scholarly journals The Transient Intermediate Plexiform Layer, a Plexiform Layer-like Structure Temporarily Existing in the Inner Nuclear Layer in Developing Rat Retina

2018 ◽  
Vol 27 (1) ◽  
pp. 28-33
Author(s):  
Hyung Wook Park ◽  
Hong-Lim Kim ◽  
Yong Soo Park ◽  
In-Beom Kim
2000 ◽  
Vol 17 (1) ◽  
pp. 1-9 ◽  
Author(s):  
DAVID V. POW ◽  
ANITA E. HENDRICKSON

Previous studies show that glycine transporter-1 (glyt-1) is a consistent membrane marker of adult retinal neurons that are likely to release glycine at their synaptic terminals (Pow, 1998; Vaney et al., 1998; Pow & Hendrickson, 1999). The current study investigated when glyt-1 immunoreactivity appeared in the postnatal rat retina, and whether all glycine-containing neurons also labelled for glyt-1. Ganglion cells, horizontal cells, and photoreceptors showed transient labelling. Many cells in the ganglion cell layer are immunoreactive for both glycine and glyt-1 at postnatal day (Pd) 1 but both are minimal by Pd5. Transient immunoreactivity for both glyt-1 and glycine was observed in presumptive horizontal cells between Pd5 and Pd10. At Pd1 many cells in the outer part of the retina which resembled immature photoreceptors were heavily labelled for glycine, but did not express glyt-1; these disappeared at older ages. These findings suggest diverse mechanisms and transient roles for glycine in the developing rat retina. In the adult rat retina, a subpopulation of amacrine cells are prominently immunoreactive for both glycine and glyt-1. These cells labelled for glycine at Pd1, but did not express significant levels of glyt-1 until Pd5. Processes from these amacrine cells did not reach the inner half of the inner plexiform layer until Pd10–14. Bipolar cells became glycine-IR between Pd10 and Pd14, but consistently lacked any glyt-1 immunoreactivity. This temporal pattern of labelling strongly indicates that bipolar cells label for glycine when gap junctions become functional between glycine/glyt-1 immunoreactive amacrine cells and cone bipolar cells.


1990 ◽  
Vol 5 (5) ◽  
pp. 441-452 ◽  
Author(s):  
Jens Nicolai Brink Larsen ◽  
Maurizio Bersani ◽  
James Olcese ◽  
Jens Juul Holst ◽  
Morten Møller

AbstractSpecific antisera, raised in rabbits, against somatostatin 1-14, somatostatin 1-28, the fragment 1-12 of somatostatin 1-28, and prosomatostatin 20-36 were used for immunohistochemistry and gel filtration of the rat retina.With all antisera, immunoreactive perikarya could be located in the inner nuclear and ganglion cell layers. In the inner nuclear layer, amacrine cells with processes extending predominantly into the first sublayer of the inner plexiform layer were observed. Some processes extended also to the ganglion cell layer. In addition, somatostatin-immunoreactive interplexiform cells were present in the inner nuclear layer.In the ganglion cell layer, perikarya were found located in the midperiphery and in the far periphery of the retina. The neurons located in the midperiphery of the retina possessed a round perikaryon from which processes could be followed going into the inner plexiform layer, where they dichotomized in the third and first sublayers. The perikarya in the far periphery of the retina near the ora serrata exhibited an ovoid-shaped cell body from which processes extended horizontally in a bipolar manner in the layer itself.By use of an [35S]-labeled antisense oligonucleotide probe, in situ hybridization of the rat retina showed the presence of perikarya in the inner nuclear layer and ganglion cell layer containing mRNA encoding for prosomatostatin.Gel filtration of the retinal extracts followed by radioimmunoassay showed the presence of somatostatin 1-14, the fragment 1-12 of somatostatin 1-28, and prosomatostatin 1-64. However, somatostatin 1-28 was not detected.The results obtained in this study verify the presence of somatostatin 1-14 in the rat retina located in perikarya and processes in the inner nuclear and ganglion cell layers. The positive in-situ hybridization signals show that the intraneuronal somatostatin immunoreactivity is due to synthesis of the peptide and not uptake in the neurons. The presence of the somatostatin propeptide and fragments of this propeptide, in both intraretinal perikarya and fibers, indicate a posttranslational modification of this neuropeptide in the perikarya and the processes as well.


1991 ◽  
Vol 6 (4) ◽  
pp. 383-391 ◽  
Author(s):  
Danru Zhang ◽  
Hermes H. Yeh

AbstractThis study describes a phenomenon of transient expression of corticotropin releasing factor-like immunoreactivity (CRF-LI) in immature horizontal cells of the developing rat retina. These cells could be distinguished from those destined to become CRF-LI amacrine cells in the adult by their location within the outer portion of the neuroblastic layer (NBL) and by their ontogenetic pattern. Upon initial detection on postnatal day 3 (PD-3), faint CRF-LI cellular profiles were found in the outer portion of the NBL, limited to the central region of the retina. Subsequently, on PD-5, these profiles began to appear in the periphery, forming a single horizontal row along the outermost aspect of the developing inner nuclear layer (INL), concomitant with the establishment of the outer plexiform layer (OPL). The results of our birth-dating study combining immunohistochemistry and [3H]-thymidine autoradiography indicated that these cells were generated between embryonic day 14 and 18. These findings are consistent with them being horizontal cells. Between PD-7 and PD-9, CRF-LI in horizontal cells began to diminish progressively following a center-to-periphery gradient such that only sporadic, faintly immunoreactive patches of cells could be seen by the time of eye opening (PD-15). Around PD-19, it declined to levels below immunohistochemical detection. However, when rats were reared in complete darkness beginning at birth until PD-21, the period of CRF-LI expression in horizontal cells was prolonged and persisted throughout the first three postnatal weeks of development.


2000 ◽  
Vol 861 (2) ◽  
pp. 399-407 ◽  
Author(s):  
Toru Nakazawa ◽  
Itsuko Nakano ◽  
Tatsuo Furuyama ◽  
Hiroshi Morii ◽  
Makoto Tamai ◽  
...  

2000 ◽  
Vol 17 (3) ◽  
pp. 484-484 ◽  
Author(s):  
DAVID V. POW ◽  
ANITA E. HENDRICKSON

Due to technical difficulties that have since been rectified, the photomicrographs in this article did not reproduce at the best resolution possible. Also, Figure 12 has been revised and a corrected version of the article is reproduced on pp. 1R–9R, which follows. Cambridge University Press regrets any inconvenience that this inadvertent error may have caused.


Author(s):  
In-Beom Kim ◽  
Eun-Jin Lee ◽  
Mun-Kyu Kim ◽  
Dae-Kyoon Park ◽  
Myung-Hoon Chun

2002 ◽  
Vol 34 (2) ◽  
pp. 63-69
Author(s):  
Fumiyuki Uehara ◽  
Norio Ohba ◽  
Masayuki Ozawa

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