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Early development of amacrine cells in the mouse retina: An electron microscopic, serial section analysis
Author(s) -
Hinds James W.,
Hinds Patricia L.
Publication year - 1978
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/cne.901790204
Subject(s) - retina , biology , inner plexiform layer , retinal waves , intrinsically photosensitive retinal ganglion cells , bistratified cell , ganglion , inner nuclear layer , amacrine cell , giant retinal ganglion cells , ganglion cell layer , parasol cell , neuroscience , microbiology and biotechnology , anatomy , retinal ganglion cell
The development of retinal amacrine cells in mice at the fifteenth day of gestation (E‐15) has been analyzed by reconstructing large numbers of cells from serial thin sections. This information has been supplemented by reconstructing cells from E13 and E17 retinas as well as autoradiographic studies of time of origin of cells arising in the period before E15. The presence of bipolar amacrine cells in the outer ventricular layer, first suggested by Cajal, has been confirmed by reconstructing cells from the E17 retina when a clearly defined inner plexiform layer (IPL) is first found. The less mature bipolar amacrine cells present at E17 resemble similar cells found in the E15 retina; they are distinguished from the pre‐axonic, migratory stage of ganglion cells by their flattened rather than cylindrical processes, the darker cytoplasm of these processes, and the position of their centrioles closer to the nucleus. Examination of large numbers of reconstructed cells throughout the thickness of the E15 retina has revealed no forms directly transitional from ventricualr cells to bipolar amacrine cells; insted, bipolar amacrine cells appear to be derived by retrograde (sclerally directed) migration of cells in the ganglion cell layer that resemble normal ganglion cells but lack axons. The origin of these anaxonic cells of the ganglion cell layer is not certain but several findings, including evidence of degenerating axons in the optic nerve, sugest that they are derived by loss of the primitive axons of ganglion cells. Thus amacrine cells may be formed by a relatively late differentiating event that occurs after migration of cells to the ganglion cell layer. Such a developmental origin would offer a plausible explanation for the displaced amacrine cells in the ganglion cell layer and IPL described in the adult, as well as perhaps the close similarity of the dendritic trees of certain subtypes of normal, nondisplaced, ganglion and amacrine cells.