In this study we evaluated the time dependence in cadmium-nicotine interaction and its effect on motor function, anxiety linked behavioural changes, serum electrolytes, and weight after acute and chronic treatment in adult male mice. Animals were separated randomly into four groups of n = 6 animals each. Treatment was done with nicotine, cadmium, or nicotine-cadmium for 21 days. A fourth group received normal saline for the same duration (control). Average weight was determined at 7-day interval for the acute (D1-D7) and chronic (D7-D21) treatment phases. Similarly, the behavioural tests for exploratory motor function (open field test) and anxiety were evaluated. Serum electrolytes were measured after the chronic phase. Nicotine, cadmium, and nicotine-cadmium treatments caused no significant change in body weight after the acute phase while cadmium-nicotine and cadmium caused a decline in weight after the chronic phase. This suggests the role of cadmium in the weight loss observed in tobacco smoke users. Both nicotine and cadmium raised serum Ca2+ concentration and had no significant effect on K+ ion when compared with the control. In addition, nicotine-cadmium treatment increased bioaccumulation of Cd2+ in the serum which corresponded to a decrease in body weight, motor function, and an increase in anxiety. 1. Introduction Wide arrays of behavioural and physiological responses have reportedly been observed following nicotine use either in tobacco smoke or as a pure drug [1]. In human abusers and rodent models, weight loss, anxiety, depression, and motor dysfunctions are among the most frequently reported behavioural changes [2–4]. Long and short term use of nicotine in tobacco smoke alter synaptic function, neurotransmitter level, and the anatomical structure of the brain to varying extents. Similarly, the addictive effect of nicotine in tobacco smoke is known to potently alter the expression of cholinergic receptors, serum level of ions, and neurotransmission (central and peripheral) [5]. Primarily, nicotine, being a structural analogue of acetylcholine, potentiates the receptors and facilitates the increase in intracellular Ca2+ concentration, vesicle formation, and neurotransmission at synapses and neuromuscular junctions. However, prolonged excitation of cholinergic synapses by nicotine leads to excitotoxicity and synaptic dysfunction, observed in prolonged use and abuse of nicotine [6–11]. Although nicotine gets into the body through various means—such as chewing of tobacco leaves and absorption of nicotine through the skin [12, 13]—the most
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