Central and peripheral changes in oxygenation and temperatures induced by intravenous nicotine in freely moving male rats.

It is well established that nicotine exerts reinforcing effects through actions on central nicotinic receptors. However, systemically delivered nicotine acts on numerous central and peripheral receptors, inducing generalized neural activation and changing multiple physiological parameters. In this study, we used oxygen sensors coupled with amperometry to examine changes in oxygen levels in the nucleus accumbens (NAc) and a peripheral location induced in freely moving male rats by intravenous nicotine. At low, physiologically relevant doses, nicotine (10, 30, and 90 µg/kg) dose-dependently increased oxygen levels in the NAc while decreasing oxygen levels in the subcutaneous space. NAc oxygen increases emerged within seconds of injection onset and preceded peripheral oxygen decreases. These responses were negatively correlated, with the strongest relationship observed at the 90 µg/kg dose. Nicotine also dose-dependently increased NAc temperature and decreased it in the subcutaneous space. In contrast to second-scale oxygen increases, brain temperature increases developed gradually and persisted for several minutes after oxygen levels had returned to baseline. Oxygen and temperature changes in the subcutaneous space were strongly correlated, whereas NAc oxygen and temperature exhibited a more complex temporal relationship, characterized by rapid oxygen increases followed by delayed temperature elevations. These findings demonstrate that intravenous nicotine rapidly induces opposite oxygen responses within central and peripheral domains, consistent with peripheral vasoconstriction and cerebral vasodilation. The exceptionally short latency of brain oxygen increases supports the view that peripheral nicotinic receptor activation and sensory signaling contribute to nicotine-induced neural activation and associated physiological responses.