The dosage used for pre-treatment was applied in the study evaluating chronic lithium treatment starting at 22 hpi, and resulted in serum levels of max. 0.22 mmol/l at P35. An increase to 110 mg kg21 d21 did not increase serum concentrations at P35, although lithium serum concentrations of 1.97 mmol/l and 2.64 mmol/l were measured in two infected animals euthanized on P16. An effect of LiCl therapy, at the measured serum concentrations, may be due to the higher lithium serum levels that are reached at a younger age since serum concentrations primarily depend on renal function which is lower in infant rats. This is due to the fact that lithium is not metabolized or Eupalinilide-B bound to any proteins and urinary concentrating ability is fully developed at around 6 weeks of age. Alterations of renal clearance, volume of distribution or other adaptations in the infant rat may be responsible for the different lithium serum concentrations measured at a different age. In the present study in rats that survived PM, lithium led to significantly improved learning performance during probe trials compared to NaCl. The time and distance to reach the platform during training trials decreased in all groups, without reaching statistical significance when comparing animals with LiCl therapy to their littermates receiving NaCl. In earlier studies, chronic lithium treatment improved spatial memory assessed in a water maze during different conditions, Chrysophanol-8-O-β-D-glucopyranoside traumatic brain injury. A correlation between hippocampal neurogenesis and learning has been described earlier. Lithium has been shown to increase neurogenesis, e.g. evidenced by enhanced BrdU labelling of cells in the DG and double-labelling with NeuN. Also, an effect on long-term potentiation has been observed earlier. Immature neurons appear to become involved in spatial memory at 15–20 days of age in rats. Most immature cells die within the first 2 weeks after proliferation, while training during days 6–10 following BrdU injection enhanced survival. PM increases the proliferation of neuronal progenitor cells in the first week after infection with a peak around 2 days post-infection and thereafter declines to basal levels. However, this increase in proliferation does not prevent learning deficits.