Glutamate hyperpolarizes retinal depolarizing bipolar cells (DBCs) by decreasing a non-specific cation conductance. We have investigated this action of glutamate using whole-cell voltage clamp of DBCs in larval tiger salamander retinal slices and here report two observations: a wash-out of the glutamate response and a concomitant decrease in resting membrane conductance. The wash-out may be due to the loss of a second messenger-mediated mechanism linking the receptor to the response. The decrease in resting membrane conductance suggests that this second messenger may be required to maintain DBC glutamate channels in an open state in the absence of the receptor ligand.
- 2-Amino-4-phosphonobutyrate receptor
- Bipolar cell
- Retinal slice
- Second messenger
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