PMID- 14977334 OWN - NLM STAT- MEDLINE DCOM- 20040329 LR - 20190917 IS - 0952-5238 (Print) IS - 0952-5238 (Linking) VI - 20 IP - 5 DP - 2003 Sep-Oct TI - Activation of glutamate transporters in rods inhibits presynaptic calcium currents. PG - 557-66 AB - We found that L-glutamate (L-Glu) inhibits L-type Ca2+ currents (ICa) in rod photoreceptors. This inhibition was studied in isolated rods or rods in retinal slices from tiger salamander using perforated patch whole cell recordings and Cl(-)-imaging techniques. Application of L-Glu inhibited ICa by approximately 20% at 0.1 mM and approximately 35% at 1 mM. L-Glu also produced an inward current that reversed around ECl. The metabotropic glutamate receptor (mGluR) agonists t-ADA (Group I), DCG-IV (Group II), and L-AP4 (Group III) had no effect on ICa. However, the glutamate transport inhibitor, TBOA (0.1 mM), prevented L-Glu from inhibiting ICa. D-aspartate (D-Asp), a glutamate transporter substrate, also inhibited ICa with significantly more inhibition at 1 mM than 0.1 mM. Using Cl imaging, L-Glu (0.1-1 mM) and D-Asp (0.1-1 mM) were found to stimulate a Cl- efflux from terminals of isolated rods whereas the ionotropic glutamate receptor agonists NMDA, AMPA, and kainate and the mGluR agonist, 1S,3R-ACPD, did not. Glutamate-evoked Cl- effluxes were blocked by the glutamate transport inhibitors TBOA and DHKA. Cl- efflux inhibits Ca2+ channel activity in rod terminals (Thoreson et al. (2000), Visual Neuroscience 17, 197). Consistent with the possibility that glutamate-evoked Cl- efflux may play a role in the inhibition, reducing intraterminal Cl- prevented L-Glu from inhibiting ICa. In summary, the results indicate that activation of glutamate transporters inhibits ICa in rods possibly as a consequence of Cl- efflux. The neurotransmitter L-Glu released from rod terminals might thus provide a negative feedback signal to inhibit further L-Glu release. FAU - Rabl, Katalin AU - Rabl K AD - Department of Ophthalmology, University of Nebraska Medical Center, Omaha 68198-5540, USA. FAU - Bryson, Eric J AU - Bryson EJ FAU - Thoreson, Wallace B AU - Thoreson WB LA - eng GR - R01 EY010542/EY/NEI NIH HHS/United States GR - R01 EY010542-08/EY/NEI NIH HHS/United States GR - EY-10542/EY/NEI NIH HHS/United States PT - Comparative Study PT - Journal Article PT - Research Support, Non-U.S. Gov't PT - Research Support, U.S. Gov't, P.H.S. PL - England TA - Vis Neurosci JT - Visual neuroscience JID - 8809466 RN - 0 (2-amino-4-phosphono-propinate) RN - 0 (Amino Acid Transport System X-AG) RN - 0 (Anticonvulsants) RN - 0 (Calcium Channels) RN - 0 (Cyclopropanes) RN - 0 (Propionates) RN - 0 (benzyloxyaspartate) RN - 127310-57-0 (azetidine-2,4-dicarboxylic acid) RN - 147782-19-2 (2-(2,3-dicarboxycyclopropyl)glycine) RN - 30KYC7MIAI (Aspartic Acid) RN - 3KX376GY7L (Glutamic Acid) RN - 4SR0Q8YD1X (D-Aspartic Acid) RN - 52497-36-6 (dihydrokainic acid) RN - 5GZ3E0L9ZU (Azetidinecarboxylic Acid) RN - SIV03811UC (Kainic Acid) RN - SY7Q814VUP (Calcium) RN - TE7660XO1C (Glycine) SB - IM MH - Amino Acid Transport System X-AG/antagonists & inhibitors/*metabolism MH - Animals MH - Anticonvulsants/pharmacology MH - Aspartic Acid/pharmacology MH - Azetidinecarboxylic Acid/*analogs & derivatives/pharmacology MH - Calcium/*metabolism MH - Calcium Channels/drug effects MH - Calcium Signaling/drug effects/*physiology MH - Cells, Cultured MH - Cyclopropanes/pharmacology MH - D-Aspartic Acid/pharmacology MH - Dose-Response Relationship, Drug MH - Drug Interactions MH - Glutamic Acid/pharmacology MH - Glycine/*analogs & derivatives/pharmacology MH - In Vitro Techniques MH - Kainic Acid/*analogs & derivatives/pharmacology MH - Membrane Potentials/drug effects MH - Neural Conduction/drug effects MH - Neural Inhibition/drug effects MH - Patch-Clamp Techniques MH - Presynaptic Terminals/*drug effects MH - Propionates/pharmacology MH - Retinal Rod Photoreceptor Cells/*drug effects/metabolism MH - Urodela EDAT- 2004/02/24 05:00 MHDA- 2004/03/30 05:00 CRDT- 2004/02/24 05:00 PHST- 2004/02/24 05:00 [pubmed] PHST- 2004/03/30 05:00 [medline] PHST- 2004/02/24 05:00 [entrez] AID - S0952523803205095 [pii] AID - 10.1017/s0952523803205095 [doi] PST - ppublish SO - Vis Neurosci. 2003 Sep-Oct;20(5):557-66. doi: 10.1017/s0952523803205095.