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.
The Journal of Physiology – Wiley
Published: Apr 1, 1992
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