Laura Medina-Ceja1, Flavio Sandoval-García, Kenia Pardo-Peña. 1. Laboratorio de Neurofisiología y Neuroquímica, Departamento de Biología Celular y Molecular, CUCBA, Universidad de Guadalajara, Guadalajara, Jalisco, Mexico. lmedina@cucba.udg.mx
Abstract
BACKGROUND AND AIMS: Glutamate and GABA transporters are cell surface proteins localized on neurons and glial cells that mediate the reuptake of glutamate and GABA from the extracellular space. In different models of the acquisition of epilepsy, important changes in the expression of these transporters have been demonstrated, although to date no such studies have been performed using the monosodium glutamate (MSG)-induced seizure model in neonatal rats. METHODS: Following repeated MSG administration, we used immunofluorescence techniques to quantify the number of cells expressing the EAAT-3 and GAT-1 transporters at postnatal days (PD) 14 and 60 in the dentate gyrus (DG) and CA1 region of the hippocampus. RESULTS: EAAT-3 and GAT-1 were expressed around the soma of granular cells and in the soma and dendrites of pyramidal cells in both experimental (MSG) and control (NaCl) rats. In the DG, MSG administration significantly increased the number of granular cells double-labelled for EAAT-3/Neun at PD 60 but not PD 14. No significant changes were observed at either PD 14 or 60 in terms of the number of cells expressing GAT-1 in the DG or CA1. CONCLUSIONS: The findings suggest that the selective long-term increase in EAAT-3 expression in granular cells following neonatal MSG treatment reflects an important compensatory or protective response to the excitotoxic and seizure-promoting effects of early glutamate exposure in adult animals.
BACKGROUND AND AIMS: Glutamate and GABA transporters are cell surface proteins localized on neurons and glial cells that mediate the reuptake of glutamate and GABA from the extracellular space. In different models of the acquisition of epilepsy, important changes in the expression of these transporters have been demonstrated, although to date no such studies have been performed using the monosodium glutamate (MSG)-induced seizure model in neonatal rats. METHODS: Following repeated MSG administration, we used immunofluorescence techniques to quantify the number of cells expressing the EAAT-3 and GAT-1 transporters at postnatal days (PD) 14 and 60 in the dentate gyrus (DG) and CA1 region of the hippocampus. RESULTS:EAAT-3 and GAT-1 were expressed around the soma of granular cells and in the soma and dendrites of pyramidal cells in both experimental (MSG) and control (NaCl) rats. In the DG, MSG administration significantly increased the number of granular cells double-labelled for EAAT-3/Neun at PD 60 but not PD 14. No significant changes were observed at either PD 14 or 60 in terms of the number of cells expressing GAT-1 in the DG or CA1. CONCLUSIONS: The findings suggest that the selective long-term increase in EAAT-3 expression in granular cells following neonatal MSG treatment reflects an important compensatory or protective response to the excitotoxic and seizure-promoting effects of early glutamate exposure in adult animals.