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The Journal of Neurophysiology Vol. 81 No. 6 June 1999, pp. 2923-2936
Copyright ©1999 by the American Physiological Society
Department of Anatomy and Cell Biology, University of Bergen, N-5009 Bergen, Norway
Hartveit, Espen
Reciprocal Synaptic Interactions Between Rod Bipolar Cells and
Amacrine Cells in the Rat Retina. J. Neurophysiol. 81: 2923-2936, 1999.
Reciprocal synaptic interactions between rod bipolar cells and amacrine
cells in the rat retina. Reciprocal synaptic transmission between rod bipolar cells and presumed A17 amacrine cells was studied
by whole cell voltage-clamp recording of rod bipolar cells in a rat
retinal slice preparation. Depolarization of a rod bipolar cell evoked
two identifiable types of Ca2+ current, a T-type current
that activated at about
70 mV and a current with L-type pharmacology
that activated at about
50 mV. Depolarization to greater than
or equal to
50 mV also evoked an increase in the frequency of
postsynaptic currents (PSCs). The PSCs reversed at
~ECl (the chloride equilibrium potential), followed changes in ECl, and were blocked by
-aminobutyric acidA (GABAA) and
GABAC receptor antagonists and thus were identified as
GABAergic inhibitory PSCs (IPSCs). Bipolar cells with cut axons displayed the T-type current but lacked an L-type current and depolarization-evoked IPSCs. Thus L-type Ca2+ channels are
placed strategically at the axon terminals to mediate transmitter
release from rod bipolar cells. The IPSCs were blocked by the
non-N-methyl-D-aspartate (non-NMDA) receptor
antagonist 6-cyano-7-nitroquinoxaline-2,3-dione, indicating that
non-NMDA receptors mediate the feed-forward bipolar-to-amacrine
excitation. The NMDA receptor antagonist
3-((RS)-2-carboxypiperazin-4-yl)-propyl-1-phosphonic acid had no
consistent effect on the depolarization-evoked IPSCs, indicating that
activation of NMDA receptors is not essential for the feedforward
excitation. Tetrodotoxin (a blocker of voltage-gated Na+
channels) reversibly suppressed the reciprocal response in some cells
but not in others, indicating that graded potentials are sufficient for
transmitter release from A17 amacrine cells, but suggesting that
voltage-gated Na+ channels, under some conditions, can
contribute to transmitter release.
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