Lithium is a primary treatment for patients with bipolar disorder, effectively managing the extreme mood swings. However, side effects of lithium treatment including increased thirst often lead to significant discomfort and potentially impact patient compliance with the medication regimen. In an effort to understand the underlying mechanisms of lithium-induced thirst, we have conducted studies using mice as a model organism. These studies involve administering lithium chloride (LiCl) either through intraperitoneal injections or by supplementing lithium salts into the animals' diet. Observations from these experiments indicate that mice exhibit a noticeable increase in water intake following lithium treatment, suggesting a direct effect of lithium on thirst regulation. To further understand the neurobiological underpinnings of this phenomenon, we conducted electrophysiological recordings from specific types of neurons in brain areas known to regulate thirst and fluid balance. By investigating the central mechanisms through which lithium salts induce thirst in mice, we aim to gain insights that could lead to improved management of this side effect in humans, enhancing the overall effectiveness and tolerability of lithium therapy for bipolar disorder. This research not only contributes to our understanding of lithium's pharmacological profile but also underscores the importance of addressing side effects to optimize therapeutic outcomes for patients with psychiatric conditions.