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The Journal of Neuroscience, April 1, 1999, 19(7):2568-2579

Immunohistological Studies of Metabotropic Glutamate Receptor Subtype 6-Deficient Mice Show No Abnormality of Retinal Cell Organization and Ganglion Cell Maturation

Yoshiaki Tagawa¹, Hajime Sawai², Yoshiki Ueda¹, Masaki Tauchi², and Shigetada Nakanishi¹

¹ Department of Biological Sciences, Kyoto University Faculty of Medicine, Yoshida, Sakyo-ku, Kyoto 606-8501, Japan, and ² Department of Welfare System and Health Science, Okayama Prefectural University, Kuboki, Souja, Okayama 719-1197, Japan

Immature retinal ganglion cells (RGCs) initially show a multistratified dendritic pattern, and, during the postnatal period, these dendrites gradually monostratify into ON and OFF sublaminae. The selective agonist of group III metabotropic glutamate receptors (mGluR), L-2-amino-4-phosphonobutyrate (L-AP-4), hyperpolarizes ON bipolar cells and reduces glutamate release. On the basis of L-AP-4-evoked inhibitory effects on ON-OFF segregation of developing RGCs, it has been hypothesized that glutamate-mediated synaptic activity is crucial for formation of the ON-OFF network. Gene-targeted ablation of mGluR6 specifically expressed in ON bipolar cells blocks normal ON responses but has been predicted to enhance glutamate release from ON bipolar cells. The mGluR6 knock-out mouse therefore provides a unique opportunity to investigate whether glutamate release and ON responses are important factors in the development of ON-OFF segregation. The combination of several different morphological analyses indicates that ON bipolar cells, as well as several distinct amacrine cells, in mGluR6 knock-out mice are normally distributed and correctly extend their terminals to defined retinal laminae. Importantly, both  and  RGCs in adult mGluR6 knock-out mice are found monostratified into cell type-specific layers. Furthermore, no difference between wild-type and mGluR6 knock-out mice is observed in the maturation and dendritic stratification of developing RGCs. Hence, despite a deficit in normal ON responses, mGluR6 deficiency causes no abnormality in the retinal cellular organization nor in the stratifications of both ON bipolar cells and developing and mature RGCs. Based on these findings, we discuss several possible mechanisms that may underlie ON-OFF segregation of RGCs.

Key words: metabotropic glutamate receptor subtype 6; knock-out and transgenic mice; Lucifer yellow injection; immunohistology; ON response; dendritic stratification; retinal cells

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Copyright © 1999 Society for Neuroscience  0270-6474/99/1972568-12$05.00/0

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