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This Article Full Text Full Text (PDF) All Versions of this Article: 586/18/4385    most recent jphysiol.2008.159327v1 Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via HighWire Google Scholar Articles by McCall, M. A. Articles by Gregg, R. G. PubMed PubMed Citation Articles by McCall, M. A. Articles by Gregg, R. G. Related Collections Perspectives Neuroscience

Departments of
¹ Ophthalmology & Visual Sciences
² Biochemistry & Molecular Biology, University of Louisville, Louisville, KY 40202, USA

In the most simplistic view, the retinal circuit can be divided into vertical excitatory pathways that use glutamate as their neurotransmitter and lateral inhibitory pathways in the outer and inner synaptic layers that modulate excitation via glycine and GABA. Within the vertical excitatory pathways, the visual signal is initiated in the rod, cone or both photoreceptors, depending on the adaptation state of the retina. This signal is transmitted to the rest of the retina through the bipolar cells, which can be subdivided based on: the photoreceptor that provides their input, their dendritic and axonal morphology, and the polarity of their response evoked by a luminance increment, e.g. depolarizing or hyperpolarizing responses. The polarity of this response is controlled by the type of glutamatergic postsynaptic receptor that is expressed on their dendritic terminals. Hyperpolarizing bipolar cells express AMPA/kainate receptors, whereas depolarizing bipolar cells (DBCs) express the metabotropic glutamate receptor 6 (Grm6). The electroretinogram (ERG) is a non-invasive method used to assess overall retinal function. The initiation of the visual signal in the photoreceptors is reflected in the ERG a-wave and the ensuing depolarization of DBCs in the b-wave. When there is failure of signal transmission from photoreceptors to DBCs or signalling within DBCs, the ERG a-wave is present, while the b-wave is absent or significantly reduced. This ERG phenotype has been found in the human population and is referred to as congenital stationary night blindness. Until recently, it had been assumed that the absence of a b-wave was indicative of a lack of signalling through the On pathway, leaving the Off pathway unaffected. Here we review recent findings that demonstrate that many mouse mutants share a no b-wave ERG phenotype but their retinal morphology and RGC responses differ significantly, suggesting very different effects of the underlying mutations on output from the DBCs to the rest of the retinal circuit.

(Received 7 July 2008; accepted after revision 21 July 2008; first published online 24 July 2008)
Corresponding author M. A. McCall: University of Louisville, Psychological & Brain Sciences, Life Sciences Building, Belknap Campus, University of Louisville, Louisville, KY 40292, USA.  Email: mo.mccall{at}louisville.edu

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				Z. J. Zhou and M. A. McCall Retinal ganglion cells in model organisms: development, function and disease J. Physiol., September 15, 2008; 586(18): 4343 - 4345. [Full Text] [PDF]