The Hippocampal Glutamate/GABA System is Affected by Aging but not by an Alzheimer’s Disease-Like Pathology in Rats

Abstract

Glutamate and GABA are the most abundant neurotransmitters in the CNS and play a critical role in synaptic stability and plasticity. Glutamate and GABA homeostasis is important for healthy aging and for reducing the risk for various neurological diseases including Alzheimer’s disease (AD). Here we analyzed age-dependent alterations of expression of glutamate, GABA, and enzymes that synthesize them (glutaminase, glutamine synthetase, GABA-T, and GAD67), transporters (GLAST, GLT1, and GAT1), and relevant receptors (GluA1, NMDAR1, NMDA2B, and GABAAr1) in the whole hippocampus of Wistar rats and of senescence-accelerated OXYS rats. The latter are considered a suitable model of the most common (sporadic) type of AD. Our results suggest that in the hippocampus, there is a significant decline of glutamate and GABA signaling with aging (in Wistar rats), but in OXYS rats, there are no significant changes or compensatory enhancements in this system within the hippocampus during the development of neurodegenerative processes that are characteristic of AD.