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Spatiotemporal gradients of kainate-sensitivity in the developing chicken retina
1Institute of Anatomy, University of Lausanne, Switzerland.
Insights
Kainate (KA) exposure causes cell death in developing chick retinas, with sensitivity emerging by embryonic day 10 (E10) and expanding over time. Significant cell depletion occurs after E12, affecting ganglion and amacrine cells.
Area of Science:
- Neuroscience
- Developmental Biology
- Ophthalmology
Background:
- The developing visual system undergoes critical periods of cell vulnerability.
- Understanding kainate excitotoxicity is crucial for studying neuronal development and injury.
Purpose of the Study:
- To investigate the age-dependent effects of kainate (KA) on chick retinal development.
- To characterize the spatiotemporal progression of KA-induced cell death and depletion.
Main Methods:
- Intravitreal injections of kainate into chick embryos and chicks at various developmental stages.
- Histological analysis to identify pyknotic cells (early cell death) and assess cell depletion after longer survival periods.
Main Results:
- Kainate induced pyknotic cells starting at embryonic day 10 (E10) in the ventrotemporal retina.
- Sensitivity to KA spread tangentially, affecting amacrine and later bipolar sublayers.
- Substantial cell depletion in inner nuclear and ganglion cell layers occurred with injections after E12, expanding with later stages.
Conclusions:
- The chick retina exhibits a specific developmental window of vulnerability to kainate excitotoxicity.
- The spatiotemporal pattern of KA effects suggests a programmed developmental sensitivity.
- Ganglion cells undergo a period of heightened sensitivity to KA during development.
Abstract:
We have studied the age-dependence of the effects of kainate (KA) on the chick retina as a prelude to the accompanying paper on the effects of target-removal on the isthmo-optic nucleus. KA was injected into the eyes of chick embryos and chicks at different ages, and the retinas were fixed a few hours or several days later. The former group of retinas was scanned for pyknotic cells. The earliest age at which KA caused pyknosis was embryonic day 10 (E10), when pyknotic cells appeared in a ventrotemporal patch in the amacrine sublayer near the fundus. Over the next two days the sensitive region expanded tangentially, reaching the periphery first temporally, then nasally. Only after E12 did the KA cause pyknotic cells to occur also in the bipolar sublayer, where the sensitivity spread in the same spatiotemporal sequence as the initial wave, but two days later. Cell loss was examined in embryos that survived a week or more after the KA injection. Substantial cell depletion was found in both the inner nuclear and ganglion cell layers, but only when the injection had been made after E12. With progressively later injections, the depleted zone expanded in the same spatiotemporal sequence as described above, until at E15 the injections caused depletion throughout the entire extent of the retina. The reasons for the lack of cell depletion after KA injections made before E12 are discussed. Cell counts in the ganglion cell layer and studies of anterograde transport of intravitreally injected peroxidase along the retinofugal fibers showed that about half the ganglion cells (including the displaced ganglion cells) pass through a period of vulnerability to the KA injections, to which they subsequently become sensitive.