May 2006
Volume 47, Issue 13
ARVO Annual Meeting Abstract  |   May 2006
Extrasynaptic Release of GABA by Retinal Dopaminergic Neurons
Author Affiliations & Notes
  • H. Hirasawa
    Neurobiology, Harvard Medical School, Boston, MA
  • M. Puopolo
    Neurobiology, Harvard Medical School, Boston, MA
  • E. Raviola
    Neurobiology, Harvard Medical School, Boston, MA
  • Footnotes
    Commercial Relationships  H. Hirasawa, None; M. Puopolo, None; E. Raviola, None.
  • Footnotes
    Support  NIH grant EY01344
Investigative Ophthalmology & Visual Science May 2006, Vol.47, 1509. doi:
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      H. Hirasawa, M. Puopolo, E. Raviola; Extrasynaptic Release of GABA by Retinal Dopaminergic Neurons . Invest. Ophthalmol. Vis. Sci. 2006;47(13):1509.

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

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Purpose: : In the vertebrate retina, a class of amacrine or interplexiform cells release dopamine over their entire surface. This modulator diffuses throughout the retina and causes many of the events that lead to neural adaptation to light. Dopaminergic amacrine (DA) cells also contain γ–aminobutyric acid (GABA) and its synthetic enzyme glutamic acid decarboxylase. Furthermore, postsynaptic GABAA receptors were observed at the site of the synapses between DA and A2 amacrine cells. Thus, it is possible that DA cells also release GABA as a second neurotransmitter in addition to dopamine. In this study we investigated the release of GABA by isolated bodies of DA cells.

Methods: : We carried out whole cell patch clamp recordings in DA cell bodies isolated from the retina of transgenic mice in which catecholaminergic neurons expressed human placental alkaline phosphatase on their membrane surface. Since immunocytochemistry showed that GABAA receptors were present over the entire surface of DA cell bodies, we monitored the events of GABA release by measuring the Clcurrent transients generated by the very same cell in response to the release of its own transmitter.

Results: : DA cell bodies exhibited at irregular intervals spontaneous inward current transients when the intracellular solution contained Ca2+ and high Cl. GABAA receptor antagonists (20µM SR 95531 or 100µM bicuculline) blocked the current events. Thus, DA cell bodies released GABA which in turn activated GABAA receptors at the cell surface. Depletion of vesicular transmitter contents by bafilomycin A1, a blocker of the vesicular proton pump, abolished the GABAergic current events. After recording in the current clamp mode the action potentials spontaneously generated by a DA cell, we used them as a voltage command to depolarize the isolated cell bodies. Depolarization by trains of action potential waveforms caused multiple GABAergic current events that were abolished by Cd2+.

Conclusions: : DA cell bodies release packets of GABA by exocytosis. This vesicular GABA release was triggered by voltage changes that cause Ca2+ influx through voltage–gated Ca2+ channels. Since DA cell bodies do not contain presynaptic active zones, GABA release was by necessity extrasynaptic.

Keywords: dopamine • inhibitory neurotransmitters • retina: proximal (bipolar, amacrine, and ganglion cells) 

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