Coupling from aII amacrine cells to ON cone bipolar cells is bidirectional

Citation
Eb. Trexler et al., Coupling from aII amacrine cells to ON cone bipolar cells is bidirectional, J COMP NEUR, 437(4), 2001, pp. 408-422
Citations number
32
Categorie Soggetti
Neurosciences & Behavoir
Journal title
JOURNAL OF COMPARATIVE NEUROLOGY
ISSN journal
00219967 → ACNP
Volume
437
Issue
4
Year of publication
2001
Pages
408 - 422
Database
ISI
SICI code
0021-9967(20010903)437:4<408:CFAACT>2.0.ZU;2-5
Abstract
The All amacrine cell is a critical interneuron in the rod pathway of the m ammalian retina. Rod signals pass into cone pathways by means of gap juncti ons between All amacrine cells and ON cone bipolar cells. Filling All amacr ine cells with Neurobiotin produces labeling of cone bipolar cells by means of these gap junctions. However, tracer injections into bipolar cells do n ot produce labeling of the All network (Vaney [1997] Invest Ophthalmol Vis Sci. 38:267-273), which suggests that the AII/bipolar gap junctions allow t he passage of tracer in only one direction. This mechanism stands in contra st to physiological results, which indicate that light adapted signals can pass from ON cone bipolar cells into the All network (Xin and Bloomfield [1 999] Vis Neurosci. 16:653-665). Here, we report that a variety of ON and OF F bipolar cells are sometimes anomalously coupled to the A-type horizontal cell network. These relatively rare examples do not result from dye injecti on errors, but seem to represent minor developmental errors. However, this provides a method to obtain Neurobiotin-filled cone bipolar cells without t he necessity of impaling them with a microelectrode. Under these conditions , Neurobiotin spreads from ON cone bipolar cells into neighboring All amacr ine cells. The dye-coupled All amacrine cells, positively identified by dou ble labeling with an antibody against calretinin, were centered around anom alously coupled ON bipolar culls. These results indicate that AII/bipolar c ell gap junctions allow tracer coupling in both directions, consistent with previous physiological results. The previous failure to detect the passage of neuronal tracer from injected bipolar cells to All amacrine cells may r eflect electrode damage or perhaps the asymmetrical voltage sensitivity of a heterotypic gap junction. J. Comp. Neurol. 437:408-422, 2001. (C) 2001 Wi ley-Liss, Inc.