title: Sodium channels in transient retinal bipolar cells enhance visual responses in ganglion cells.
abstract: Retinal bipolar cells are slow potential neurons that respond to photoreceptor inputs with graded potentials and do not fire action potentials. We found that transient ON bipolar cells recorded in retinal slices possess voltage-gated sodium channels located on either their dendrites or somas. The sodium currents in these neurons did not generate spikes but enhanced voltage responses evoked by visual stimulation, which selectively boosted transmission to transient ganglion cells. In contrast, sodium currents were not found in sustained ON bipolar cells, and light responses in sustained bipolar cells and ganglion cells were not affected by TTX. The presence of sodium channels in transient ON bipolar cells contributed to the separation of transient and sustained signals by selectively enhancing the responses of ON transient ganglion cells to light. Our results suggest that bipolar cell sodium channels augment transient signals and contribute to the temporal segregation of visual information.
authors.affiliation: Department of Ophthalmology and Visual Sciences, Washington University School of Medicine, St. Louis, Missouri 63110, USA.
authors.forename: Tomomi
authors.initials: T
authors.lastname: Ichinose
authors.forename: Colleen R
authors.initials: CR
authors.lastname: Shields
authors.forename: Peter D
authors.initials: PD
authors.lastname: Lukasiewicz
mesh_terms: D000557:Ambystoma / Q000254:growth & development; D000818:Animals; D002794:Choline / Q000494:pharmacology; D003712:Dendrites / Q000502:physiology; D007395:Interneurons / Q000502:physiology* / Q000648:ultrastructure; D015640:Ion Channel Gating; D007814:Larva; D008012:Lidocaine / Q000031:analogs & derivatives / Q000494:pharmacology; D018408:Patch-Clamp Techniques; D010775:Photic Stimulation; D020419:Photoreceptor Cells, Vertebrate / Q000502:physiology; D012165:Retinal Ganglion Cells / Q000502:physiology* / Q000648:ultrastructure; D012964:Sodium / Q000378:metabolism; D026941:Sodium Channel Blockers / Q000494:pharmacology; D015222:Sodium Channels / Q000187:drug effects / Q000502:physiology*; D013779:Tetrodotoxin / Q000494:pharmacology; D013997:Time Factors; D014795:Visual Pathways / Q000502:physiology*
chemical_list: D026941:Sodium Channel Blockers; D015222:Sodium Channels; C012647:QX-314; D013779:Tetrodotoxin; D008012:Lidocaine; D012964:Sodium; D002794:Choline
references.citation: Nat Neurosci. 1998 Dec;1(8):714-9
references.pmid: 10196588
references.citation: J Neurophysiol. 2000 Apr;83(4):1817-29
references.pmid: 10758094
references.citation: J Neurosci. 2000 Jun 15;20(12):4462-70
references.pmid: 10844015
references.citation: J Neurosci. 2000 Jun 15;20(12):4471-9
references.pmid: 10844016
references.citation: J Neurosci. 2000 Sep 15;20(18):7087-95
references.pmid: 10995856
references.citation: J Neurophysiol. 2000 Nov;84(5):2564-71
references.pmid: 11067998
references.citation: Nature. 2001 Mar 29;410(6828):583-7
references.pmid: 11279496
references.citation: J Neurosci. 2001 Jul 1;21(13):4543-50
references.pmid: 11425883
references.citation: J Neurosci. 2001 Jul 1;21(13):4852-63
references.pmid: 11425912
references.citation: J Neurophysiol. 2001 Oct;86(4):1671-84
references.pmid: 11600631
references.citation: J Neurosci. 2002 Apr 15;22(8):3285-92
references.pmid: 11943830
references.citation: Jpn J Pharmacol. 2002 Apr;88(4):365-77
references.pmid: 12046980
references.citation: Neuroscience. 2002;115(1):163-72
references.pmid: 12401331
references.citation: J Neurophysiol. 2003 May;89(5):2449-58
references.pmid: 12611993
references.citation: J Physiol. 1953 Apr 28;120(1-2):171-204
references.pmid: 13062231
references.citation: J Neurophysiol. 1985 Jan;53(1):153-70
references.pmid: 2579215
references.citation: J Neurophysiol. 1988 Sep;60(3):1122-42
references.pmid: 3171660
references.citation: J Neurosci. 1988 Dec;8(12):4470-81
references.pmid: 3199187
references.citation: Proc Natl Acad Sci U S A. 1986 Mar;83(5):1509-12
references.pmid: 3456599
references.citation: J Neurophysiol. 1969 May;32(3):339-55
references.pmid: 4306897
references.citation: J Gen Physiol. 1974 Jan;63(1):88-110
references.pmid: 4359065
references.citation: J Neurophysiol. 1978 Mar;41(2):472-83
references.pmid: 650277
references.citation: J Physiol. 1978 May;278:79-99
references.pmid: 671342
references.citation: Vision Res. 1982;22(2):257-60
references.pmid: 7101761
references.citation: Neuron. 1995 Nov;15(5):1065-76
references.pmid: 7576650
references.citation: Neurosci Lett. 1995 Apr 14;189(2):109-12
references.pmid: 7609913
references.citation: Pflugers Arch. 1993 Feb;422(5):481-91
references.pmid: 7682688
references.citation: Science. 1995 Apr 14;268(5208):301-4
references.pmid: 7716525
references.citation: J Neurosci. 1994 Jun;14(6):3852-61
references.pmid: 7911519
references.citation: J Neurophysiol. 1994 Jun;71(6):2562-5
references.pmid: 7931536
references.citation: Nature. 1994 Jan 6;367(6458):69-72
references.pmid: 8107777
references.citation: J Neurosci. 1994 Mar;14(3 Pt 1):1202-12
references.pmid: 8120620
references.citation: J Neurosci. 1993 Feb;13(2):660-73
references.pmid: 8381170
references.citation: J Physiol. 1977 Jan;264(3):767-85
references.pmid: 845823
references.citation: J Neurophysiol. 1995 Nov;74(5):2220-4
references.pmid: 8592214
references.citation: J Neurophysiol. 1997 Nov;78(5):2662-73
references.pmid: 9356416
references.citation: J Neurosci. 1998 Mar 15;18(6):2301-8
references.pmid: 9482814
references.citation: J Physiol. 1999 Jan 15;514 ( Pt 2):343-50
references.pmid: 9852318