The brain-derived neurotrophic factor BDNF, which regulates neurogenesis and brain plasticity, mediates the neuroprotective action of the mood stabilizer lithium, which is commonly used in psychiatry. However, it remains unclear whether lithium affects BDNF levels in neonatal brain structures that differ in the maturity levels during ontogeny. Here, we studied the acute effects of lithium chloride (LiCl) treatment on the BDNF levels and levels of the apoptosis marker active caspase-3 in the brainstem and cortex of 3-day-old rats. Lithium increased the BDNF levels in both the brainstem and cortex of rat pups 2 h after injection. In the brainstem, which is more developed at postnatal day 3 in comparison to the cortex, the lithium-induced increase in the BDNF levels was accompanied by a 2-fold decrease in the levels of active caspase-3. These results show that the neuroprotective effects of LiCl treatment in the developing mammalian brain depend on the maturity level of the neonatal brain regions that are affected by the mood stabilizer.