Oral Administration of Probiotic Bifidobacterium breve Improves Facilitation of Hippocampal Memory Extinction via Restoration of Aberrant Higher Induction of Neuropsin in an MPTP-Induced Mouse Model of Parkinson's Disease

We previously reported that 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine-induced Parkinson's disease (PD) model mice (PD mice) facilitate hippocampal memory extinction, which may be the cause of cognitive impairment in PD. Recent studies on the consumption of probiotics have reported a variety of beneficial effects on the central nervous system via the microbiota-gut-brain axis. In this study, we investigated the effects of oral administration of Bifidobacterium breve strain A1 [MCC1274] (B. breve A1) on the facilitation of hippocampal memory extinction observed in PD mice. We found that four-day consecutive oral administration of B. breve A1 restored facilitation of contextual fear extinction in PD mice. Hippocampal mRNA expression levels of postsynaptic density protein-95 and synaptophysin significantly decreased in the PD mice, but mRNA and protein expression levels of neuropsin increased. Furthermore, CA1 apical spine density was significantly reduced in PD mice. On the other hand, administration of B. breve Al to PD mice recovered all these expression levels and the CA1 spine density to control levels. These results suggest that increased induction of neuropsin is involved in abnormal changes in hippocampal synaptic plasticity, and that B. breve A1 imposes reins on its expression, resulting in the restoration of abnormal hippocampal synaptic plasticity and the facilitation of fear extinction in PD mice.

Automated summary

The study showed that oral administration of Bifidobacterium breve strain A1 could reverse the facilitation of hippocampal memory extinction in PD mice, restoring abnormal changes in synaptic plasticity and facilitating fear extinction through regulating neuropsin expression levels.