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Journal Article

Glutamate responses of bipolar cells in a slice preparation of the rat retina

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Euler,  Thomas
Retinal Signal Processing, Max Planck Institute for Medical Research, Max Planck Society;
Department of Biomedical Optics, Max Planck Institute for Medical Research, Max Planck Society;

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Citation

Euler, T., Schneider, H., & Wässle, H. (1996). Glutamate responses of bipolar cells in a slice preparation of the rat retina. The Journal of Neuroscience, 16(9), 2934-2944. Retrieved from http://www.jneurosci.org/content/16/9/2934/tab-article-info.


Cite as: https://hdl.handle.net/11858/00-001M-0000-0019-A72F-E
Abstract
Whole-cell currents from >70 voltage-clamped bipolar cells were recorded in a slice preparation of the rat retina. The recorded cells were identified and classified by intracellular staining with Lucifer yellow. Glutamate, the specific agonists (+/-)-2-amino-4-phosphonobutyric acid (AP-4) and kainate (KA), and the antagonist 6-cyanoquinoxaline-2,3-dione (CNQX) were applied. The cells could be isolated from presynaptic influences by the co-application of bicuculline, strychnine, and cobalt ions. Responses to AP-4 were elicited only from bipolar cells with axons stratifying in the inner part of the inner plexiform layer (IPL). AP-4 caused an outward current in these cells attributable to the closure of nonspecific cation channels. Responses to kainate representing a direct action of the drug on the recorded cells were observed only in bipolar cells with axons stratifying in the outer part of the IPL. KA caused a CNQX-sensitive inward current in these cells, associated with openings of nonspecific cation channels. The results predict that cone bipolar (CB) cells with axons terminating in the outer IPL are OFF-bipolars, whereas those with axons terminating in the inner IPL are ON-bipolars. Most of the cells expressed GABA-gated Cl- conductances. In rod bipolar and in some CB cells, only part of the GABA-induced currents could be blocked by the application of bicuculline, suggesting the presence of GABAc receptors in addition to GABAA receptors.