Abstract 1412 Nicotine-Induced Changes in Microglial ATP Responses: Role of Mitochondrial and ER Calcium Regulation

Nicotine exposure contributes to cardiovascular and neurodegenerative diseases through its modulatory effects on inflammatory processes. In the brain, microglia serve as primary immune cells whose functions, including cytokine release, phagocytosis, and synaptic maintenance, are critically regulated by ATP-dependent purinergic signaling. While nicotine acts through nicotinic acetylcholine receptors (nAChRs) to influence microglial activity, its effects on purinergic signaling remain unclear. Using human microglia HMC3 cells, we investigated how nicotine exposure (1-10 μM, 72 hours) alters calcium signaling dynamics.