Introduction: Alzheimer's disease (AD) is a neurodegenerative central nervous system (CNS) disorder. AD is characterized pathophysiologically by regional neuronal loss. This loss may result from an excitotoxic process in which glutamate transporters may play an important role. Amyloid precursor protein (APP23) transgenic mice, a unique AD model, are known to cause early-onset familial AD. Until now, not much is known with respect to the glutamate transporters in AD. These transporters regulate excitatory neurotransmission and prevent glutamate-mediated excitotoxicity in the CNS. Three vesicular glutamate transporters (vGlut1-3) load glutamate up into synaptic vesicles. Glutamate transporter-1 (Glt-1) and glutamate aspartate transporter (Glast), the 2 glial high-affinity Na+/K+-dependent glutamate transporters, are responsible for removing extracellular glutamate in the CNS.
Aim: In the present study, the possible changes in hippocampal expression level of the vGlut1-3, Glt-1 and Glast are examined by means of semi-quantitative Western blotting in 8 month old wild type (WT) and APP23 mice.
Results: There is no change in expression in vGlut1 and vGlut2. On the contrary, there is a tendency to a downregulated expression in vGlut3 in APP23. Glast is significantly downregulated in APP23 mice compared to the WT mice and this is also the tendency for Glt-1.
Discussion: The possible elevation of glutamate in the synaptic cleft is probably not due to an enhanced expression of the vGlut1, but can be a consequence of a decreased expression of Glt-1 and Glast.
Original languageEnglish
Title of host publicationBelgisch Genootschap voor Fundamentele en Klinische Fysiologie en Farmacologie
Publication statusPublished - 17 Nov 2007

    Research areas

  • glutamate transporters, APP23 model

ID: 1751521