![]() ![]() 1995 a) and goldfish bipolar cells ( Palmer et al. Thanks to this neurotransmitter-gated conductance, glutamate transporters act as a presynaptic receptor enabling the cell to measure its own glutamate release in salamander cone photoreceptors ( Picaud et al. 2005) as well as at an invertebrate neuromuscular junction ( Dudel & Schramm, 2003) and in mammalian cerebellar Purkinje cells ( Otis et al. 1995 b) and subsequently reported in salamander rod photoreceptors ( Grant & Werblin, 1996), teleost retinal bipolar cells ( Grant & Dowling, 1995, 1996 Palmer et al. 1988 Tachibana & Kaneko, 1988 Eliasof & Werblin, 1993 Picaud et al. Such a Cl − conductance with the pharmacological characteristics of glutamate transporters was first demonstrated in salamander and turtle cone photoreceptors ( Sarantis et al. 1997), which both have a large Cl − conductance gated by Na + and glutamate. This is particularly relevant for the glutamate transporters EAAT4 ( Fairman et al. ![]() Second, transporters can behave as neurotransmitter-gated ionic channels (reviewed in Sonders & Amara, 1996). Depending on the transport stoichiometry, this usually generates a transport-associated current of small amplitude, but which still can have a direct influence on the cell excitability as recently shown for postsynaptic GAT-1 ( Bagley et al. First, neurotransmitter uptake is tightly coupled to the flux of ions. Transporters can also have roles beyond the control of the extracellular and intracellular neurotransmitter concentrations, by modulating neuronal activity through their electrogenic properties. Through their buffering and uptake capacities, neurotransmitter transporters help shape synaptic events, especially when release levels are high, and limit neurotransmitter spill-over between neighbouring synapses. This feedback mechanism could control glutamate release at the ribbon synapses of a non-spiking neuron and increase the temporal contrast in the rod photoreceptor pathway. These results indicate that EAAT5 acts as a major inhibitory presynaptic receptor at mammalian rod bipolar cell axon terminals. In conditions for which reciprocal inhibition could be monitored, the charge carried by the EAAT5 current was 1.5 times larger than the one carried by the inhibitory postsynaptic currents received from amacrine cells. For 2 ms depolarizations evoking maximal responses, the EAAT5-mediated current carried between 2 and 8 times more charge as an average inhibitory GABA or glycine postsynaptic current received spontaneously from amacrine cells, with 10 m m or 0.5 m m intracellular EGTA, respectively. Its kinetics indicated that EAAT5 was located close to the glutamate release site. Furthermore, short depolarizations of the bipolar cells evoked a dl-tBOA and Cd 2+-sensitive current whose amplitude was comparable to the glutamate-evoked current. ![]() In these later cells, application of glutamate on the axon terminal evoked a current that reversed at E Cl, was insensitive to bicuculline, TPMPA, strychnine, dl-AP5, CNQX and MCPG, but blocked by the glutamate transporter inhibitor dl-tBOA. In the mouse retina, we located EAAT5 in both cone and rod photoreceptor terminals and in axon terminals of rod bipolar cells. This conductance is particularly large in the retina-specific EAAT5 isoform. In addition, excitatory amino acid transporters (EAAT) have a Cl − conductance which is gated by the joint binding of Na + and glutamate, but thermodynamically uncoupled to the flux of glutamate. ![]() Membrane neurotransmitter transporters control the concentration of their substrate in the synaptic clefts, through the thermodynamic coupling of uptake to the movement of Na + and other ions. ![]()
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