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J Physiol. 1992 Apr;449:589-606.

Two types of glutamate receptors differentially excite amacrine cells in the tiger salamander retina.

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Department of Ophthalmology, University of California, San Francisco 94143-0730.


1. Excitatory inputs to amacrine cells in the salamander retinal slice preparation were examined using whole-cell patch pipette voltage-clamp techniques. In strychnine (500 nM) and bicuculline (100 microM), two types of amacrine cell were easily distinguished by their light-evoked excitatory responses: transient and sustained. 2. In transient amacrine cells the current-voltage (I-V) relation for the peak light-evoked current was non-linear with a negative slope region between -50 and -70 mV. Responses reversed near +10 mV and were prolonged at more positive holding potentials. 3. In DL-2-amino-phosphonoheptanoate (AP7, 30 microM), a selective N-methyl-D-aspartate (NMDA) receptor antagonist, both the negatively sloped region of the light I-V relation and the prolongation of the response at positive potentials were eliminated. In 6-cyano-7-nitroquinoxaline-2,3-dione (CNQX, 2 microM), a selective non-NMDA receptor antagonist, light-evoked currents at the most hyperpolarized holding potentials were eliminated. At potentials positive to -85 mV the light-evoked currents lacked a fast onset. The light I-V relation in CNQX had a negative slope region between -35 and -80 mV. 4. With synaptic transmission blocked, kainate evoked responses in transient cells with a resultant I-V relation that was nearly linear, whereas glutamate and NMDA elicited responses with non-linear I-V relations. 5. Light-evoked currents in sustained amacrine cells had a nearly linear I-V relation and reversed near +10 mV. AP7 at a concentration of 30 microM did not affect the light-evoked currents in sustained cells, but 2 microM-CNQX eliminated all light-evoked currents in these cells. 6. With synaptic transmission blocked, sustained amacrine cells responded only to glutamate and kainate, not NMDA. The resultant I-V relations were linear. 7. We conclude that the light-evoked responses of transient amacrine cells are mediated by concomitant activation of both non-NMDA and NMDA receptors whereas the responses of sustained amacrine cells are mediated only by non-NMDA receptors. Furthermore, these data provide supportive evidence that the primary light-evoked excitatory neurotransmitter activating amacrine cells is glutamate.

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