May 2006
Volume 47, Issue 13
ARVO Annual Meeting Abstract  |   May 2006
Enhancing Distal Synapses by Glycinergic Interplexiform Cells
Author Affiliations & Notes
  • W. Shen
    Department of Biomedical Science, Florida Atlantic University, Boca Raton, FL
  • B. Li
    Department of Biomedical Science, Florida Atlantic University, Boca Raton, FL
  • Footnotes
    Commercial Relationships  W. Shen, None; B. Li, None.
  • Footnotes
    Support  NIH grant EY14161
Investigative Ophthalmology & Visual Science May 2006, Vol.47, 2309. doi:
  • Views
  • Share
  • Tools
    • Alerts
      This feature is available to authenticated users only.
      Sign In or Create an Account ×
    • Get Citation

      W. Shen, B. Li; Enhancing Distal Synapses by Glycinergic Interplexiform Cells . Invest. Ophthalmol. Vis. Sci. 2006;47(13):2309.

      Download citation file:

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

  • Supplements

Purpose: : We studied the effect of glycinergic interplexiform cells (IPCs) in the distal synapse from photoreceptors to horizontal cells (HCs). It has been known that glutamate depolarizes HCs resulting in a GABA release that contributes to a center–surrounding organization in the distal retina. The glycine feedback input from IPCs is pronounced in the distal retina. The function of glycine in the distal spatial sensitivity is largely unknown yet.

Methods: : Combined techniques of whole cell patch clamp recording and immunofluorescence labeling were used to investigate the function and localization of glycine input in the distal retina. The experiments were performed on tiger salamander retina. HCs were voltage clamped at the dark membrane potential and stimulated by a central spot (250nm) and a full–field light stimulus in dark–adapted retinal slices.

Results: : Applications of 10µM glycine depolarized HCs and increased the light response. These effects could be blocked by CNQX, a glutamate receptor inhibitor. 200µM glycine largely depolarized HCs, but shunted light response, which was insensitive to CNQX. These indicate that glycine positively controls glutamate and GABA releases in the distal retina. Immunoantibody labeling results indicate that HCs and photoreceptor terminals express a high level of NKCC, a transporter uptake chloride. This could be a key factor that glycine causes a chloride efflux and depolarizes these neurons. We also find that 10µM glycine preferentially increased a full field light response in HCs, but not a spot light stimulus. SR95531, a GABAA receptor inhibitor, partially reversed the effect of glycine, suggesting that glycine input promoted GABA activation between HCs. A distribution pattern of glycinergic IPCs, a glycine input source, in the OPL was identified by antibody staining of glycine transporter II (GlyT2). The double–labeling experiments indicate that glycinergic IPCs directly contact to photoreceptor terminals and HC’s processes.

Conclusions: : Glycine not only directly depolarizes HCs, but also increases glutamate release. Both effects are highly related a high ECl in the local neurons. Also glycine input increases spatial sensitivity in HCs. This effect could be a network caused by the enhancement of interaction between HCs.

Keywords: signal transduction • receptors: pharmacology/physiology • retinal connections, networks, circuitry 

This PDF is available to Subscribers Only

Sign in or purchase a subscription to access this content. ×

You must be signed into an individual account to use this feature.