Procalcitonin contributes to hippocampal neuronal damage and impairment of LTP: implications for cognitive dysfunction in LPS-induced neuroinflammation rat model.

Abstract

Bacterial meningitis (BM) can lead to cognitive impairment, seriously affecting patients' quality of life. Our previous study demonstrated a significant increase in procalcitonin (PCT) levels in cerebrospinal fluid (CSF) in BM patients, but the functional implications remain unknown. We found high expression of PCT in the hippocampus of LPS-induced neuroinflammation models. PCT had a neurotoxic effect on the primarily cultured hippocampal neurons. The high dose of PCT induced neuronal apoptosis. The low dose of PCT impaired the arborization of hippocampal neurons and reduced the expression of the growth-associated protein-43 (GAP-43) and synaptophysin (SYN). Furthermore, long-term potentiation (LTP) in hippocampal brain slices was decreased after PCT perfusion ex vivo. Our results indicated that PCT had neurotoxic effects on neuronal survival and synaptic plasticity, potentially leading to cognitive impairment after BM.