Alzheimer’s disease is a progressive neurodegenerative disease associated with the buildup of amyloid-β protein. Toxic amyloid-β oligomers (AβOs) are known to impair the function of excitatory synapses of the hippocampus, leading to deficits in synaptic plasticity, loss of synaptic structure, and eventual neuronal death. Pannexin-1 (Panx1) is a membrane channel which has an emerging role in central nervous system physiology and pathophysiology. My thesis investigates the contribution of Panx1 to these AβO induced degenerative events by using fluorescence imaging, immunoblotting, and electrophysiology techniques on in vitro primary neuronal cultures and acute hippocampal slices. Here I demonstrate that the activity of Panx1 channels is facilitated by AβO treatment following the stimulation of NMDA receptors. However, KO of Panx1 failed to ameliorate AβO induced synaptic degeneration or deficits in long-term potentiation.