Skip Navigation

Integrative and Comparative Biology 2005 45(4):658-664; doi:10.1093/icb/45.4.658
This Article
Right arrow Full Text Freely available
Right arrow FREE Full Text (PDF) Freely available
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Services
Right arrow Email this article to a friend
Right arrow Similar articles in this journal
Right arrow Similar articles in ISI Web of Science
Right arrow Alert me to new issues of the journal
Right arrow Add to My Personal Archive
Right arrow Download to citation manager
Right arrow Request Permissions
Google Scholar
Right arrow Articles by Hoffpauir, B. K.
Right arrow Articles by Gleason, E. L.
Right arrow Search for Related Content
Social Bookmarking
 Add to CiteULike   Add to Connotea   Add to Del.icio.us  
What's this?

The Society for Integrative and Comparative Biology

Modulation of Synaptic Function in Retinal Amacrine Cells1

Brian K. Hoffpauir2,1 and Evanna L. Gleason3,1
1 Department of Biological Sciences, Louisiana State University, Baton Rouge, Louisiana 70803

Amacrine cells are interneurons that have diverse functions in retinal signal processing. In order to study signaling and modulation in retinal amacrine cells, we employ a simplified culture system containing identifiable GABAergic amacrine cells. Immunocytochemistry experiments indicate that GABAergic amacrine cells express metabotropic glutamate receptor 5 (mGluR5), a group I mGluR usually linked to the IP3 signaling pathway. Ca2+ imaging experiments using an mGluR5-specific agonist indicate that these receptors are functional and when activated, can stimulate temporally diverse Ca2+ elevations. To begin to establish the role of these receptors in modulating amacrine cell function, we have used electrophysiological methods to ask whether ion channels are the targets of mGluR5-dependent modulation. Here we discuss our results indicating that activation of mGluR5 leads to enhancement of currents through GABAA receptors. This enhancement is dependent upon elevations in cytosolic Ca2+ and activation of protein kinase C (PKC). To explore the consequences of Ca2+ elevations in another context, we have used nitric oxide (NO) donors to mimic the effects of activating the Ca2+-dependent synthetic enzyme for NO, neuronal nitric oxide synthase. We find that exposure to NO donors also enhances the amplitude of currents through GABAA receptors. Together, these results indicate that glutamate from presynaptic bipolar cells has the potential to work through multiple mechanisms to regulate the function of amacrine-to-amacrine cell GABAergic synapses.


Add to CiteULike CiteULike   Add to Connotea Connotea   Add to Del.icio.us Del.icio.us    What's this?




Disclaimer:
Please note that abstracts for content published before 1996 were created through digital scanning and may therefore not exactly replicate the text of the original print issues. All efforts have been made to ensure accuracy, but the Publisher will not be held responsible for any remaining inaccuracies. If you require any further clarification, please contact our Customer Services Department.