Kainate activation of horizontal, bipolar, amacrine, and ganglion cells in the rabbit retina

Marc, Robert E.

doi:10.1002/(sici)1096-9861(19990428)407:1<65::aid-cne5>3.0.co;2-1

Cited by 94 publications

(66 citation statements)

References 66 publications

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“…They do for some other cell types. Horizontal cells (Marc et al, 1995;Marc, 1999b) and starburst amacrine cells (Marc, 1999b) can be extracted via their distinctive signatures, and other cell types display strong superclasses; e.g., mammalian cone ONcenter and OFF-center bipolar cells have distinctive signatures (Kalloniatis et al, 1996). This does not prove that all natural classes should have characteristic signatures, even when excitation signals are added to the data.…”

Section: Structural Correlates Of Classesmentioning

confidence: 98%

“…Brace, 1992;Penn et al, 1994;Jacoby et al, 1996;Stafford and Dacey, 1997;Xin and Bloomfield, 1997). Most amacrine cells are GABA immunoreactive, and GABA-immunoreactive dendrites comprise ϳ80% of the mass of the inner plexiform layer (Marc, 1992(Marc, , 1999bMarc et al, 1995Marc et al, , 1998. GABA is a 97 Da molecule and would clearly leak from GABA in amacrine cells (containing ϳ10 mM GABA) through gap junctions at nearly diffusion-limited rates into ganglion cells.…”

Section: Coupling Signaturesmentioning

confidence: 99%

“…On the basis of previous analyses, we expected that the signatures of natural ganglion cell classes would be poorly separable (Marc, 1999a,b), but when we expanded the set of molecular targets to include aspartate, glutamate, glycine, glutamine, GABA, and taurine signals, strongly heterogeneous multispectral signatures emerged in the ganglion cell layer, suggesting that detailed phenotyping was indeed possible. Excitation signatures based on mapping AMPA-activated 1-amino-4-guanidobutane (AGB) permeation (Marc, 1999b) proved decisive. Fusion of excitation and intrinsic signals permitted the demonstration that the rabbit retinal ganglion cell layer contains no fewer than 14 natural types of ganglion cells, and some are further characterized by cell size, patterning, and population fraction.…”

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confidence: 99%

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Molecular Phenotyping of Retinal Ganglion Cells

2002

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Classifying all of the ganglion cells in the mammalian retina has long been a goal of anatomists, physiologists, and cell biologists. The rabbit retinal ganglion cell layer was phenotyped using intrinsic small molecule signals (aspartate, glutamate, glycine, glutamine, GABA, and taurine) and glutamate receptorgated 1-amino-4-guanidobutane excitation signals as the clustering dimensions for formal classification. Intrinsic signals alone yielded 7 ganglion cell superclasses and 1 amacrine cell superclass; the addition of excitation signals ultimately resolved 14 natural ganglion cell classes and 3 amacrine cell classes. Ganglion cells comprise two-thirds to three-quarters of the cells in the ganglion cell layer and exhibited distinct metabolic, coupling, and excitation phenotypes, as well as characteristic sizes, population fractions, and patterns. Metabolic signatures (mixtures of glutamate, aspartate, glutamine, and GABA) chemically discriminated ganglion from amacrine cells. Coupling signatures reflected heterologous coupling states across ganglion cells: (1) uncoupled, (2) coupled to GABAergic amacrine cells, and (3) coupled to glycinergic amacrine cells. Excitation signatures reflected differential channel permeation rates across classes after AMPA activation. Extraction of unique size and patterning features from the data sets further validated the robustness of the classification. Because the classifications were explicitly blinded to structure, this is strong evidence that molecular phenotype classes are natural classes. Correspondences of molecular phenotype classes to functional classes were inferred from size, coupling, encounter, and physiological attributes. Ganglion cell classes display markedly different ionotropic drives, which may partly explain the physiological brisk-sluggish spectrum of ganglion cell spiking patterns.

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Section: Structural Correlates Of Classesmentioning

confidence: 98%

Section: Coupling Signaturesmentioning

confidence: 99%

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confidence: 99%

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Molecular Phenotyping of Retinal Ganglion Cells

2002

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“…In the rabbit retina, kainate responses were recorded from various types of neuronal cells (Marc, 1999). The light responses of most retinal neurons are mediated primarily by AMPA receptors that desensitize to a maintained plateau (Thoreson and Witkovsky, 1999).…”

Section: Functional Relevancementioning

confidence: 99%

Glutamate-Evoked Alterations of Glial and Neuronal Cell Morphology in the Guinea Pig Retina

Uckermann¹,

Vargová²,

Ulbricht³

et al. 2004

J. Neurosci.

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Neuronal activity is accompanied by transmembranous ion fluxes that cause cell volume changes. In whole mounts of the guinea pig retina, application of glutamate resulted in fast swelling of neuronal cell bodies in the ganglion cell layer (GCL) and the inner nuclear layer (INL) (by ϳ40%) and a concomitant decrease of the thickness of glial cell processes in the inner plexiform layer (IPL) (by ϳ40%) that was accompanied by an elongation of the glial cells, by a thickening of the whole retinal tissue, and by a shrinkage of the extracellular space (by ϳ18%). The half-maximal effect of glutamate was observed at ϳ250 M, after ϳ4 min. The swelling was caused predominantly by AMPAkainate receptor-mediated influx of Na ϩ into retinal neurons. Similar but transient morphological alterations were induced by high K ϩ and dopamine, which caused release of endogenous glutamate and subsequent activation of AMPA-kainate receptors. Apparently, retinal glutamatergic transmission is accompanied by neuronal cell swelling that causes compensatory morphological alterations of glial cells. The effect of dopamine was elicitable only during light adaptation but not in the dark, and glutamate and high K ϩ induced stronger effects in the dark than in the light. This suggests that not only the endogenous release of dopamine but also the responsiveness of glutamatergic neurons to dopamine is regulated by light-dark adaptation. Similar morphological alterations (neuronal swelling and decreased glial process thickness) were observed in whole mounts isolated immediately after experimental retinal ischemia, suggesting an involvement of AMPA-kainate receptor activation in putative neurotoxic cell swelling in the postischemic retina.Key words: glutamate; dopamine; ATP; neuroglia; circadian phase; ischemia; retina IntroductionGlial cells play crucial roles in supporting neuronal survival and information processing (Newman and Reichenbach, 1996): they regulate the extracellular homeostasis of relevant ions including K ϩ , control the water content of the extracellular space, and mediate the rapid termination of neuronal activity by transmitter uptake from the synaptic cleft (Matsui et al., 1999). In the retina, neuronally released K ϩ , water, and glutamate are cleared from the extracellular space mainly by the radial glial (Müller) cells. Retinal glial cells display a complex pattern of K ϩ channel expression in their plasma membranes that directs the flow of neuronally released K ϩ into the glial cell bodies and farther into the vitreous and the blood vessels (Kofuji et al., 2002). Parallel water fluxes were suggested to be coupled to the transglial K ϩ fluxes (Nagelhus et al., 1999). The K ϩ and water fluxes, generated by neuronal activity and mediated by glial cells, are accompanied by swelling of cells and shrinkage of the extracellular space caused by the decreased extracellular osmolality (Dietzel et al., 1980;Jendelová and Syková, 1991;Syková, 1991). Cell volume alterations are important, particularly under pathological conditions such as ...

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“…19,20 Previous experiments have shown that only calcium blockers prevented agmatine from entering synaptosomes. 21 Although other channels may be involved in different cell membrane locations, it is highly likely that calcium or nonspecific cation channels are responsible for the uptake of agmatine in our experiments.…”

Section: Discussionmentioning

confidence: 99%

Gonadotropin-Releasing Hormone Modulates Vomeronasal Neuron Response to Male Salamander Pheromone

et al. 2012

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Abstract:Electrophysiological studies have shown that gonadotropin-releasing hormone (GnRH) modifies chemosensory neurons responses to odors. We have previously demonstrated that male Plethodon shermani pheromone stimulates vomeronasal neurons in the female conspecific. In the present study we used agmatine uptake as a relative measure of the effects of GnRH on this pheromoneinduced neural activation of vomeronasal neurons. Whole male pheromone extract containing 3 millimolar agmatine with or without 10 micromolar GnRH was applied to the nasolabial groove of female salamanders for 45 minutes. Immunocytochemical procedures were conducted to visualize and quantify relative agmatine uptake as measured by labeling density of activated vomeronasal neurons. The relative number of labeled neurons did not differ between the two groups: pheromone alone or pheromone-GnRH. However, vomeronasal neurons exposed to pheromone-GnRH collectively demonstrated higher labeling intensity, as a percentage above background (75%) as compared with neurons exposed to pheromone alone (63%, P , 0.018). Since the labeling intensity of agmatine within neurons signifies the relative activity levels of the neurons, these results suggest that GnRH increases the response of female vomeronasal neurons to male pheromone.

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Kainate activation of horizontal, bipolar, amacrine, and ganglion cells in the rabbit retina

Cited by 94 publications

References 66 publications

Molecular Phenotyping of Retinal Ganglion Cells

Molecular Phenotyping of Retinal Ganglion Cells

Glutamate-Evoked Alterations of Glial and Neuronal Cell Morphology in the Guinea Pig Retina

Gonadotropin-Releasing Hormone Modulates Vomeronasal Neuron Response to Male Salamander Pheromone

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