retinal ganglion cells, the circuitry that mediates surround inhibition remains controversial. We examined the contribution of horizontal cells and amacrine cells to the surround of parasol ganglion cells of macaque and baboon retina by measuring receptive field structure before and during the application of drugs that have been shown previously to affect surrounds in a range of mammalian and nonmammalian species. Carbenoxolone and cobalt, thought to attenuate feedback from horizontal cells to cones, severely reduced the surround. Tetrodotoxin, which blocks sodium spiking in amacrine cells, and picrotoxin, which blocks the inhibitory action of GABA, only slightly reduced the surround. These data are consistent with the hypothesis that the surrounds of light-adapted parasol ganglion cells are generated primarily by non-GABAergic horizontal cell feedback in the outer retina, with a small contribution from GABAergic amacrine cells of the inner retina.

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“…Because blocking GABA A R inhibition with BIC only reduced but did not eliminate the inhibitory effects of NO on GLY release, most notably in the INL, it is possible that GABA A R inhibition was not the only pathway by which NO inhibits glycinergic neurons. GABA C Rs are predominantly located on bipolar cell axon terminals (Vitanova et al, 2001), and GABA C Rs have been shown to interact with glycinergic neurons (Cook et al, 2000). Enhanced feedback inhibition onto bipolar cells through GABA C R may reduce the excitatory drive to glycinergic neurons, resulting in reduced GLY release.…”

Section: No Inhibits Glycine Release Through the Modulation Of Gaba Rmentioning

confidence: 99%

Nitric oxide stimulates γ‐aminobutyric acid release and inhibits glycine release in retina

Eldred

2005

J of Comparative Neurology

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Nitric oxide (NO) modulates the uptake and/or release of neurotransmitters through a variety of cellular mechanisms. However, the pharmacological and biochemical processes underlying these neurochemical effects of NO often remain unclear. In our study, we used immunocytochemical methods to study the effects of NO, cyclic guanosine monophosphate (cGMP), and peroxynitrite on the uptake and release of γ-aminobutyric acid (GABA) and glycine in the turtle retina. In addition, we examined the involvement of glutamate receptors, calcium, and the GABA transporter in this GABA uptake and release. We also tested for interactions between the GABAergic and glycinergic systems. In general, we show that NO stimulated GABA release and inhibited glycine release. The NO-stimulated GABA release involved calcium-dependent or calcium-independent synaptic release or reversal of the GABA transporter. Some effects of NO on GABA release involved glutamate, cGMP, or peroxynitrite. NO promoted glycine uptake and inhibited its release, and this inhibition of glycine release was influenced by GABAergic modulation. These findings indicate that NO modulates the levels of the inhibitory transmitters GABA and glycine through several specific biochemical mechanisms in different retinal cell types and layers. Thus it appears that some of the previously described reciprocal interactions between GABA and glycine in the retina function through specific NO signaling pathways. Keywords turtle; neurotransmitter; release, uptake; modulation Nitric oxide (NO) plays diverse roles in the regulation of neurotransmission mediated by conventional neurotransmitters. In the brain or retina of different species, NO has been found to affect the release of acetylcholine

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GABA_CReceptors Control Adaptive Changes in a Glycinergic Inhibitory Pathway in Salamander Retina

Cited by 19 publications

References 22 publications

Inhibitory network properties shaping the light evoked responses of cat alpha retinal ganglion cells

Inhibitory network properties shaping the light evoked responses of cat alpha retinal ganglion cells

The Classical Receptive Field Surround of Primate Parasol Ganglion Cells Is Mediated Primarily by a Non-GABAergic Pathway

Nitric oxide stimulates γ‐aminobutyric acid release and inhibits glycine release in retina

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GABACReceptors Control Adaptive Changes in a Glycinergic Inhibitory Pathway in Salamander Retina

Cited by 19 publications

References 22 publications

Inhibitory network properties shaping the light evoked responses of cat alpha retinal ganglion cells

Inhibitory network properties shaping the light evoked responses of cat alpha retinal ganglion cells

The Classical Receptive Field Surround of Primate Parasol Ganglion Cells Is Mediated Primarily by a Non-GABAergic Pathway

Nitric oxide stimulates γ‐aminobutyric acid release and inhibits glycine release in retina

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GABA_CReceptors Control Adaptive Changes in a Glycinergic Inhibitory Pathway in Salamander Retina