Amyloid Precursor Protein Immunohistochemical Changes in the Occipital Cerebral Cortex of Newborn Mice Affected by Prenatal Ketamine Exposure

Background: B-amyloid plaque is a lesion in the brain’s gray matter, imaging studies show significant Ab aggregation in the occipital lobes. This inflammatory reaction causes neuronal impairment and neurotoxicity. Ketamine, an NMDA receptor blocker used in pediatrics, can cause neuronal death or neurodegeneration during embryonic phases, as animal trials have shown.

Objectives: The study investigates the effects of therapeutic doses of ketamine on the occipital cerebral cortices of newborn mice to inform scientific decisions on its potential adverse effects.

Materials and Methods: This experiment involved 60 pregnant female mice from a lab. The mice were divided into control and experimental groups. After birth, the newborn mice were preserved in formalin, and brain tissue was embedded. Immunohistochemical staining was performed on the brain tissue, and the pattern of anti-amyloid precursor protein expression was determined. The results were analyzed using a t test and SPSS version 26.

Results: The study analyzed the immunohistochemical labeling patterns in the occipital cerebral cortex of neonate mice. The control group showed a negative pattern with no visible tissue or cell arrangements. The experimental group showed brown staining and immunohistochemical labeling with varying intensity and shapes. Brown DAP depositions were observed in both superficial and deep layers. The study found a significant difference (P ≤ 0.000) in strongly positive pixels in the experimental group compared to the control group.

Conclusion: The study reveals varying amyloid precursor protein reactivity and apoptosis in mice following prenatal ketamine therapy, with β-amyloid accumulation potentially contributing to these changes.