Poster Session 1 - B1
1,3Aeen Ebrahim Amini, 1John Georgiou, 2Changiz Taghibiglou, 1,3Graham L. Collingridge
1 Lunenfeld-Tanenbaum Research Institute, Mount Sinai Hospital; 2 Department of Pharmacology, University of Saskatchewan; 3 Department of Physiology, University of Toronto
α-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid receptors (AMPARs) are the major neurotransmitter receptors in the brain that are involved in glutamate-based neuronal communication. Increases and decreases in AMPAR number, distribution, and efficacy represent some of the mechanisms that neurons employ to modulate their communication strength, which is known as synaptic plasticity. Defects in synaptic plasticity may be responsible for many brain disorders including Alzheimer’s disease (AD). It has been shown that beta-amyloid oligomers bind the cellular prion protein (PrPC), a cell-surface glycoprotein with many physiological functions such as cellular differentiation, adhesion and control of cell morphology. However, the role of PrPC in synaptic plasticity and learning and memory remains obscure. We used electrophysiological techniques to explore the function of PrPC at CA1 synapses in the hippocampus, a region critical for learning and memory and preferentially affected in AD. Preliminary data suggest that C57BL/6J-Prnp knockout mice have enhanced long-term potentiation. The input/output function of synaptic transmission and paired-pulse potentiation were unaffected. Ongoing investigations will confirm these initial findings and examine the role of glutamate receptors in PrPC–dependent modulation of synaptic plasticity. We conclude that PrPC may serve to limit synaptic potentiation.