title: Glial glutamate transporter 1 regulates the spatial and temporal coding of glutamatergic synaptic transmission in spinal lamina II neurons.
abstract: Glutamatergic synaptic transmission is a dynamic process determined by the amount of glutamate released by presynaptic sites, the clearance of glutamate in the synaptic cleft, and the properties of postsynaptic glutamate receptors. Clearance of glutamate in the synaptic cleft depends on passive diffusion and active uptake by glutamate transporters. In this study, we examined the role of glial glutamate transporter 1 (GLT-1) in spinal sensory processing. Excitatory postsynaptic currents (EPSCs) of substantia gelatinosa neurons recorded from spinal slices of young adult rats were analyzed before and after GLT-1 was pharmacologically blocked by dihydrokainic acid. Inhibition of GLT-1 prolonged the EPSC duration and the EPSC decay phase. The EPSC amplitudes were increased in neurons with weak synaptic input but decreased in neurons with strong synaptic input upon inhibition of GLT-1. We suggest that presynaptic inhibition, desensitization of postsynaptic AMPA receptors, and glutamate "spillover" contributed to the kinetic change of EPSCs induced by the blockade of GLT-1. Thus, GLT-1 is a key component in maintaining the spatial and temporal coding in signal transmission at the glutamatergic synapse in substantia gelatinosa neurons.
authors.affiliation: Department of Anesthesiology and Pain Medicine, The University of Texas M. D. Anderson Cancer Center, 1400 Holcombe Boulevard, Unit 42, Houston, TX 77030-4009, USA. hrweng@mdanderson.org
authors.forename: H-R
authors.initials: HR
authors.lastname: Weng
authors.forename: J H
authors.initials: JH
authors.lastname: Chen
authors.forename: Z Z
authors.initials: ZZ
authors.lastname: Pan
authors.forename: H
authors.initials: H
authors.lastname: Nie
mesh_terms: D000818:Animals; D001581:Benzothiadiazines / Q000494:pharmacology; D004307:Dose-Response Relationship, Radiation; D004347:Drug Interactions; D004558:Electric Stimulation; D004791:Enzyme Inhibitors / Q000494:pharmacology; D027342:Excitatory Amino Acid Transporter 2 / Q000502:physiology*; D019706:Excitatory Postsynaptic Potentials / Q000187:drug effects / Q000502:physiology / Q000528:radiation effects; D018698:Glutamic Acid / Q000378:metabolism* / Q000494:pharmacology; D066298:In Vitro Techniques; D007608:Kainic Acid / Q000031:analogs & derivatives / Q000494:pharmacology; D008297:Male; D009474:Neurons / Q000187:drug effects / Q000502:physiology* / Q000528:radiation effects; D009842:Oligopeptides / Q000494:pharmacology; D018408:Patch-Clamp Techniques / Q000379:methods; D051381:Rats; D017207:Rats, Sprague-Dawley; D013116:Spinal Cord / Q000166:cytology*; D009435:Synaptic Transmission / Q000187:drug effects* / Q000502:physiology
chemical_list: D001581:Benzothiadiazines; D004791:Enzyme Inhibitors; D027342:Excitatory Amino Acid Transporter 2; D009842:Oligopeptides; C048439:gamma-glutamyl-glycyl-glycine; D018698:Glutamic Acid; C020889:dihydrokainic acid; C004639:cyclothiazide; D007608:Kainic Acid