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Glycinergic amacrine cells of the rat retina
Author(s) -
Menger Nicole,
Pow David V.,
Wässle Heinz
Publication year - 1998
Publication title -
journal of comparative neurology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.855
H-Index - 209
eISSN - 1096-9861
pISSN - 0021-9967
DOI - 10.1002/(sici)1096-9861(19981109)401:1<34::aid-cne3>3.0.co;2-p
Subject(s) - amacrine cell , inner plexiform layer , retina , glycine receptor , neuroscience , immunolabeling , biology , glycine , inner nuclear layer , lucifer yellow , microbiology and biotechnology , interneuron , retinal , anatomy , intracellular , inhibitory postsynaptic potential , biochemistry , immunohistochemistry , immunology , amino acid , gap junction
Abstract Physiological studies of neurons of the inner retina, e.g., of amacrine cells, are now possible in a mammalian retinal slice preparation. The present anatomical study characterizes glycinergic amacrine cells of the rat retina and thus lays the ground for such future physiological and pharmacological experiments. Rat retinae were immunolabeled with antibodies against glycine and the glycine transporter‐1 (GLYT‐1), respectively. Glycine immunoreactivity was found in approximately 50% of the amacrine and 25% of the bipolar cells. GLYT‐1 immunoreactivity was restricted to glycinergic amacrine cells. They were morphologically characterized by the intracellular injection of Lucifer Yellow followed by GLYT‐1 immunolabeling. Eight different types of glycinergic amacrine cells could be distinguished. They were all small‐field amacrine cells with bushy dendritic trees terminating at different levels within the inner plexiform layer. The well‐known AII amacrine cell was encountered most frequently. From our measurements of the dendritic field sizes and the density of glycinergic cells, we estimate that there are enough glycinergic amacrine cells available to make sure that all eight types and possibly more tile the retina regularly with their dendritic fields. J. Comp. Neurol. 401:34–46, 1998. © 1998 Wiley‐Liss, Inc.