Paracetamol is one of the most frequently used drugs against pain and fever in both adults and children. It has earlier been shown that neonatal paracetamol administration can cause altered adult spontaneous behavior and cognitive dysfunction in mice. There is also evidence from epidemiological studies showing association between prenatal exposure to paracetamol and adverse outcomes later in life. These adverse effects may have been produced by changes in proteins important for normal brain development, during the brain growth spurt.
Mice were exposed to either paracetamol, cannabinoid receptor type 1 (CB1R) agonist Win 55212-2 or the combination of both substances on postnatal day 10 (PND10). Slot blot analysis was used to determine the levels of the neuroprotein markers CaMKII, GAP-43, GluR1, PSD95, tau and synaptophysin in both frontal and parietal cortex. Analysis showed a significant decrease in protein levels for GluR1, PSD95 and synaptophysin in parietal cortex for mice, neonatally exposed to paracetamol. These results support earlier findings and we conclude, that paracetamol acts as a neurological toxin during brain development.