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This Article Full Text Full Text (PDF) Supplemental Figures All Versions of this Article: 102/3/1945    most recent 00142.2009v1 Alert me when this article is cited Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in Web of Science Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Google Scholar Articles by Abd-El-Barr, M. M. Articles by Wu, S. M. PubMed PubMed Citation Articles by Abd-El-Barr, M. M. Articles by Wu, S. M.

Genetic Dissection of Rod and Cone Pathways in the Dark-Adapted Mouse Retina

¹Departments of Ophthalmology and ²Neuroscience, Baylor College of Medicine; ³College of Optometry, University of Houston, Houston; ⁴Department of Medical Education, Texas Tech University Health Sciences Center, El Paso, Texas; ⁵Casey Eye Institute, Oregon Health and Science University, Portland, Oregon; ⁶Department of Ophthalmology, Tufts University School of Medicine; and ⁷Department of Neurobiology, Harvard Medical School, Boston, Massachusetts

Submitted 17 February 2009; accepted in final form 2 July 2009

Abstract

A monumental task of the mammalian retina is to encode an enormous range (>10⁹-fold) of light intensities experienced by the animal in natural environments. Retinal neurons carry out this task by dividing labor into many parallel rod and cone synaptic pathways. Here we study the operational plan of various rod- and cone-mediated pathways by analyzing electroretinograms (ERGs), primarily b-wave responses, in dark-adapted wildtype, connexin36 knockout, depolarizing rod–bipolar cell (DBC_R) knockout, and rod transducin alpha-subunit knockout mice [WT, Cx36(–/–), Bhlhb4(–/–), and Tr(–/–)]. To provide additional insight into the cellular origins of various components of the ERG, we compared dark-adapted ERG responses with response dynamic ranges of individual retinal cells recorded with patch electrodes from dark-adapted mouse retinas published from other studies. Our results suggest that the connexin36-mediated rod–cone coupling is weak when light stimulation is weak and becomes stronger as light stimulation increases in strength and that rod signals may be transmitted to some DBC_Cs via direct chemical synapses. Moreover, our analysis indicates that DBC_R responses contribute about 80% of the overall DBC response to scotopic light and that rod and cone signals contribute almost equally to the overall DBC responses when stimuli are strong enough to saturate the rod bipolar cell response. Furthermore, our study demonstrates that analysis of ERG b-wave of dark-adapted, pathway-specific mutants can be used as an in vivo tool for dissecting rod and cone synaptic pathways and for studying the functions of pathway-specific gene products in the retina.