May 2007
Volume 48, Issue 13
ARVO Annual Meeting Abstract  |   May 2007
Dendritic ‘Hotspots’ of Visually-Evoked Ca2+ Signaling in Starburst Amacrine Cells
Author Affiliations & Notes
  • X. Castell
    Biomedical Optics, Max Planck Institute for Medical Research, Heidelberg, Germany
  • W. Denk
    Biomedical Optics, Max Planck Institute for Medical Research, Heidelberg, Germany
  • T. Euler
    Biomedical Optics, Max Planck Institute for Medical Research, Heidelberg, Germany
  • Footnotes
    Commercial Relationships X. Castell, None; W. Denk, None; T. Euler, None.
  • Footnotes
    Support the MPG and the DFG (EU 42/3-1)
Investigative Ophthalmology & Visual Science May 2007, Vol.48, 5965. doi:
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      X. Castell, W. Denk, T. Euler; Dendritic ‘Hotspots’ of Visually-Evoked Ca2+ Signaling in Starburst Amacrine Cells. Invest. Ophthalmol. Vis. Sci. 2007;48(13):5965.

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      © ARVO (1962-2015); The Authors (2016-present)

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Purpose:: Forty years after the discovery of retinal direction selectivity (DS) the underlying biophysical mechanisms are still not fully understood. As synaptic input to retinal DS ganglion cells (DSGC) is directionally-tuned, motion direction must be presynaptically computed, likely in starburst amacrine cells (SAC), which generate DS Ca2+ signals in their dendrites (Euler et al., 2002, Nature 418:845-852). In these experiments SACs were filled with Ca2+ indicator using sharp microelectrodes. However, during patch-clamp experiments in many cases visually-evoked Ca2+ signals vanished but not DS electrical responses (Hausselt et al., 2004, SfN #299.4). After removal of the patch electrode visually-evoked Ca2+ signals often recover. This suggests the involvement of a dialysis-sensitive signaling mechanism as Ca2+ release from internal stores, which have been shown to participate in transmitter release from cultured retinal amacrine cells (Warrier et al., 2005, J Neurophysiol 94:4196-4208).We aim at determining the distribution of visually-evoked Ca2+ signals along SACs dendritic branches and whether internal Ca2+ stores are involved.

Methods:: Displaced (ON) SACs in whole-mounted rabbit retina were briefly filled with Ca2+ indicator via microelectrodes, which then were retracted. Dendritic Ca2+ responses to visual stimuli were recorded using 2-photon imaging. Inhibitors were applied with the perfusion medium or locally via pipettes.

Results:: The strongest Ca2+ responses were localized to varicosities on the SAC distal dendrites(consistent with earlier observations), which correspond to the output region. The Ca2+ signal distribution was heterogeneous: some branchlets (‘hotspots’) responded strongly to the stimuli, while neighboring ones stayed silent. Moreover, some hotspots were DS while neighboring ones were not. In hotspots Ca2+ signals could be observed during the entire recording time (more than 3 hours). Application of a combination of intracellular-Ca2+-signaling-pathways inhibitors (cyclopiazonic acid, 2-APB, and Ryanodine, inhibiting SERCA pumps, IP3- and Ryanodine-receptors respectively) strongly reduced or abolished visually evoked Ca2+ signals.

Conclusions:: Our pharmacological data suggest the involvement of internal Ca2+- stores in the generation of visually-evoked Ca2+ responses in SACs possibly via a Ca2+-induced-Ca2+-release mechanism. Internal Ca2+- stores could support a functional compartmentalization of dendritic Ca2+ signals; this compartmentalization may be reflected by the Ca2+ activity ‘hotspots’ we observed in SAC dendrites.

Keywords: imaging/image analysis: non-clinical • amacrine cells • calcium 

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