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R. Farajian, S. A. Bloomfield; Synaptic Mechanisms Responsible for Masking ON Signals in OFF Alpha Ganglion Cells. Invest. Ophthalmol. Vis. Sci. 2009;50(13):4556.
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© ARVO (1962-2015); The Authors (2016-present)
To study the synaptic mechanisms responsible for masking the ON visual signals received by OFF alpha ganglion cells in the rabbit retina.
OFF alpha ganglion cells were visualized with the vital dye Azure B under IR transcleral illumination of a flattened, retina-eyecup preparation of the albino rabbit. OFF alpha cells were selectively targeted and their light-evoked responses were recorded with extracellular and intracellular microelectrodes. OFF alpha cells were subsequently labeled with Neurobiotin for morphological identification.
As we have previously reported, application of 100 µM picrotoxin unmasks a transient, short-latency ON response in OFF alpha ganglion cells. Application of L-AP4 (100 µM) reversibly blocked the unmasked ON response, indicating that it is generated by the ON pathway. Simultaneous application of the GABAA receptor blocker SR-95531 (20 µM) and the GABAC receptor blocker TPMPA (100 µM) unmasked the ON response, although each drug alone did not. Neither the GABAB receptor antagonist CGP-55845 (50 µM), nor the GABAB receptor agonist baclofen (100 µM) were able to unmask the ON response. Likewise, strychnine (1 µM) did not unmask the ON response, indicating that glycinergic inhibition does not play a role. Blockade of gap junctions with MFA (100 µM) or 18β-glycyrrhetinic acid (25 µM) eliminated the unmasked ON response, suggesting that it is received via the gap junctions OFF alpha cells make with neighboring wide-field amacrine cells. To further define the synaptic mechanisms responsible for masking the ON response, we blocked postsynaptic inhibition in OFF alpha cells by intracellular injection of the chloride channel blocker DNDS (500 µM). While DNDS increased the background firing of alpha cells, it did not unmask the ON response. Co-administration of TPMPA with DNDS also did not unmask the ON response, indicating that the postsynaptic activation of GABAA receptors on OFF alpha cells was not involved in the masking process.
Our results indicate that OFF alpha cells receive ON signals via gap junctions made with neighboring amacrine cells. However, the ON response is suppressed by GABAergic inhibition under normal recording conditions. Both GABAA and GABAC, but not GABAB, receptors are activated during the suppression of the ON response. Our results indicate that presynaptic inhibition of bipolar and/or amacrine cells is responsible for masking the ON response, whereas direct inhibition of OFF alpha cells does not play a role.
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