In vitro effects of kainate on embryonic and posthatching chick retina

Gibson, Barbara L.; Reif‐Lehrer, Liane

doi:10.1016/0165-3806(84)90144-5

Cited by 21 publications

(13 citation statements)

References 8 publications

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“…Exposure of embryonic chick retina to KA results in damage to neurons within the inner region of the INL at an earlier age than neurons in the outer region of the INL [Gibson and Reif-Lehrer, 1984]. These results suggest that amacrine cells develop sensitivity to KA earlier than bipolar cells, a feature consistent with morphological studies that indicate that amacrine cells develop ear lier than bipolar cells [see Grun, 1982].…”

Section: Introductionsupporting

confidence: 78%

“…In the posthatch chick retina, a concentration of 0.5 and 5.0 juM KA is re quired to elicit a neurotoxic response in bi polar and amacrine cells, respectively [Sattayasai and Ehrlich, 1987], In the embryonic retina, the adult threshold response for amacrine cells is attained at E-12 and for bipolar cells at D -l. Gibson and Reif-Lehrer [1984], in a similar study, reported that the adult pattern of KA neurotoxicity is estab lished between E-8 and E-15. However, their study was based on relative high doses of KA which precluded comparisons of sensitivity, since even the lowest reported dose (0.1 mM) had profound neurotoxic effects on the INL.…”

Section: Discussionmentioning

confidence: 78%

“…In the study of Gibson and Reif-Lehrer [1984], there was no report of horizontal cell damage. We found that the dose required to damage horizontal cells was similar to the dose reported to damage them in posthatch retina [Ingham and Morgan, 1983].…”

Section: Discussionmentioning

confidence: 99%

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Neurotoxic Effects of Kainic Acid on Developing Chick Retina

Nardis

Sattayasai²,

Zappia³

et al. 1988

Dev Neurosci

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The neurotoxic effects of kainic acid (KA) on developing neurons in the chick retina was investigated in an in vitro preparation. Eyecups from chick embryos at 6 (E-6), 8, 10, 12, 14, 16, and 20 days of incubation and from chicks on day 1 posthatch (D-1) were exposed to different doses of KA for 30 min and then processed for light microscopy. Neurotoxic damage was evaluated by the presence of swollen cell bodies, containing pale cytoplasm and pyknotic nuclei. At E-8, amacrine cells first became sensitive to KA and displayed neurotoxic damage at a threshold concentration of 20 µM. Their sensitivity to KA increased over the following 4 days, so that by E-12 they attained a threshold sensitivity of 5.0 µMKA. At E-14, one third of the retinae showed amacrine cell damage at 0.5–2.0 µM KA, less than the threshold dose of 5.0 µM KA required at D-1. Bipolar cells first become sensitive to KA at E-12, at a threshold concentration of 5.0 µM. The threshold concentration decreased over the following 10 days: 2.0 µM at E-16,1.0 µM at E-20, and 0.5 µM at D-1. At E-8 and E-10, horizontal cells were susceptible to a relatively high concentration of 80 µM KA. The sensitivity to KA is evident prior to the formation of photoreceptor input. These results indicate that amacrine and horizontal cells are susceptible to KA at an earlier age than bipolar cells. Both amacrine and bipolar cells exhibit an age-dependent relationship with the threshold concentration of KA required to cause neurotoxicity; in general, the older the embryo, the lower the dose of KA. However, the increased susceptibility of amacrine cells at E-14 suggests a transient hypersensitivity to KA during this period which may reflect an overproduction of the receptor-ionic channel complex necessary for KA to exert its effect.

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Section: Introductionsupporting

confidence: 78%

Section: Discussionmentioning

confidence: 78%

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Neurotoxic Effects of Kainic Acid on Developing Chick Retina

Nardis

Sattayasai²,

Zappia³

et al. 1988

Dev Neurosci

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“…In chick retina, ␥-amino-butyric acid (GABA) receptors and calcium channels are active from early days of development (Yamashita and Fukuda, 1993), and muscarinic acetylcholine responses (Yamashita et al, 1994b), as well as glutamate evoked currents (Allcorn et al, 1996;Sugioka et al, 1998), were also observed. Also, in chick retina cells in culture, glutamic acid decarboxylase expression (de Mello et al, 1991) and GABA evoked currents have been studied (Yamashita et al, 1994a), as well as calcium channels (Yamashita et al, 1994a;Capela et al, 1997), and kainate toxicity (Gibson and Reif-Lehrer, 1984;Ferreira et al, 1998).…”

Section: Introductionmentioning

confidence: 99%

Expression of AMPA/kainate receptors during development of chick embryo retina cells: in vitro versus in vivo studies

Cristóvão

Oliveira

Carvalho

2002

Intl J of Devlp Neuroscience

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The activity and the subunit expression of alpha-amino-3-hydroxy-5-methylisoxazole-4-propionate (AMPA)/kainate ionotropic glutamate receptors were studied in retina cells developing in chick embryos and in retina cells cultured as retinospheroids, at the same stages of development. In the retinospheroids, the activity of the AMPA/kainate receptors was monitored by following the changes in the intracellular free calcium concentration ([Ca(2+)](i)), in response to AMPA, kainate or to L-glutamate, and the expression of the receptor subunits GluR1, GluR2/3, GluR4 and GluR6/7 was determined in the retinospheroids and in chick retinas by immunodetection using polyclonal antibodies. The changes in [Ca(2+)](i) in response to 400 microM kainate increased from 5h in vitro to 3 days, and remained constant until day 14, whereas the [Ca(2+)](i) in response to 500 microM L-glutamate or 400 microM AMPA increased from 5h in vitro to 3 days, and thereafter decreased slightly until day 14. The [Ca(2+)](i) responses to kainate are mainly due to AMPA receptor stimulation, since the signals were abolished by LY303070, the AMPA receptor antagonist, and were not affected by MK-801, the NMDA receptor antagonist. In retinospheroids, the levels of expression of GluR1 subunit increased from 5h in vitro until day 7, then decreased until day 14. The levels of expression of GluR2/3 and GluR4 subunits increased from 5h in vitro until day 10, and remained constant until day 14. The levels of kainate receptor subunits GluR6/7 increased from 5h in vitro until day 3, and thereafter decreased slightly until day 14. In the retinas, the expression of GluR1 and GluR6/7 subunits increased from day 8 until day 15, and then decreased until day 22 (post-natal 1). The subunits GluR2/3 and GluR4 increased from day 8 until day 18, and remained constant until day 22. The results suggest that AMPA/kainate receptors are expressed at early embryonic stages, although at low levels and before synapse formation (E12). However, the AMPA receptors are not completely functional at the first stage studied since they do not respond to the agonist AMPA. Also, the patterns of AMPA/kainate receptor subunit expression in retinospheroids of chick embryo retina cells cultured in vitro and in retina cells developing in the embryo (in vivo) were similar, indicating that the AMPA/kainate receptor subunits expression in these primary cultures mimics their expression in the developing chick retina.

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“…The need for a simple system to test the validity and the relative potency of different GN analogs and derivatives as neuroprotectors has prompted us to explore the suitability of the chick retina as a model to analyze the ability of GNs to antagonize the toxic actions of excitatory amino acids. Although early descriptions of the deleterious effects of glutamate on the mouse retina [13]were based on the parenteral administration of the amino acid (see [14]for a discussion), the use of the ex vivo chick (or mouse) retinal preparation for excitotoxicity analysis was later successfully adopted in several laboratories [15–21]. We have taken advantage of a further adaptation of this retinal model to set up a simple and sensitive system to evaluate the neuroprotective effects of GNs and other EAA antagonists on the acute and delayed effects of a single dose of kainate.…”

Section: Introductionmentioning

confidence: 99%

Guanine nucleotides protect against kainate toxicity in an ex vivo chick retinal preparation

et al. 1998

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Ex vivo preparations of chick neural retina have been successfully used in the assessment of excitotoxicity and in the evaluation of the protective effects of glutamate antagonists. Using a variation of this approach, and measuring the acute and delayed toxic effects of kainate (KA) in terms of lactate dehydrogenase release, we have shown that guanine nucleotides behave as effective neuroprotecting agents. The anti-excitotoxic potency of guanine nucleotides (in the case of GMP and GDPL LS it is about 100 times lower than that of DNQX, a powerful kainate antagonist) correlates well with their ability to displace KA from retinal KA receptors.z 1998 Federation of European Biochemical Societies.

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In vitro effects of kainate on embryonic and posthatching chick retina

Cited by 21 publications

References 8 publications

Neurotoxic Effects of Kainic Acid on Developing Chick Retina

Neurotoxic Effects of Kainic Acid on Developing Chick Retina

Expression of AMPA/kainate receptors during development of chick embryo retina cells: in vitro versus in vivo studies

Guanine nucleotides protect against kainate toxicity in an ex vivo chick retinal preparation

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