| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH |
|
|
|
|||||||
|
|||||||||
| ||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
Received July 29, 2006
Revised September 4, 2006
Accepted after revision September 4, 2006
1 INSERM U592, H&ocirpital St-Antoine et Université Pierre et Marie Curie-Paris6, Paris, France
2 IGBMC, 1 rue Laurent Fries, BP10142, 67404 Illkirch, France
3 Discipline of Anatomy, School of Biomedical Sciences, University of Newcastle, NSW 2308, Australia
* To whom correspondence should be addressed. E-mail: mjroux{at}igbmc.u-strasbg.fr.
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. 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. This conductance is particularly large in the retina-specific EAAT5 isoform. In the mouse retina, we located EAAT5 in both cone and rod photoreceptor terminals and in axon terminals of rod bipolar cells. In these later cells, application of glutamate on the axon terminal evoked a current that reversed at ECl, was insensitive to bicuculline, TPMPA, strychnine, DL-AP5, CNQX and MCPG, but blocked by the glutamate transporter inhibitor DL-tBOA. Furthermore, short depolarizations of the bipolar cells evoked a DL-tBOA and Cd2+ sensitive current which amplitude was comparable to the glutamate-evoked current. Its kinetics indicated that EAAT5 was located close to the glutamate release site. For 2 ms depolarizations evoking maximal responses, the EAAT5-mediated current carried between twice and 8 times more charge as an average inhibitory GABA or glycine postsynaptic current received spontaneously from amacrine cells, with 10 mM or 0.5 mM intracellular EGTA, respectively. In conditions for which reciprocal inhibition could be monitored, the charge carried by the EAAT5 current was 1.5-time larger than the one carried by the inhibitory postsynaptic currents received from amacrine cells. These results indicate that EAAT5 acts as a major inhibitory presynaptic receptor at mammalian rod bipolar cell axon terminals. 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.
This article has been cited by other articles:
|
|
 |
|
  G. P. Leary, E. F. Stone, D. C. Holley, and M. P. Kavanaugh The Glutamate and Chloride Permeation Pathways Are Colocalized in Individual Neuronal Glutamate Transporter Subunits J. Neurosci., March 14, 2007; 27(11): 2938 - 2942. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
H. P. Koch, R. Lane Brown, and H. P. Larsson The Glutamate-Activated Anion Conductance in Excitatory Amino Acid Transporters Is Gated Independently by the Individual Subunits J. Neurosci., March 14, 2007; 27(11): 2943 - 2947. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 L. Oltedal, S. H. Morkve, M. L. Veruki, and E. Hartveit Patch-Clamp Investigations and Compartmental Modeling of Rod Bipolar Axon Terminals in an In Vitro Thin-Slice Preparation of the Mammalian Retina J Neurophysiol, February 1, 2007; 97(2): 1171 - 1187. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
D.-Q. Zhang, T.-R. Zhou, and D. G. McMahon Functional Heterogeneity of Retinal Dopaminergic Neurons Underlying Their Multiple Roles in Vision J. Neurosci., January 17, 2007; 27(3): 692 - 699. [Abstract] [Full Text] [PDF]
|
|
| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH |
