Post-translational regulation of an Aplysia glutamate transporter during long-term facilitation

Authors

Maria Sol Collado, University of Houston, Department of Biology & Biochemistry, 369 Science and Research II, Houston, TX 77204-5001
Omar Khabour, University of Houston, Department of Biology & Biochemistry, 369 Science and Research II, Houston, TX 77204-5001
Diasinou Fioravante, University of Texas Medical School at Houston, Department of Neurobiology and Anatomy, Houston, TX 77225
John H. Byrne, University of Texas Medical School at Houston, Department of Neurobiology and Anatomy, Houston, TX 77225
Arnold Eskin, University of Houston, Department of Biology & Biochemistry, 369 Science and Research II, Houston, TX 77204-5001

Publication Date

1-2009

Journal

Journal of Neurochemistry

Abstract

Regulation of glutamate transporters accompanies plasticity of some glutamatergic synapses. The regulation of glutamate uptake at the Aplysia sensorimotor synapse during long-term facilitation (LTF) was investigated. Previously, increases in levels of ApGT1 (Aplysia glutamate transporter 1) in synaptic membranes were found to be related to long-term increases in glutamate uptake. In this study, we found that regulation of ApGT1 during LTF appears to occur post-translationally. Serotonin (5-HT) a transmitter that induces LTF did not increase synthesis of ApGT1. A pool of ApGT1 appears to exist in sensory neuron somata, which is transported to the terminals by axonal transport. Blocking the rough endoplasmic reticulum-Golgi-trans-Golgi network (TGN) pathway with Brefeldin A prevented the 5-HT-induced increase of ApGT1 in terminals. Also, 5-HT produced changes in post-translational modifications of ApGT1 as well as changes in the levels of an ApGT1-co-precipitating protein. These results suggest that regulation of trafficking of ApGT1 from the vesicular trafficking system (rough endoplasmic reticulum-Golgi-TGN) in the sensory neuron somata to the terminals by post-translational modifications and protein interactions appears to be the mechanism underlying the increase in ApGT1, and thus, glutamate uptake during memory formation.

Keywords

Animals, Aplysia, Brefeldin A, Cells, Cultured, Colchicine, Electric Stimulation, Excitatory Amino Acid Transporter 2, Ganglia, Invertebrate, Gene Expression Regulation, Glutamic Acid, Long-Term Potentiation, Protein Synthesis Inhibitors, Sensory Receptor Cells, Serotonin, Synaptosomes, Time Factors

Comments

PMCID: PMC2684684