Nicotine and Integrin Linked Kinase Interplay Modulates Synaptic Plasticity Mechanisms Required for Memory

Abstract

Integrin Linked Kinase (ILK) has been associated with forms of synaptic plasticity required for memory. Nicotine, at low-concentration improves memory but higher concentrations impart learning and memory deficits. The relationship between nicotine and ILK, with regards to learning and memory, has yet to be investigated. In this study, I demonstrate the effect of different concentrations of nicotine on ILK and subsequent downstream signaling using H-19 rat hippocampal cells. In addition, I also show the differential modulation of synaptic plasticity by varying concentrations of nicotine is due to altered expression and function of synaptic nicotinic receptors. Our results indicate that nicotine affects cell viability, modulates ILK activity, micro-spine formation, and long term potentiation. Furthermore, nicotine also differentially modulated extracellular signal regulated kinase 1/2 (ERK1/2) required for synaptic plasticity. My data provides a novel mechanism by which nicotine modulates synaptic transmission and plasticity required for learning and memory.